p.1
2024 ESC Guidelines for the management
of peripheral arterial and aortic diseases
Developed by the task force on the management of peripheral arterial and aortic diseases of the European Society of Cardiology (ESC) Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS), the European Reference Network on Rare Multisystemic Vascular Diseases (VASCERN), and the European Society of Vascular Medicine (ESVM) Authors/Task Force Members: Lucia Mazzolai *†, (Chairperson) (Switzerland), Gisela Teixido-Tura ‡, (Task Force Co-ordinator) (Spain), Stefano Lanzi ‡, (Task Force Co-ordinator) (Switzerland), Vinko Boc (Slovenia), Eduardo Bossone (Italy), Marianne Brodmann 1 (Austria), Alessandra Bura-Rivière (France), Julie De Backer 2 (Belgium), Sebastien Deglise (Switzerland), Alessandro Della Corte (Italy), Christian Heiss (United Kingdom), Marta Kałużna-Oleksy (Poland), Donata Kurpas (Poland), Carmel M. McEniery (United Kingdom), Tristan Mirault (France), Agnes A. Pasquet (Belgium), Alex Pitcher (United Kingdom), Hannah A.I. Schaubroeck (Belgium), Oliver Schlager (Austria), Per Anton Sirnes (Norway), Muriel G. Sprynger (Belgium), Eugenio Stabile (Italy), Françoise Steinbach (France), Matthias Thielmann (Germany), Roland R.J. van Kimmenade (Netherlands), Maarit Venermo (Finland), Jose F. Rodriguez-Palomares *†, (Chairperson) (Spain), and ESC Scientific Document Group
* Corresponding authors: Lucia Mazzolai, Department of Angiology, Lausanne University Hospital (CHUV), and Medical School, Lausanne University (UNIL) Lausanne, Switzerland. Tel: +41 (0)21 314 0750. Email: Lucia. Mazzolai@chuv.ch; and Jose F. Rodriguez-Palomares, Cardiovascular Imaging Section and Aortic Diseases Unit (VASCERN), Department of Cardiology, Vall d’Hebron Hospital Universitari, Vall d’Hebron Barcelona Hospital Campus, Vall d′Hebron Institut de Recerca (VHIR), Barcelona, Spain, and Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares, Instituto de Salud Carlos III, Madrid, Spain, and Department of Medicine, Universitat Autònoma de Barcelona, Spain. Tel: +34 93 882 3881. Email: josefernando.rodriguez@vallhebron.cat
† The two Chairpersons contributed equally to the document and are joint corresponding authors. ‡ The two Task Force Co-ordinators contributed equally to the document. Author/Task Force Member affiliations are listed in author information. 1 Representing the European Society of Vascular Medicine (ESVM) 2 Representing the European Reference Network on Rare Multisystemic Vascular Diseases (VASCERN) ESC Clinical Practice Guidelines (CPG) Committee: listed in the Appendix. ESC subspecialty communities having participated in the development of this document: Associations: Association for Acute CardioVascular Care (ACVC), Association of Cardiovascular Nursing & Allied Professions (ACNAP), European Association of Cardiovascular Imaging (EACVI), European Association of Preventive Cardiology (EAPC), European Association of Percutaneous Cardiovascular Interventions (EAPCI), Heart Failure Association (HFA). Councils: Council for Cardiology Practice, Council on Hypertension. Working Groups: Adult Congenital Heart Disease, Aorta and Peripheral Vascular Diseases, Cardiovascular Surgery, Thrombosis. Patient Forum © The European Society of Cardiology 2024. All rights reserved. For permissions, please email: journals.permissions@oup.com. No part of this publication may be reproduced, stored in a retrieval system, transmitted, used for text and data mining, or used for training artificial intelligence, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by license or under terms agreed with the appropriate reprographics rights organization. Inquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above. ESC Guidelines are protected by copyright. As per opt out option under Article 4 §3 of EU Directive 2019/790, the European Society of Cardiology (ESC) reserves all rights to license uses of ESC Guidelines to train or develop generative artificial intelligence (AI) models, large language models or other deep learning or machine learning models.
European Heart Journal (2024) 45, 3538–3700 https://doi.org/10.1093/eurheartj/ehae179
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.2
Document Reviewers: Alessia Gimelli, (CPG Review Co-ordinator) (Italy), Jean-Baptiste Ricco, (CPG Review Co-ordinator) (France), Elena Arbelo (Spain), Christian-Alexander Behrendt (Germany), Michael Böhm (Germany), Michael A. Borger (Germany), Margarita Brida (Croatia), Sergio Buccheri (Sweden), Gill Louise Buchanan (United Kingdom), Christina Christersson (Sweden), Gert J. de Borst (Netherlands), Marco De Carlo (Italy), Roman Gottardi (Austria), Lydia Hanna (United Kingdom), Lynne Hinterbuchner (Austria), Borja Ibanez (Spain), Ignatios Ikonomidis (Greece), Stefan James (Sweden), Thomas Kahan (Sweden), Klaus Kallenbach2 (Luxemburg), Lars Køber (Denmark), Konstantinos C. Koskinas (Switzerland), Juraj Madaric1 (Slovakia), Blandine Maurel (France), John William McEvoy (Ireland), Gil Meltzer (Israel), Borislava Mihaylova (United Kingdom), Richard Mindham (United Kingdom), Ioana Mozos (Romania), Jens Cosedis Nielsen (Denmark), Eva Prescott (Denmark), Amina Rakisheva (Kazakhstan), Barbara Rantner (Germany), Bianca Rocca (Italy), Xavier Rossello (Spain), Jean Paul Schmid (Switzerland), Daniel Staub (Switzerland), Sabine Steiner (Germany), Isabella Sudano (Switzerland), Martin Teraa (Netherlands), Ilonca Vaartjes (Netherlands), Rafael Vidal-Perez (Spain), Christiaan Vrints (Belgium), and Katja Zeppenfeld (Netherlands)
All experts involved in the development of these guidelines have submitted declarations of interest which are reported in a supplementary document to the guidelines. See the European Heart Journal online or https://www.escardio.org/Guidelines for supplementary documents as well as evidence tables
Disclaimer. The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientific and medical knowledge and the evidence available at the time of their publication. The ESC is not responsible in the event of any contradiction, discrepancy and/or ambiguity between the ESC Guidelines and any other official recommendations or guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged to take the ESC Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the implementation of preventive, diagnostic or therapeutic medical strategies; however, the ESC Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient’s health condition and in consultation with that patient and, where appropriate and/or necessary, the patient’s caregiver. Nor do the ESC Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient’s case in light of the scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professional’s responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription. The ESC warns readers that the technical language may be misinterpreted and declines any responsibility in this respect.
Permissions. The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only. No commercial use is authorized. No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC. Permissions can be obtained upon submission of a written request to Oxford University Press, the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC (journals.permissions@oup.com).
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - Keywords Guidelines • Acute aortic syndrome • Aortic aneurysm • Aortic atherosclerosis • Aortic dissection • Aortic surgery • Carotid artery disease • Chronic limb-threatening ischaemia • Endovascular repair • Exercise • Genetic aortic diseases • Intramural haematoma • Lower extremity artery disease • Penetrating atherosclerotic ulcer • Peripheral arterial disease • Polyvascular disease • Renal artery disease
ESC Guidelines 3539
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.3
Table of contents
1. Preamble .............................................................................................................. 3547 2. Introduction ....................................................................................................... 3548 3. What is new ....................................................................................................... 3550 4. Epidemiology and risk factors ..................................................................... 3558 4.1. Epidemiology ............................................................................................ 3558 4.2. Risk factors ................................................................................................ 3559 5. Evaluation of peripheral arteries and aorta .......................................... 3560 5.1. Clinical history and examination, and laboratory assessment, in patients with peripheral arterial and aortic diseases .................. 3560 5.2. Functional and quality of life assessment in patients with peripheral arterial and aortic diseases ................................................... 3560 5.3. Vascular examination of peripheral arteries ............................... 3561 5.3.1. Duplex ultrasound ......................................................................... 3562 5.3.2. Digital subtraction angiography, computed tomography angiography, and magnetic resonance angiography ..................... 3562 5.4. Evaluation of the aorta ......................................................................... 3562 5.4.1. Aortic measurements ................................................................... 3562 5.4.2. Normal aortic values ..................................................................... 3565 5.4.3. Chest X-ray and electrocardiogram ....................................... 3565 5.4.4. Echocardiography ........................................................................... 3565 5.4.5. Duplex ultrasound imaging of the abdominal aorta ........ 3566 5.4.6. Cardiovascular computed tomography ................................ 3566 5.4.7. Cardiovascular magnetic resonance ....................................... 3566 5.4.8. Positron emission tomography ................................................. 3566 5.4.9. Intravascular ultrasound ............................................................... 3567 5.4.10. Digital subtraction aortography ............................................. 3567 6. Screening for carotid, peripheral arterial, and aortic diseases ..... 3567 6.1. Screening for carotid and peripheral arterial diseases ........... 3567 6.1.1. Lower-extremity peripheral arterial disease ....................... 3567 6.1.2. Carotid artery stenosis ................................................................ 3567 6.1.3. Multisite artery disease ................................................................. 3567 6.2. Screening for aortic diseases ............................................................. 3568 6.2.1. Screening for abdominal aortic aneurysm ........................... 3568 6.2.2. Screening for thoracic aortic aneurysm ................................ 3568 7. Optimal medical treatment ......................................................................... 3568 7.1. Lifestyle, exercise, patient education ............................................. 3568 7.1.1. Diet ....................................................................................................... 3568 7.1.2. Physical activity ................................................................................ 3569 7.1.3. Smoking ............................................................................................... 3570 7.1.4. Patient education ............................................................................ 3570 7.1.5. Risk scoring models in secondary prevention .................... 3570 7.2. Principles of pharmacological medical therapy .......................... 3571 7.2.1. Antithrombotic therapy ............................................................... 3571 7.2.2. Antihypertensive therapy ............................................................ 3571 7.2.2.1. Renovascular hypertension ................................................ 3571 7.2.3. Lipid-lowering therapy ................................................................. 3572 7.2.3.1. Statins .......................................................................................... 3572 7.2.3.2. Ezetimibe ................................................................................... 3572 7.2.3.3. Proprotein convertase subtilisin/kexin type 9 inhibitors .................................................................................................... 3572 7.2.3.4. Bempedoic acid ....................................................................... 3572 7.2.3.5. Hypertriglyceridaemia .......................................................... 3572 7.2.4. Diabetes and pre-diabetes conditions ................................... 3573 7.2.5. Other pharmacological therapy ............................................... 3574 8. Peripheral arterial disease ............................................................................ 3574 8.1. Lower-extremity peripheral arterial disease .............................. 3574 8.1.1. Peripheral arterial disease syndromes ................................... 3574 8.1.1.1. Clinical presentation and diagnosis ................................. 3574 8.1.1.1.1. Diagnostic tests .............................................................. 3575 8.1.1.1.2. Imaging methods ............................................................ 3576 8.1.1.2. Medical treatment .................................................................. 3578 8.1.1.2.1. Exercise therapy ............................................................ 3578 8.1.1.2.2. Pharmacological treatment ....................................... 3582 8.1.1.2.3. Aorto-iliac lesion revascularization ........................ 3583 8.1.1.2.4. Femoro-popliteal lesion revascularization .......... 3584 8.1.1.2.5. Below-the-knee artery revascularization ........... 3584 8.1.1.3. Follow-up ................................................................................... 3585 8.1.2. Chronic limb-threatening ischaemia ....................................... 3585 8.1.2.1. Clinical presentation and diagnosis ................................. 3585 8.1.2.1.1. Definition .......................................................................... 3585 8.1.2.1.2. Initial assessment and risk of amputation ........... 3585 8.1.2.1.3. Imaging ............................................................................... 3585 8.1.2.1.4. Mortality risk assessment ........................................... 3585 8.1.2.2. Medical treatment .................................................................. 3586 8.1.2.3. Interventional treatment ..................................................... 3586 8.1.2.3.1. Revascularization ............................................................ 3586 8.1.2.3.2. Spinal cord stimulation ................................................ 3587 8.1.2.3.3. Amputation ...................................................................... 3587 8.1.2.4. Follow-up ................................................................................... 3587 8.1.3. Acute limb ischaemia .................................................................... 3587 8.1.3.1. Clinical presentation and diagnosis ................................. 3587 8.1.3.1.1. Clinical examination ..................................................... 3588 8.1.3.1.2. Imaging and functional tests ...................................... 3588 8.1.3.2. Medical treatment .................................................................. 3588 8.1.3.3. Surgical and interventional treatment ........................... 3588 8.1.3.4. Follow-up ................................................................................... 3590 8.2. Extracranial carotid and vertebral artery disease ..................... 3590 8.2.1. Clinical presentation and diagnosis ......................................... 3590 8.2.1.1. Clinical presentation ............................................................. 3590 8.2.1.2. Diagnosis .................................................................................... 3590 8.2.2. Asymptomatic carotid artery stenosis .................................. 3591 8.2.2.1. Medical treatment .................................................................. 3591 8.2.2.1.1. Lipid-lowering therapy ................................................ 3591 8.2.2.1.2. Antihypertensive therapy ........................................... 3591 8.2.2.1.3. Glucose-lowering therapy ......................................... 3591 8.2.2.1.4. Antithrombotic therapy ............................................. 3591 8.2.2.2. Interventional treatment ..................................................... 3592 8.2.2.2.1. Open surgery vs. medical therapy ......................... 3592 8.2.2.2.2. Carotid revascularization: surgery vs. stenting . 3592 8.2.3. Symptomatic carotid artery stenosis ..................................... 3594 8.2.3.1. Medical treatment .................................................................. 3594 8.2.3.1.1. Lipid-lowering therapy ................................................ 3594 8.2.3.1.2. Antihypertensive therapy ........................................... 3594 8.2.3.1.3. Glucose-lowering therapy ......................................... 3594 8.2.3.1.4. Antithrombotic therapy ............................................. 3594 8.2.3.2. Interventional treatment ..................................................... 3595 8.2.3.2.1. Open surgery .................................................................. 3595 8.2.3.2.2. Endovascular therapy vs. open surgery ................ 3595 8.2.3.2.3. Vertebral arteries .......................................................... 3595 8.2.3.3. Follow-up ................................................................................... 3596 8.3. Other arterial locations ....................................................................... 3596 8.3.1. Subclavian artery disease ............................................................. 3596 8.3.1.1. Clinical presentation and diagnosis ................................. 3596 8.3.1.2. Treatment strategy (medical and interventional) ..... 3597 8.3.1.3. Follow-up ................................................................................... 3597 8.3.2. Renal artery disease ....................................................................... 3598 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.4
8.3.2.1. Clinical presentation and diagnosis ................................. 3598 8.3.2.1.1. Epidemiology ................................................................... 3598 8.3.2.1.2. Clinical presentation ..................................................... 3598 8.3.2.1.3. Diagnosis of renal artery disease ............................ 3598 8.3.2.1.4. Prognosis ........................................................................... 3598 8.3.2.2. Treatment strategy (medical and interventional) ..... 3598 8.3.2.2.1. Medical therapy .............................................................. 3598 8.3.2.2.2. Revascularization ............................................................ 3598 8.3.2.3. Follow-up ................................................................................... 3600 8.3.3. Visceral artery disease .................................................................. 3600 8.3.3.1. Acute mesenteric ischaemia .............................................. 3600 8.3.3.1.1. Clinical presentation and diagnosis ........................ 3600 8.3.3.1.2. Treatment strategy ....................................................... 3600 8.3.3.1.3. Follow-up .......................................................................... 3601 8.3.3.2. Chronic mesenteric artery disease ................................. 3601 8.3.3.2.1. Clinical presentation and diagnosis ........................ 3601 8.3.3.2.2. Treatment strategy ....................................................... 3602 8.3.3.2.3. Follow-up .......................................................................... 3602 9. Aorta ..................................................................................................................... 3602 9.1. Atheromatous disease of the aorta ............................................... 3602 9.1.1. General concepts ............................................................................ 3602 9.1.2. Treatment .......................................................................................... 3602 9.1.2.1. Primary prevention ................................................................ 3602 9.1.2.2. Secondary prevention .......................................................... 3602 9.2. Aortic aneurysms ................................................................................... 3603 9.2.1. General concepts ............................................................................ 3603 9.2.1.1. Definitions ................................................................................. 3603 9.2.2. Thoracic aortic aneurysms ......................................................... 3603 9.2.2.1. Aetiology, risk factors, and natural history ................. 3603 9.2.2.2. Ascending thoracic aorta and arch aneurysms ......... 3603 9.2.2.3. Descending thoracic aorta and thoracoabdominal aorta aneurysms ..................................................................................... 3604 9.2.2.4. Surveillance ............................................................................... 3607 9.2.3. Abdominal aortic aneurysms ..................................................... 3607 9.2.3.1. General concepts ................................................................... 3607 9.2.3.2. Aetiology, risk factors, and natural history ................. 3607 9.2.3.3. Surveillance ............................................................................... 3607 9.2.4. Optimal medical treatment of aortic aneurysms .............. 3609 9.2.5. Surgical management of aortic aneurysms .......................... 3609 9.2.5.1. Surgical treatment of aortic root and ascending aorta ............................................................................................................ 3609 9.2.5.2. Surgical treatment of aortic arch aneurysms ............. 3611 9.2.5.3. Surgical treatment of the thoracic descending aorta 3612 9.2.5.3.1. General considerations ............................................... 3612 9.2.5.3.2. Open repair ..................................................................... 3612 9.2.5.3.3. Endovascular repair ...................................................... 3612 9.2.5.4. Surgical treatment of thoracoabdominal aorta aneurysms ................................................................................................. 3612 9.2.5.4.1. General considerations ............................................... 3612 9.2.5.4.2. Open repair ..................................................................... 3612 9.2.5.4.3. Endovascular repair ...................................................... 3612 9.2.5.5. Surgical treatment of abdominal aorta aneurysms .. 3613 9.2.5.5.1. General considerations ............................................... 3613 9.2.5.5.2. Pre-operative cardiovascular evaluation and choice of treatment ......................................................................... 3613 9.2.5.5.3. Open abdominal aorta aneurysm repair ............. 3615 9.2.5.5.4. Endovascular abdominal aorta aneurysm repair 3615 9.2.6. Endoleaks ........................................................................................... 3615 9.2.7. Long-term follow-up after aortic repair ............................... 3617 9.2.7.1. Follow-up after thoracic aortic aneurysm treatment 3617 9.2.7.2. Follow-up after abdominal aortic aneurysm treatment ................................................................................................... 3617 9.3. Acute thoracic aortic syndromes .................................................... 3618 9.3.1. General concepts ............................................................................ 3618 9.3.1.1. Epidemiology and risk factors ........................................... 3618 9.3.1.1.1. Sex differences ................................................................ 3620 9.3.1.1.2. Chronobiology ................................................................ 3621 9.3.1.1.3. Outcomes ......................................................................... 3621 9.3.1.2. Clinical presentation ............................................................. 3622 9.3.1.3. Diagnostic work-up ............................................................... 3622 9.3.1.4. Therapeutic intervention in acute aortic dissection 3622 9.3.1.4.1. Initial treatment .............................................................. 3622 9.3.1.4.2. Type A aortic dissection interventional treatment .............................................................................................. 3623 9.3.1.4.3. Acute type B aortic dissection interventional treatment .............................................................................................. 3628 9.3.1.4.4. Chronic type B aortic dissection interventional treatment .............................................................................................. 3629 9.3.1.4.5. Management during pregnancy ................................ 3629 9.3.2. Intramural haematoma ................................................................. 3630 9.3.2.1. Diagnostic work-up ............................................................... 3630 9.3.2.2. Clinical outcomes ................................................................... 3630 9.3.2.3. Geographical variations ....................................................... 3630 9.3.2.4. Management ............................................................................. 3630 9.3.2.4.1. Type A intramural haematoma ............................... 3630 9.3.2.4.2. Type B intramural haematoma ................................ 3630 9.3.3. Penetrating atherosclerotic ulcer ............................................ 3631 9.3.3.1. Diagnosis .................................................................................... 3631 9.3.3.2. Treatment ................................................................................. 3631 9.3.4. Aortic pseudo-aneurysm ............................................................. 3632 9.3.5. Traumatic aortic injury ................................................................. 3633 9.3.5.1. Diagnosis and therapeutic interventions ...................... 3633 9.3.5.2. Long-term surveillance in traumatic aortic injury .... 3633 9.3.6. Iatrogenic aortic injuries .............................................................. 3633 9.3.7. Long-term follow-up of acute aortic syndrome ............... 3633 9.3.7.1. Follow-up after invasive treatment ................................ 3634 9.3.7.2. Follow-up under medical treatment (chronic type B aortic dissection, intramural haematoma, penetrating atherosclerotic ulcer) ........................................................................... 3636 10. Genetic and congenital diseases of the aorta ................................... 3637 10.1. Genetic and chromosomal diseases ............................................ 3637 10.1.1. Turner syndrome ......................................................................... 3638 10.1.1.1. Diagnosis, clinical presentation, and natural history 3638 10.1.1.2. Medical treatment ............................................................... 3640 10.1.1.3. Surgery of aortic aneurysms ........................................... 3640 10.1.1.4. Pregnancy and physical exercise ................................... 3640 10.1.2. Vascular Ehlers–Danlos syndrome ....................................... 3641 10.1.2.1. Diagnosis, clinical presentation, and natural history 3641 10.1.2.2. Surveillance and imaging ................................................... 3641 10.1.2.3. Medical treatment ............................................................... 3641 10.1.2.4. Surgical treatment ............................................................... 3641 10.1.2.5. Pregnancy ................................................................................ 3641 10.1.3. Marfan syndrome ......................................................................... 3641 10.1.3.1. Diagnosis, clinical presentation, and natural history 3641 10.1.3.2. Imaging surveillance ............................................................ 3641 10.1.3.3. Medical treatment ............................................................... 3642 10.1.3.4. Aortic surgery ....................................................................... 3642 10.1.3.5. Pregnancy and physical exercise ................................... 3643
ESC Guidelines 3541
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.5
10.1.4. Other syndromic and non-syndromic heritable thoracic aortic diseases and/or arterial disorders ........................................... 3643 10.1.4.1. Loeys–Dietz syndrome ..................................................... 3643 10.1.4.1.1. Diagnosis, clinical presentation, and natural evolution ............................................................................................... 3643 10.1.4.2. ACTA2-related heritable thoracic aortic disease .... 3645 10.2. Aortic disease associated with bicuspid aortic valves .......... 3646 10.3. Coarctation of the aorta and aortic arch variants ................ 3648 10.3.1. Coarctation of the aorta ........................................................... 3648 10.3.1.1. Diagnostic work-up ............................................................ 3648 10.3.1.2. Treatment and follow-up ................................................. 3648 10.3.2. Aortic arch anatomic variants ................................................ 3650 10.3.3. Aberrant subclavian artery and Kommerell’s diverticulum ................................................................................................... 3650 11. Polyvascular peripheral arterial disease and peripheral arterial disease in patients with cardiac diseases ..................................................... 3650
11.1. Polyvascular disease ............................................................................ 3650 11.1.1. Epidemiology and prognosis .................................................... 3650 11.1.2. Screening for atherosclerosis in other arterial territories ....................................................................................................... 3650 11.1.2.1. Screening for coronary artery disease in patients with symptomatic peripheral arterial disease ............................ 3651 11.1.2.2. Screening for peripheral arterial disease in patients with coronary artery disease ............................................................ 3651 11.1.2.3. Screening for coronary artery disease in patients with carotid stenosis ............................................................................ 3651 11.1.2.4. Screening for carotid stenosis in patients with coronary artery disease ....................................................................... 3651 11.1.3. Management of patients with polyvascular disease ....... 3651 11.2. Peripheral arterial disease and heart failure ............................. 3651 11.3. Peripheral arterial disease and AF ................................................ 3652 11.4. Peripheral arterial disease and aortic stenosis ........................ 3652 12. Key messages .................................................................................................. 3652 13. Gaps in evidence ............................................................................................ 3653 14. Sex differences ............................................................................................... 3653 15. ‘What to do’ and ‘What not to do’ messages from the guidelines .................................................................................................................. 3653 16. Evidence tables ............................................................................................... 3661 17. Data availability statement ......................................................................... 3661 18. Author information ...................................................................................... 3661 19. Appendix ........................................................................................................... 3662 20. References ........................................................................................................ 3663
Tables of Recommendations Recommendation Table 1 — Recommendations for clinical and laboratory, and for functional and quality of life, assessment in patients with peripheral arterial and aortic disease (see also Evidence Table 1) 3560 Recommendation Table 2 — Recommendations for diagnostic tests in patients with peripheral arterial disease ................................................ 3562 Recommendation Table 3 — Recommendations for imaging of the aorta (see also Evidence Table 2) .................................................................. 3565 Recommendation Table 4 — Recommendations for thoracic aortic measurements ........................................................................................................ 3566 Recommendation Table 5 — Recommendations for peripheral arterial disease screening (see also Evidence Table 3) .......................... 3568 Recommendation Table 6 — Recommendations for abdominal aortic aneurysm screening ................................................................................ 3568 Recommendation Table 7 — Recommendations for lifestyle, physical activity, and patient education (see also Evidence Table 4) 3570 Recommendation Table 8 — Recommendations for antihypertensive therapy in patients with peripheral and aortic disease ........................................................................................................................ 3571 Recommendation Table 9 — Recommendations for lipid-lowering therapy in patients with peripheral arterial and aortic diseases ....... 3572 Recommendation Table 10 — Recommendations for the medical management of patients with peripheral arterial and aortic diseases and diabetes ............................................................................................................ 3573 Recommendation Table 11 — Recommendations for diagnostic tests in patients with peripheral arterial disease and diabetes, renal failure, and wounds .............................................................................................. 3577 Recommendation Table 12 — Recommendations for imaging in patients with peripheral arterial disease ..................................................... 3577 Recommendation Table 13 — Recommendations for exercise therapy in patients with peripheral arterial disease (see also Evidence Table 5) ..................................................................................................................... 3582 Recommendation Table 14 — Recommendations for antithrombotic therapy in patients with peripheral arterial disease (see also Evidence Table 6) .............................................................................. 3582 Recommendation Table 15 — Recommendations for interventional treatment of asymptomatic and symptomatic peripheral arterial disease (general) .................................................................................................... 3584 Recommendation Table 16 — Recommendations for interventional treatment of patients with symptomatic peripheral arterial disease (per arterial bed) ................................................................................................... 3585 Recommendation Table 17 — Recommendations in patients with peripheral arterial disease: follow-up of patients with peripheral arterial disease ........................................................................................................ 3585 Recommendation Table 18 — Recommendations for the management of chronic limb-threatening ischaemia ............................. 3586 Recommendation Table 19 — Recommendations for medical treatment in patients with chronic limb-threatening ischaemia (see also Evidence Table 7) ........................................................................................ 3586 Recommendation Table 20 — Recommendations for interventional treatment of chronic limb-threatening ischaemia ................................... 3587 Recommendation Table 21 — Recommendations for follow-up in patients with chronic limb-threatening ischaemia .................................. 3587 Recommendation Table 22 — Recommendations for the management of patients presenting with acute limb ischaemia (see also Evidence Table 8) ........................................................................................ 3590 Recommendation Table 23 — Recommendations for carotid artery stenosis assessment ............................................................................................. 3590 Recommendation Table 24 — Recommendations for antithrombotic treatment in patients with carotid stenosis .............. 3592 Recommendation Table 25 — Recommendations for interventional treatment in patients with asymptomatic carotid artery stenosis ... 3594 Recommendation Table 26 — Recommendations for evaluation and medical treatment in patients with symptomatic carotid artery stenosis ...................................................................................................................... 3594 Recommendation Table 27 — Recommendations for interventions in patients with symptomatic carotid artery stenosis ........................... 3596 Recommendation Table 28 — Recommendations for follow-up in patients with carotid artery stenosis ............................................................ 3596 Recommendation Table 29 — Recommendations for the management of subclavian artery stenosis (see also Evidence Table 9) ..................................................................................................................... 3597 Recommendation Table 30 — Recommendations for diagnostic strategies for renal artery disease .................................................................. 3600 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.6
Recommendation Table 31 — Recommendations for treatment strategies for renal artery disease (see also Evidence Table 10) ...... 3600 Recommendation Table 32 — Recommendations in patients with visceral artery stenosis ........................................................................................ 3602 Recommendation Table 33 — Recommendations for primary and secondary prevention in aortic atheromatous plaques ........................ 3602 Recommendation Table 34 — Recommendations for initial evaluation of thoracic aortic aneurysm and abdominal aortic aneurysm .................................................................................................................. 3603 Recommendation Table 35 — Recommendation for the surveillance of patients with thoracic aortic aneurysms (non-heritable thoracic aortic disease) ......................................................................................................... 3607 Recommendation Table 36 — Recommendations for surveillance of patients with abdominal aortic aneurysm .................................................. 3609 Recommendation Table 37 — Recommendations for medical treatment in patients with thoracic aorta or abdominal aortic aneurysms ................................................................................................................ 3609 Recommendation Table 38 — Recommendations for surgery in aortic root and ascending aorta dilatation associated with tricuspid aortic valve (see also Evidence Table 11) ................................................... 3611 Recommendation Table 39 — Recommendations for surgery in aortic arch aneurysms ......................................................................................... 3611 Recommendation Table 40 — Recommendations for the management of patients presenting with descending thoracic aortic and thoracoabdominal aortic aneurysms ................................................... 3613 Recommendation Table 41 — Recommendations for the management of patients presenting with abdominal aortic aneurysm .................................................................................................................. 3615 Recommendation Table 42 — Recommendations for the management of patients presenting with endoleaks ............................. 3617 Recommendation Table 43 — Recommendations for follow-up after treatment of aortic aneurysms (see also Evidence Table 12) 3618 Recommendation Table 44 — Recommendations for diagnostic work-up of acute aortic syndromes ............................................................. 3622 Recommendation Table 45 — Recommendation for medical treatment in acute aortic syndromes ........................................................... 3623 Recommendation Table 46 — Recommendations for intervention in type A acute aortic dissection .................................................................... 3624 Recommendation Table 47 — Recommendations for aortic repair strategies in type A acute aortic dissection ............................................... 3624 Recommendation Table 48 — Recommendations for the management of malperfusion in the setting of acute aortic dissection .................................................................................................................. 3628 Recommendation Table 49 — Recommendations for the management of patients presenting with acute type B aortic dissection .................................................................................................................. 3629 Recommendation Table 50 — Recommendations for the management of patients presenting with chronic type B aortic dissection .................................................................................................................. 3629 Recommendation Table 51 — Recommendations for the management of intramural haematoma ...................................................... 3631 Recommendation Table 52 — Recommendations for the management of penetrating atherosclerotic ulcer ................................. 3631 Recommendation Table 53 — Recommendations for traumatic aortic injury .............................................................................................................. 3633 Recommendation Table 54 — Recommendations for follow-up after treatment of acute aortic syndrome ................................................. 3637 Recommendation Table 55 — Recommendations for the management of patients with heritable thoracic aortic disease ....... 3637 Recommendation Table 56 — Recommendations for genetic testing and aortic screening in aortic disease .......................................................... 3638 Recommendation Table 57 — Recommendations for imaging in women with Turner syndrome ...................................................................... 3638 Recommendation Table 58 — Recommendations for aortic surgery in women with Turner syndrome ................................................................. 3640 Recommendation Table 59 — Recommendations for medical treatment in patients with vascular Ehlers–Danlos syndrome (see also Evidence Table 13) ...................................................................................... 3641 Recommendation Table 60 — Recommendations for vascular imaging in Marfan syndrome ............................................................................ 3642 Recommendation Table 61 — Recommendations for medical treatment in Marfan syndrome (see also Evidence Table 14) ........... 3642 Recommendation Table 62 — Recommendations for aortic surgery in Marfan syndrome ............................................................................................. 3642 Recommendation Table 63 — Recommendations for pregnancy in women with Marfan syndrome ...................................................................... 3643 Recommendation Table 64 — Recommendations for physical exercise in patients with Marfan syndrome .............................................. 3643 Recommendation Table 65 — Recommendations for imaging follow-up in Loeys–Dietz syndrome ............................................................ 3644 Recommendation Table 66 — Recommendations for aortic root surgery in Loeys–Dietz syndrome ................................................................. 3644 Recommendation Table 67 — Recommendations for imaging and surgery in ACTA2-related heritable thoracic aortic disease (see also Evidence Table 11) ............................................................................................... 3645 Recommendation Table 68 — Recommendations for bicuspid aortic valve-associated aortopathy management ........................................................ 3647 Recommendation Table 69 — Recommendations for evaluation and medical treatment of patients with coarctation of the aorta ............ 3648 Recommendation Table 70 — Recommendations for screening and management of polyvascular disease and peripheral arterial disease with cardiac diseases (see also Evidence Table 15) ............................... 3652
List of tables
Table 1 Classes of recommendations .......................................................... 3547 Table 2 Levels of evidence ................................................................................ 3548 Table 3 New recommendations .................................................................... 3550 Table 4 Revised recommendations ............................................................... 3555 Table 5 Main aortic imaging techniques ...................................................... 3564 Table 6 High-risk populations for carotid artery stenosis .................. 3567 Table 7 Peripheral arterial disease categorized according to clinical presentation ............................................................................................................ 3574 Table 8 Assessment of the risk of amputation: the Wound, Ischaemia, and foot Infection classification ................................................ 3577 Table 9 Clinical categories of acute limb ischaemia ............................... 3588 Table 10 Peak systolic velocity criteria for grading internal carotid artery stenosis ........................................................................................................ 3591 Table 11 High-risk features associated with increased risk of stroke in patients with asymptomatic internal carotid artery stenosis on optimal medical treatment ................................................................................ 3592 Table 12 High-risk peri-operative features for carotid endarterectomy ..................................................................................................... 3595 Table 13 Clinical signs suggestive of renal artery disease .................... 3598 Table 14 Grading of atherosclerotic aortic plaques .............................. 3603 Table 15 Overview of factors favouring open vs. endovascular repair in thoracoabdominal aortic aneurysm ......................................................... 3613 Table 16 High-risk features of intramural haematoma type A and B 3630 Table 17 Need for assessment of associated atherosclerotic disease in additional vascular territories in symptomatic patients with coronary artery disease, peripheral arterial disease, or carotid stenosis ............... 3651 Table 18 ‘What to do’ and ‘What not to do’ .......................................... 3654
ESC Guidelines 3543
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.7
List of figures
Figure 1 Central illustration: from diagnosis to treatment, a holistic multidisciplinary peripheral arterial and aortic diseases approach .. 3549 Figure 2 Estimated specific prevalence of peripheral arterial disease, by sex, in people aged 40 years and older ................................................. 3558 Figure 3 Main risk factors associated with atherosclerosis in peripheral arterial and aortic diseases ......................................................... 3559 Figure 4 Haemodynamic assessment of peripheral arterial disease 3561 Figure 5 Anatomy and aortic segments and upper normal values for aortic dimensions .................................................................................................. 3563 Figure 6 Conventional measurements of the aorta at different levels by echocardiography or duplex ultrasound (A, B, C), cardiovascular computed tomography or cardiovascular magnetic resonance (D, E, F) ......................................................................................... 3564 Figure 7 Cardiovascular risk modification and healthy lifestyle interventions and targets in patients with peripheral arterial and aortic diseases ........................................................................................................ 3569 Figure 8 Cardiovascular risk in patients with peripheral arterial disease 3575 Figure 9 Diagnostic algorithm for peripheral arterial disease ............ 3576 Figure 10 Optimal medical treatment in patients with peripheral arterial disease ........................................................................................................ 3578 Figure 11 Treatment algorithm in peripheral arterial disease without wounds ................................................................................................................................ 3579 Figure 12 Treatment algorithm in peripheral arterial disease with wounds ...................................................................................................................... 3580 Figure 13 Exercise training characteristics and benefits in patients with peripheral arterial disease ....................................................................... 3581 Figure 14 Long-term antithrombotic therapy in patients with symptomatic peripheral arterial disease .......................................................... 3583 Figure 15 Patients with chronic symptomatic PAD after endovascular revascularization ........................................................................ 3584 Figure 16 Management of acute limb ischaemia ...................................... 3589 Figure 17 North American Symptomatic Carotid Endarterectomy Trial/European Carotid Surgery Trial methods ....................................... 3591 Figure 18 Algorithm of carotid artery stenosis management ............ 3593 Figure 19 Diagnostic and treatment algorithm for renal artery stenosis ...................................................................................................................... 3599 Figure 20 Algorithm of chronic mesenteric ischaemia management 3601 Figure 21 Thoracic and abdominal aortic aneurysms: aetiology, screening and diagnostic methods ................................................................. 3604 Figure 22 Classification of thoracoabdominal and abdominal aortic aneurysms ................................................................................................................ 3605 Figure 23 Risk factors for thoracic and abdominal aneurysm rupture 3606 Figure 24 Surveillance of patients with non-heritable thoracic aortic disease and abdominal aortic aneurysms ...................................... 3608 Figure 25 Peri-operative algorithm for the management of patients with surgically treated aortic root and ascending aortic aneurysm 3610 Figure 26 Algorithm for individual decision-making process in the treatment of patients with abdominal aortic aneurysm ...................... 3614 Figure 27 Algorithm for follow-up after thoracic endovascular aortic aneurysm repair, and management of endoleaks and their classification 3616 Figure 28 Anatomical and temporal classification of acute aortic syndrome .................................................................................................................. 3619 Figure 29 Aortic dissection classification system based on the 2020 Society for Vascular Surgery/Society of Thoracic Surgeons Reporting Standards and the European update of the Stanford classification—Type Entry Malperfusion classification .......................... 3620 Figure 30 Multiparametric diagnostic work-up of acute aortic syndrome .................................................................................................................. 3621 Figure 31 Medical management of acute aortic syndrome ................. 3623 Figure 32 Complications in acute aortic syndromes, clinical evidence associated with malperfusion syndrome, and in-hospital mortality associated with these complications ............................................................ 3625 Figure 33 Interventional treatment algorithm in acute aortic dissection .................................................................................................................. 3626 Figure 34 Mechanisms and clinical management of aortic branch obstruction in acute aortic dissection .......................................................... 3627 Figure 35 High-risk features in penetrating atherosclerotic ulcer and management of patients with type B penetrating atherosclerotic ulcer ............................................................................................................................ 3632 Figure 36 Classification and treatment of traumatic aortic injuries 3634 Figure 37 Aetiology, risk factors, and classification of iatrogenic aortic injuries .......................................................................................................... 3635 Figure 38 Algorithm for follow-up after acute aortic syndrome ..... 3636 Figure 39 Algorithm for genetic and imaging screening in patients with thoracic aortic disease .............................................................................. 3639 Figure 40 Algorithm for surveillance in women (≥15 years) with Turner syndrome .................................................................................................. 3640 Figure 41 Algorithm for imaging surveillance in patients with syndromic and non-syndromic heritable thoracic aortic disease ..... 3644 Figure 42 Suggested thresholds for prophylactic aortic root/ ascending replacement in Loeys–Dietz syndrome ................................. 3645 Figure 43 Bicuspid aortic valve, valvulo-aortopathy nomenclature . 3646 Figure 44 Criteria for significant coarctation/re-coarctation of the aorta and management algorithm .................................................................. 3649 Figure 45 Reported rate ranges of other localizations of atherosclerosis in patients with a specific arterial disease .................. 3650
Abbreviations and acronyms
18F–NaF Fluorine-18–sodium fluoride 6MWD Six-minute walking distance 6MWT Six-minute walk test AA Abdominal aorta AAA Abdominal aortic aneurysm AAD Acute aortic dissection AAE Aortic adverse events AAL Ascending aortic length AAS Acute aortic syndrome ABI Ankle–brachial index ACAS Asymptomatic Carotid Atherosclerosis Study ACB Asymptomatic Cervical Bruit Study ACC/AHA American College of Cardiology and American Heart Association ACEI Angiotensin-converting enzyme inhibitor ACS Acute coronary syndrome ACST Asymptomatic Carotid Surgery Trial ACTA2 Alpha-actin gene AD Aortic dissection ADAM American Aneurysm Detection and Management ADD-RS Aortic dissection detection-risk score AF Atrial fibrillation AHI Aortic height index ALI Acute limb ischaemia AMI Acute mesenteric ischaemia AP Antero-posterior ARB Angiotensin receptor blocker ARR Absolute risk reduction ASCVD Atherosclerotic cardiovascular disease ASE American Society of Echocardiography Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.8
ASI Aortic size index BASIL Bypass versus Angioplasty in Severe Ischaemia of the Leg trial BAV Bicuspid aortic valve BB Beta-blocker BEST-CLI Best Endovascular versus Best Surgical Therapy for Patients with Critical Limb Ischemia trial b.i.d. Bis in die (twice daily) BMI Body mass index BP Blood pressure b.p.m. Beats per minute BSA Body surface area BTK Below-the-knee CABG Coronary artery bypass grafting CAD Coronary artery disease CANTOS Canakinumab Anti-Inflammatory Thrombosis Outcomes Study CANVAS Canagliflozin Cardiovascular Assessment Study CAS Carotid artery stenting CCA Common carotid artery CCB Calcium channel blocker CCT Cardiovascular computed tomography CDT Catheter-based thrombectomy cdTLR Clinically driven target lesion revascularization CEA Carotid endarterectomy CEUS Contrast-enhanced ultrasound CHA2DS2-VASc Congestive heart failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65 to 74 and sex category (female) CI Confidence interval cIMT Carotid intima media thickness CK Creatinine kinase CKD Chronic kidney disease CLTI Chronic limb-threatening ischaemia CMI Chronic mesenteric ischaemia CMR Cardiovascular magnetic resonance CoA Coarctation of the aorta COMPASS Cardiovascular Outcomes for People Using Anticoagulation Strategies COPD Chronic obstructive pulmonary disease CP Carotid plaque CREDENCE Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation CREST-2 Carotid Revascularization Endartectomy vs. Stenting Trial 2 CRP C-reactive protein CS Carotid artery stenosis CSA/h Cross-sectional area-to-height ratio CT Computed tomography CTA Computed tomography angiography CV Cardiovascular CVD Cardiovascular disease CVRF Cardiovascular risk factor DAPT Dual antiplatelet therapy DBP Diastolic blood pressure DD D-dimer DISSECT Duration, Intimal tear, Size, Segmental Extent, Clinical complications, Thrombosis DPI Dual pathway inhibition DSA Digital subtraction angiography DTA Descending thoracic aorta DUS Duplex ultrasound DWI Diffusion-weighted imaging ECG Electrocardiogram ECST European Carotid Surgery Trial eGFR Estimated glomerular filtration rate EMPA-REG OUTCOME
(Empagliflozin) Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients ESC European Society of Cardiology ESH European Society of Hypertension ESRD End-stage renal disease EUCLID Examining Use of tiCagreLor In peripheral artery Disease FDA (United States) Food and Drug Administration FDG Fluorodeoxyglucose FDR First-degree relative FET Frozen elephant trunk FID Focal intimal disruption FL False lumen GERAADA German Registry of Acute Aortic Dissection Type A GFR Glomerular filtration rate GLP-1RA Glucagon-like peptide-1 receptor agonist GSV Great saphenous vein HADS Hospital anxiety and depression score HbA1c Glycated haemoglobin HBET Home-based exercise training HF Heart failure HITS High-intensity transient signal HOME Hyperinsulinaemia: the Outcomes of its Metabolic Effects HR Hazard ratio HRQoL Health-related quality of life hs-CRP High-sensitivity C-reactive protein HSR High surgical risk HTAD Heritable thoracic aortic disease IC Intermittent claudication ICA Internal carotid artery ID Intimal disruption IL Interleukin ILT Intensive lipid-lowering therapy IMA Inferior mesenteric artery IMH Intramural haematoma IMPROVE-AD The Improving outcomes in vascular disease— aortic dissection trial IMPROVE-IT IMProved Reduction of Outcomes: Vytorin Efficacy International Trial IPE Icosapent ethyl IRAD International Registry of Acute Aortic Dissection ISTH International Society on Thrombosis and Haemostasis i.v. Intravenous IVUS Intravascular ultrasound LDL-C Low-density lipoprotein cholesterol LEADER Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results trial LSA Left subclavian artery LV Left ventricular MACE Major adverse cardiac event
ESC Guidelines 3545
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.9
MAD Multisite artery disease MALE Major adverse limb event MAP Mean arterial pressure MESA Multi-Ethnic Study of Atherosclerosis MFS Marfan syndrome MHV Mechanical heart valve MI Myocardial infarction MRA Magnetic resonance angiography MRI Magnetic resonance imaging MWD Maximal walking distance NASCET North American Symptomatic Carotid Endarterectomy Trial OAC Oral anticoagulation o.d. Once daily OMT Optimal medical treatment OR Odds ratio PAAD Peripheral arterial and aortic diseases PA Popliteal aneurysm PAD Peripheral arterial disease PAU Penetrating atherosclerotic ulcer PC-AKI Post-contrast acute kidney injury PCSK9 Proprotein convertase subtilisin/kexin type 9 PET Positron emission tomography PET-CT PET-computed tomography PFWD Pain-free walking distance PROM Patient-reported outcome measure PSV Peak systolic velocity PSVr Peak systolic velocity ratio PVD Polyvascular disease QoL Quality of life RAR Renal-aortic peak flow velocity ratio RAS Renal artery stenosis RCT Randomized controlled trial REACH The REduction of Atherothrombosis for Continued Health REDUCE-IT Reduction of Cardiovascular Events With Icosapent Ethyl–Intervention Trial ROMS Retrograde open mesenteric stenting ROPAC Registry Of Pregnancy And Cardiac disease RPE Rate of perceived exertion RR Relative risk SAMMPRIS Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis trial SAPPHIRE Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy trial SAPT Single antiplatelet therapy SBP Systolic blood pressure SCI Spinal cord ischaemia SCS Spinal cord stimulation SET Supervised exercise training SF-36 Short-form 36-item health questionnaire SGLT2i Sodium-glucose co-transporter-2 inhibitor SMA Superior mesenteric artery SMART Secondary Manifestation of ARTerial disease SOCRATES Acute Stroke or Transient Ischaemic Attack Treated with Aspirin or Ticagrelor and Patient Outcomes trial SCORE2 Systematic Coronary Risk Evaluation 2 SCORE2-Diabetes Systematic Coronary Risk Evaluation 2 - diabetes SCORE2-OP Systematic Coronary Risk Evaluation 2–Older Persons SPACE-2 Stent Protected Angioplasty versus Carotid Endarterectomy study SPPB Short physical performance battery SRUCC Society of Radiologists in Ultrasound SS Subclavian stenosis SSFP Steady-state free precession STJ Sinotubular junction STS/AATS Society of Thoracic Surgeons/American Association for Thoracic Surgery SUSTAIN-6 Trial to Evaluate Cardiovascular and Other Long-term Outcomes with Semaglutide in Subjects with Type 2 Diabetes SVS Society for Vascular Surgery T1DM Type 1 diabetes mellitus T2DM Type 2 diabetes mellitus TAA Thoracic aortic aneurysm TAAA Thoracoabdominal aortic aneurysm TAAD Type A aortic dissection TAD Thoracic aortic disease TAI Traumatic aortic injury TAV Tricuspid aortic valve TAVI Transcatheter aortic valve implantation TBAD Type B aortic dissection TBI Toe–brachial index TCAR Transcarotid artery revascularization TcPO2 Transcutaneous oxygen pressure TOE Transoesophageal echocardiography TEM Type entry malperfusion classification TEVAR/EVAR Thoracic endovascular aortic aneurysm repair TFCAS Transfemoral carotid artery stenting THALES Acute Stroke or Transient Ischaemic Attack Treated with Ticagrelor and acetylsalicylic acid for Prevention of Stroke and Death trial TIA Transient ischaemic attack TIMI Thrombolysis in myocardial infarction TP Toe pressure TS Turner syndrome TTE Transthoracic echocardiography UEAD Upper-limb artery disease UKPDS United Kingdom Prospective Diabetes Study: clinical and therapeutic implications for type 2 diabetes uTBAD Uncomplicated type B aortic dissection VascuQoL Vascular quality of life questionnaire VAST Vertebral Artery Stenting Trial vEDS Vascular Ehlers–Danlos syndrome VIST Vertebral Artery Ischaemia Stenting Trial VKA Vitamin K antagonist WELCH Walking Estimated Limitation Calculated by History WIfI Wound, Ischaemia, foot Infection classification WIQ Walking Impairment Questionnaire Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.10
1 Preamble
Guidelines evaluate and summarize available evidence with the aim of assisting health professionals in proposing the best diagnostic or therapeutic approach for an individual patient with a given condition. Guidelines are intended for use by health professionals and the European Society of Cardiology (ESC) makes its guidelines freely available. ESC Guidelines do not override the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient’s health condition and in consultation with that patient or the patient’s caregiver where appropriate and/or necessary. It is also the health professional’s responsibility to verify the rules and regulations applicable in each country to drugs and devices at the time of prescription and to respect the ethical rules of their profession. ESC Guidelines represent the official position of the ESC on a given topic and are regularly updated when warranted by new evidence. ESC Policies and Procedures for formulating and issuing ESC Guidelines can be found on the ESC website (https://www.escardio.org/Guidelines/ Clinical-Practice-Guidelines/Guidelines-development/Writing-ESC- Guidelines). This guideline updates and replaces the previous peripheral arterial disease and aortic disease guidelines from 2017 and 2014, respectively. The Members of this task force were selected by the ESC to include professionals involved with the medical care of patients with this pathology as well as patient representatives and methodologists. The selection procedure included an open call for authors and aimed to include members from across the whole of the ESC region and from relevant ESC Subspecialty Communities. Consideration was given to diversity and inclusion, notably with respect to gender and country of origin. The task force performed a critical review and evaluation of the published literature on diagnostic and therapeutic approaches including assessment of the risk–benefit ratio. The strength of every recommendation and the level of evidence supporting them were weighed and scored according to pre-defined scales as outlined in Tables 1 and 2 below. Patient-reported outcome measures (PROMs) and patient-reported experience measures (PREMs) were also evaluated as the basis for recommendations and/or discussion in these guidelines. The task force followed ESC voting procedures and all approved recommendations were subject to a vote and achieved at least 75% agreement among voting members. Members of the task force with declared interests on specific topics were asked to abstain from voting on related recommendations.
The experts of the writing and reviewing panels provided declaration of interest forms for all relationships that might be perceived as real or potential sources of conflicts of interest. Their declarations of interest were reviewed according to the ESC declaration of interest rules which can be found on the ESC website (http://www.escardio.org/guidelines) and have been compiled in a report published in a supplementary document with the guidelines. Funding for the development of ESC Guidelines is derived entirely from the ESC with no involvement of the healthcare industry. The ESC Clinical Practice Guidelines (CPG) Committee supervises and co-ordinates the preparation of new guidelines and is responsible for the approval process. In addition to review by the CPG Committee, ESC Guidelines undergo multiple rounds of double-blind peer review by external experts, including members from across the whole of the ESC region, all National Cardiac Societies of the ESC and from relevant ESC Subspecialty Communities. After appropriate
Table 1 Classes of recommendations
©ESC 2024
Classes of recommendations Class I Evidence and/or general agreement that a given treatment or procedure is beneficial, useful, effective.
Conflicting evidence and/or a divergence of opinion about the usefulness/ efficacy of the given treatment or procedure.
Is recommended or is indicated
Wording to use Definition
Class III Evidence or general agreement that the given treatment or procedure is not useful/effective, and in some cases may be harmful. Is not recommended
Class IIb Usefulness/efficacy is less well established by evidence/opinion. May be considered
Class IIa Weight of evidence/opinion is in favour of usefulness/efficacy. Should be considered
Class II
ESC Guidelines 3547
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.11
revisions, the guidelines are signed off by all the experts in the task force. The finalized document is signed off by the CPG Committee for publication in the European Heart Journal. ESC Guidelines are based on analyses of published evidence, chiefly on clinical trials and meta-analyses of trials, but potentially including other types of studies. Evidence tables summarizing key information from relevant studies are generated early in the guideline development process to facilitate the formulation of recommendations, to enhance comprehension of recommendations after publication, and reinforce transparency in the guidelines development process. The tables are published in their own section of ESC Guidelines and reference specific recommendation tables. Off-label use of medication may be presented in this guideline if a sufficient level of evidence shows that it can be considered medically appropriate for a given condition. However, the final decisions concerning an individual patient must be made by the responsible health professional giving special consideration to: • The specific situation of the patient. Unless otherwise provided for by national regulations, off-label use of medication should be limited to situations where it is in the patient’s interest with regard to the quality, safety, and efficacy of care, and only after the patient has been informed and has provided consent. • Country-specific health regulations, indications by governmental drug regulatory agencies, and the ethical rules to which health professionals are subject, where applicable.
2 Introduction
Peripheral arterial and aortic diseases (PAAD) are highly prevalent and significantly increase cardiovascular (CV) mortality and morbidity in the general population,1,2 consequently, intensive preventive strategies are needed. However, patients with PAAD are generally underdiagnosed and undertreated3,4 compared with patients with coronary artery disease (CAD).5 Common risk factors in PAAD often coexist, requiring a multidisciplinary approach for effective management.5 Early diagnosis is crucial for better outcomes. These guidelines address PAAD, updating and merging the 2017 peripheral arterial diseases and 2014 aortic diseases guidelines. The focus is primarily on atherosclerotic arterial diseases, but they also address some non-atherosclerotic genetic conditions. While not exhaustive, these 2024 guidelines offer guidance on diagnosis, surveillance, and treatment. A number of new and revised recommendations are summarized in Tables 3 and 4, respectively. Readers should consider non-atherosclerotic conditions and refer to specific documents.6–9
A general approach to PAAD is provided in the central illustration (Figure 1). In the management of PAAD, the following aspects must be highlighted: • Shared decision-making to involve patients, explore treatment options, assess patient values, and reach decisions collaboratively. • Multidisciplinary approach (Figure 1) in expert and high-volume PAAD centres for complex patients or procedures. These centres provide diverse services, including diagnosis, treatment planning, minimally invasive procedures, open surgery, post-operative and outpatient care, and ideally, research and innovation. They should provide continuous clinical service (24/7) and have access to digital imaging. These guidelines recognize variations in healthcare systems, population sizes, and needs, impacting the definition of ‘high volume’ in PAAD care across countries.
Table 2 Levels of evidence
Level of evidence A
Level of evidence B
Level of evidence C Data derived from multiple randomized clinical trials or meta-analyses.
Data derived from a single randomized clinical trial or large non-randomized studies.
Consensus of opinion of the experts and/or small studies, retrospective studies, registries. ©ESC 2024 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.12
Diagnosis
Cardiologist
Angiologist
Vascular surgeon
Geneticist Cardiac surgeon CV radiologist
CV intensive care specialist
Neurologist Anaesthetist
Nurse Nephrologist
Exercise therapist
Follow-up
Treatment Prevention
Goals Initial steps
Clinical assessment Functional assessment QoL assessment Use of non-invasive tools Imaging, if appropriate
Optimal medical treatment Patient education CVRFs control Exercise/rehabilitation programmes Need for intervention/ surgery?
Regular follow-up Optimal medical treatment CVRFs management Patient education Patient’s tailored targets and goals Family screening, if appropriate
Increase awareness CVRFs management Screening Genetic counselling
Prevent development of peripheral and aortic atherosclerosis Prevent aortic dilation or lesions Improve patients’ QoL and functioning Reduce risk of MACE and MALE Improve survival Reduce the risk of hospitalization Reduce the need for intervention/surgery Screen patients at risk of PAAD Enable early access to treatment Ensure optimal medical treatment
Figure 1 Central illustration: from diagnosis to treatment, a holistic multidisciplinary peripheral arterial and aortic diseases approach. CV, cardiovascular; CVRFs, cardiovascular risk factors; MACE, major adverse cardiac event; MALE, major adverse limb event; PAAD, peripheral arterial and aortic diseases; QoL, quality of life.
ESC Guidelines 3549
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.13
3 What is new
Table 3 New recommendations
Recommendations Class Level
Recommendations for clinical and laboratory, and for functional quality of life, assessment in patients with peripheral arterial and aortic disease When managing PAAD, it is recommended to adopt a comprehensive approach that addresses the entirety of arterial circulation. I B Recommendations for peripheral arterial disease screening In patients with AAA, femoro-popliteal aneurysm screening with DUS should be considered. IIa C In patients needing intervention with transfemoral access, screening for iliofemoral artery disease may be considered. IIb C In patients with two or more CVRFs, screening for asymptomatic CS may be considered. IIb C Recommendations for abdominal aortic aneurysm screening Opportunistic AAA screening with DUS should be considered in symptomatic/asymptomatic PAD patients. IIa B Recommendations for lifestyle, physical activity, and patient education Use of web- or app-based secondary prevention risk calculators should be considered in the shared decision-making to improve patient adherence to treatment and lifestyle changes. IIa C E-cigarettes may be considered as an aid to quitting tobacco smoking, but it is advisable to limit their use and avoid simultaneous use with conventional cigarettes due to unknown long-term effects. IIb C Recommendations for lipid-lowering therapy in patients with peripheral arterial and aortic diseases In patients with atherosclerotic PAAD, lipid-lowering therapy is recommended. I A An ultimate LDL-C goal of <1.4 mmol/L (55 mg/dL) and a >50% reduction in LDL-C vs. baseline are recommended in patients with atherosclerotic PAAD. I A If the target LDL-C level is not achieved on maximally tolerated statins and ezetimibe, treatment with a PCSK9 inhibitor is recommended in patients with atherosclerotic PAAD, to achieve target values. I A If the target LDL-C level is not achieved, a combination of statins and ezetimibe is indicated in patients with atherosclerotic PAAD, to achieve the given target values. I B For statin-intolerant patients with atherosclerotic PAAD, at high CV risk, who do not achieve their LDL-C goal on ezetimibe, it is recommended to add bempedoic acid either alone or in combination with a PCSK9 inhibitor. I B Statins for the reduction of growth and rupture of AAA should be considered. IIa B Statins for the reduction of growth and rupture of TAA may be considered. IIb B In high-risk patients with PAAD and triglycerides >1.5 mmol/L despite lifestyle measures and statin therapy, icosapent ethyl 2 g b.i.d. may be considered in addition to a statin. IIb B Fibrates are not recommended for cholesterol lowering. III B Recommendations for exercise therapy in patients with peripheral arterial disease In patients with symptomatic PAD, SET is recommended. I A In those patients undergoing endovascular revascularization, SET is recommended as an adjuvant therapy. I A When SET is not available or feasible, a structured and monitored (calls, logbooks, connected devices) HBET programme should be considered. IIa A Walking should be considered as the first-line training modality. When walking exercise is not an option, alternative exercise modes (strength training, arm cranking, cycling, and combinations of different training modes) should also be considered. IIa A Walking training performed at high intensity (77%–95% of maximal heart rate or 14–17 self-perceived exertion on Borg’s scale) should be considered to improve walking performance, and high-intensity exercise training (various aerobic training modes) should be considered to improve cardiorespiratory fitness. IIa A Training frequency of at least three times per week, training session duration of at least 30 min, and training programme duration of at least 12 weeks should be considered. IIa B In patients with PAD, exercise training to moderate-severe claudication pain may be considered to improve walking performance. However, improvements are also achievable with lesser claudication pain severities (low-mild pain or pain-free). IIb B Based on patient’s tolerance, a progressive increase (every 1–2 weeks) in exercise training load may be considered. IIb C
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.14
Recommendations for antithrombotic therapy in patients with peripheral arterial disease Treatment with combination rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered for patients with PAD and high ischaemic risk, and non-high bleeding risk. IIa A Treatment with combination rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered for patients with PAD and non-high bleeding risk following lower-limb revascularization. IIa B Aspirin (75–100 mg) for primary prevention may be considered in patients with asymptomatic PAD and DM, in the absence of contraindications. IIb A Recommendations for interventional treatment of asymptomatic and symptomatic peripheral arterial disease (general) In patients with symptomatic PAD, after a 3 month period of OMT and exercise therapy, PAD-related QoL assessment is recommended. I B It is recommended to adapt the mode and type of revascularization options to anatomical lesion location, lesion morphology, and general patient condition. I C In patients with symptomatic PAD and impaired PAD-related QoL after a 3 month period of OMT and exercise therapy, revascularization may be considered. IIb B In patients with PAD, revascularization is not recommended if the reason is to solely prevent progression to CLTI. III B In patients with asymptomatic PAD, revascularization is not recommended. III C Recommendations for interventional treatment of patients with symptomatic peripheral arterial disease (per arterial bed) In femoro-popliteal lesions, drug-eluting treatment should be considered as the first-choice strategy. IIa A In femoro-popliteal lesions, if revascularization is indicated, an open surgical approach should be considered when an autologous vein (e.g. GSV) is available in patients with low surgical risk. IIa C In patients with severe IC undergoing endovascular femoro-popliteal revascularization, treatment of BTK arteries may be considered in the same intervention. IIb C Recommendations in patients with peripheral arterial disease: follow-up of patients with peripheral arterial disease It is recommended to regularly, at least once a year, follow-up patients with PAD, assessing clinical and functional status, medication adherence, limb symptoms, and CVRFs, with DUS assessment as needed. I C Recommendations for the management of chronic limb-threatening ischaemia Early recognition of CLTI and referral to the vascular team are recommended for limb salvage. I C Recommendations for medical treatment in patients with chronic limb-threatening ischaemia It is recommended that patients with CLTI are managed by a vascular team. I C In patients with CLTI and ulcers, offloading mechanical tissue stress is indicated to allow wound healing. I C Lower-limb exercise training is not recommended in patients with CLTI and wounds. III C Recommendations for interventional treatment of chronic limb-threatening ischaemia In CLTI patients, it is recommended to perform revascularization as soon as possible. I B In CLTI, it is recommended to use autologous veins as the preferred conduit for infra-inguinal bypass surgery. I B In multilevel vascular disease, it is recommended to eliminate inflow obstructions when treating downstream lesions. I C In CLTI patients with good autologous veins and low surgical risk (<5% peri-operative mortality, >50% 2 year survival), infra-inguinal bypass may be considered. IIb B In CLTI patients, endovascular treatment may be considered as first-line therapy, especially in patients with increased surgical risk or inadequate autologous veins. IIb B Recommendations for follow-up in patients with chronic limb-threatening ischaemia In patients with CLTI, following revascularization it is recommended to follow-up patients on a regular basis. I C At follow-up, it is recommended to assess clinical, haemodynamic and functional status, limb symptoms, treatment adherence, and CVRFs. I C Recommendations for carotid artery stenosis assessment It is recommended to use the NASCET method or its non-invasive equivalent to assess ICA stenosis. I B It is not recommended to use the ECST method for ICA stenosis assessment. III C Recommendations for the management of subclavian artery stenosis Bilateral arm BP measurement is recommended for all patients with PAAD. I B Endovascular revascularization may be considered over surgery, despite similar long-term outcomes, due to lower complication rates. IIb B Routine revascularization in patients with atherosclerotic subclavian artery disease is not recommended. III C Recommendations for diagnostic strategies for renal artery disease DUS is recommended as the first-line imaging modality in patients with suspicion of RAS. I B
Continued
ESC Guidelines 3551
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.15
Recommendations for treatment strategies for renal artery disease Revascularization In patients with atherosclerotic unilateral >70% RAS, concomitant high-risk features, and signs of kidney viability, renal artery revascularization should be considered after OMT has been established. IIa B In patients with atherosclerotic bilateral (>70%) RAS or RAS in a solitary kidney, concomitant high risk features, and signs of kidney viability, renal artery revascularization should be considered. IIa B In patients with hypertension and/or signs of renal dysfunction due to RAS caused by fibromuscular dysplasia, concomitant high-risk features, and signs of kidney viability, revascularization with primary balloon angioplasty and bailout stenting should be considered. IIa B In patients with an indication for renal artery revascularization and complex anatomy, or after failed endovascular revascularization, open surgical revascularization should be considered. IIa B In patients with atherosclerotic unilateral RAS, routine revascularization is not recommended. III A Recommendations in patients with visceral artery stenosis In patients with acute or chronic mesenteric ischaemia, assessment by a vascular team is recommended. I C Revascularization of asymptomatic atherosclerotic visceral artery stenosis is not recommended. III C Recommendations for surgery in aortic root and ascending aorta dilatation associated with tricuspid aortic valve In patients with dilatation of the tubular ascending aorta who can be offered surgery with low predicted risk, ascending aortic replacement should be considered at a maximum diameter >52 mm. IIa B In patients undergoing surgery for tricuspid aortic valve disease who have concomitant dilatation of the aortic root or ascending tubular aorta, and low predicted surgical risk, ascending aorta or root replacement should be considered at a maximum diameter ≥45 mm, otherwise ≥50 mm. IIa B SAPT with low-dose aspirin (75–100 mg/day) should be considered for the first 3 months after valve-sparing aortic surgery when there are no other baseline indications for OAC. IIa C In patients undergoing non-aortic-valve cardiac surgery who have concomitant dilatation of the ascending aorta or aortic root with a maximum diameter ≥50 mm, concomitant aortic surgery should be considered. IIa C Recommendations for surgery in aortic arch aneurysms In patients with low or intermediate operative risk with an aortic arch aneurysm and recurrent episodes of chest pain not attributable to non-aortic causes, open surgical replacement of the arch is recommended. I C In patients undergoing open surgical repair of an aortic arch aneurysm, an elephant trunk or frozen elephant trunk procedure should be considered if the aneurysmal disease extends into the proximal descending thoracic aorta. IIa C Recommendations for follow-up after treatment of aortic aneurysms After open repair of TAA, an early CCT is recommended within 1 month, and then yearly CCT follow-up for the first 2 post-operative years and every 5 years thereafter is recommended if findings are stable. I B After 5 post-operative years without complications, continuing long-term follow-up of TEVAR by CCT every 5 years should be considered. IIa B If growth of the excluded aneurysm is observed, without evidence of type I or III endoleak, repeating CCT every 6–12 months, depending on the growth rate observed, should be considered. IIa C In low-risk patients, from 1 year post-operatively after EVAR, repeating DUS/CEUS every 2 years should be considered. IIa B If any abnormality during DUS/CEUS is found, confirmation should be considered using additional CCT or CMR (based on potential artefacts). IIa B Recommendations for diagnostic work-up of acute aortic syndrome CCT from neck to pelvis is recommended as the first-line imaging technique in patients with suspected AAS since it is widely available, accurate, and provides information about the entry tear, extension, and possible complications (malperfusion, dilatation, or rupture). I C In patients with suspected AAS, TOE is recommended to guide peri-operative management and detect complications. I C Recommendations for medical treatment in acute aortic syndromes In patients with AAS who can be managed conservatively and who achieved haemodynamic targets with i.v. anti-impulse therapy, switching to oral BBs and, if necessary, up-titration of other BP-lowering agents is recommended after 24 h if gastrointestinal transit is preserved. I B If the patient has a contraindication for BBs, a non-dihydropyridine calcium blocker should be considered. IIa B Recommendations for intervention in type A acute aortic dissection In patients with acute TAAD who have extensive destruction of the aortic root, a root aneurysm, or a known genetic aortic disorder, aortic root replacement is recommended with a mechanical or biological valved conduit. I B In patients presenting with acute TAAD, transfer from a low- to a high-volume aortic centre with the presence of a multidisciplinary team should be considered to improve survival if transfer can be accomplished without significant delay in surgery. IIa B In selected patients, a valve-sparing root repair may be considered, when performed by experienced surgeons. IIb B
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.16
Recommendations for aortic repair strategies in type A acute aortic dissection In patients with acute TAAD and a partially dissected aortic root but no significant aortic valve leaflet pathology, aortic valve resuspension is recommended over valve replacement. I B In patients with acute TAAD undergoing aortic repair, an open distal anastomosis is recommended to improve survival and increase FL thrombosis rates. I B In patients with acute TAAD without an intimal tear in the arch or a significant arch aneurysm, hemi-arch repair is recommended over more extensive arch replacement. I B In patients with acute TAAD and a secondary intimal tear in the arch or proximal DTA, extended aortic repair with stenting of the proximal DTA (e.g. by the frozen elephant technique) may be considered to reduce late distal aortic complications (e.g. aneurysm evolution of the remaining dissected descending aorta). IIb C Recommendations for the management of malperfusion in the setting of acute aortic dissection In patients with acute TAAD presenting with malperfusion (cerebral, mesenteric, lower limb, or renal), immediate aortic surgery is recommended. I B In patients with acute TAAD presenting with cerebral malperfusion or non-haemorrhagic stroke, immediate aortic surgery should be considered to improve neurological outcome and reduce mortality. IIa B In patients with acute TAAD presenting with clinically significant mesenteric malperfusion syndrome, immediate invasive angiographic diagnostics to evaluate percutaneous malperfusion repair before or directly after aortic surgery, in aortic centres with expertise, should be considered. IIa C Recommendations for the management of patients presenting with acute type B aortic dissection In patients with uncomplicated acute TBAD, TEVAR in the subacute phase (between 14 and 90 days) should be considered in selected patients with high-risk features to prevent aortic complications. IIa B Recommendations for the management of patients presenting with chronic type B aortic dissection In chronic TBAD and with a descending thoracic aortic diameter ≥60 mm, treatment is recommended in patients at reasonable surgical risk. I B In patients with chronic TBAD and a descending thoracic aortic diameter ≥55 mm, an indication for intervention should be considered in patients with low procedural risk. IIa C In patients with chronic post-dissection thoracoabdominal aortic aneurysms, the use of fenestrated/branched stent grafts may be considered, when treatment is indicated. IIb C Recommendations for the management of penetrating atherosclerotic ulcer In uncomplicated type B PAU with high-risk imaging features, endovascular treatment should be considered. IIa C Recommendations for traumatic aortic injury In cases of severe aortic injury (grade 4), immediate repair is recommended. I A In minimal aortic injury (grades 1 or 2), initial medical therapy under careful clinical and imaging surveillance should be considered. IIa C In cases of progression of the IMH (grade 2), semi-elective repair (within 24–72 h) should be considered. IIa C Recommendations for follow-up after treatment of acute aortic syndrome In medically treated type B AAS or IMH, follow-up imaging is recommended at 1, 3, 6, and 12 months after onset, then yearly if imaging findings are stable. I C In medically treated PAU, follow-up imaging is recommended at 1 month after diagnosis, then every 6 months if imaging findings are stable. I C After open surgery for AAS, follow-up imaging by CCT and TTE within 6 months, then CCT at 12 months and then yearly if findings are stable, should be considered. IIa B If no complications occur within the first 5 years, CCT every 2 years thereafter should be considered. IIa B If no residual patent FL is documented for 3 post-operative years, subsequent surveillance by CCT every 2–3 years should be considered. IIa C In the follow-up of medically treated PAU, after 2 years of imaging stability, larger intervals should be considered in low-risk patients. IIa C Recommendations for the management of patients with heritable thoracic aortic disease It is recommended that medical management of patients with HTAD is individualized and based on shared decision-making. I C It is recommended that patients with known or suspected syndromic or non-syndromic HTAD are evaluated in a centre with experience in the care of this patient group. I C Recommendations for genetic testing and aortic screening in aortic disease In patients with HTAD, guidance of clinical management by the underlying gene/variant, when known, should be considered. IIa B
Continued
ESC Guidelines 3553
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.17
Recommendations for imaging in women with Turner syndrome To take the smaller body size of women (≥15 years) with TS into account, the use of the ascending ASI (ratio of aortic diameter [mm] to BSA [m2]), AHI (ratio of aortic diameter [mm] to height [m]), or aortic z-score is recommended to define the degree of aortic dilatation and assess the risk of aortic dissection. I C It is recommended to define imaging and clinical surveillance intervals according to the estimated risk for dissection, based on the ascending ASI and concomitant lesions. I C Recommendations for aortic surgery in women with Turner syndrome Elective surgery for aneurysms of the aortic root and/or ascending aorta should be considered in women with TS who are ≥15 years of age, have an ascending ASI >23 mm/m2, an AHI >23 mm/m, a z-score >3.5, and have associated risk factors for aortic dissection or are planning pregnancy. IIa C Elective surgery for aneurysms of the aortic root and/or ascending aorta may be considered for women with TS who are ≥15 years of age, have an ascending ASI >25 mm/m2, an AHI >25 mm/m, a z-score >4, and who do not have associated risk factors for aortic dissection. IIb C Recommendations for medical treatment in patients with vascular Ehlers–Danlos syndrome In patients with vEDS, regular vascular surveillance of the aorta and peripheral arteries by DUS, CCT, or CMR is recommended. I C Treatment with celiprolol should be considered in patients with vEDS. IIa B Recommendations for vascular imaging in Marfan syndrome In patients with MFS, TTE is recommended: • At least annually in patients with an aortic root diameter <45 mm in the absence of additional risk factors • At least every 6 months in patients with an aortic root diameter <45 mm in the presence of additional risk factors • At least every 6–12 months in patients with an aortic root diameter ≥45 mm in the absence of additional risk factors I C In patients without previous aortic surgery, complete peripheral vascular and thoracoabdominal aortic imaging by CMR or CCT and DUS is recommended at the first evaluation, and subsequently every 3–5 years if stable. I C Recommendations for medical treatment in Marfan syndrome In patients with MFS, treatment with either a BB or an ARB, in maximally tolerated doses (unless contraindicated), is recommended to reduce the rate of aortic dilatation. I A In patients with MFS, the use of both a BB and an ARB, in maximally tolerated doses (unless contraindicated), should be considered to reduce the rate of aortic dilatation. IIa A Recommendations for pregnancy in women with Marfan syndrome It is recommended that all women with MFS: • Have a pre-conception evaluation to address the risks of maternal CV and other complications • Have follow-up in a centre with access to a pregnancy heart and vessel team I C It is recommended that couples in which a partner has or is at risk of HTAD be offered pre-conception genetic counselling. I C Imaging of the whole aorta (by CMR/CCT) is recommended prior to pregnancy. I C Follow-up during pregnancy is recommended with a frequency determined by aortic diameter and growth. I C Intake of BBs during pregnancy is recommended. I C Prophylactic aortic root surgery is recommended in women desiring pregnancy with aortic diameters >45 mm. I C Prophylactic aortic root surgery may be considered in women desiring pregnancy with aortic diameters of 40–45 mm. IIb C Recommendations for physical exercise in patients with Marfan syndrome It is recommended to individualize physical activity in patients with MFS based on aortic diameter, family history of aortic dissection, and pre-existing fitness. I C Regular moderate aerobic exercise with a level of intensity informed by aortic diameter is recommended in most patients with MFS. I C For patients who present with aortic dissection and/or have undergone aortic surgery, post-operative cardiac rehabilitation aiming at improving both physical and mental health should be considered. IIa B Recommendations for imaging follow-up in Loeys–Dietz syndrome In patients with Loeys–Dietz syndrome, TTE at baseline and subsequently every 6–12 months, depending on aortic diameter and growth, is recommended. I C In patients with Loeys–Dietz syndrome, a baseline arterial imaging study from head to pelvis with CMR or CCT and subsequent surveillance with CMR or CCT or DUS every 1–3 years is recommended. I C Recommendations for imaging and surgery in ACTA2-related heritable thoracic aortic disease Annual monitoring of the aortic root/ascending aorta with TTE to evaluate for aortic root/ascending aorta enlargement is recommended. I C Imaging of the aorta with CMR/CCT every 3–5 years is recommended. I C Prophylactic aortic root surgery should be considered with a diameter ≥45 mm, or lower in cases with other risk factors. IIa C
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.18
Recommendations for bicuspid aortic valve-associated aortopathy management Surgery for bicuspid aortopathy of the root phenotype is recommended when the maximum aortic diameter is ≥50 mm. I B Screening by TTE in FDRs of BAV patients with root phenotype aortopathy and/or isolated aortic regurgitation is recommended. I C In patients with low surgical risk, surgery for bicuspid aortopathy of ascending phenotype should be considered when the maximum aortic diameter is >52 mm. IIa B Recommendations for evaluation and medical treatment of patients with coarctation of the aorta In patients with native or repaired coarctation, lifelong follow-up is recommended, including regular imaging of the aorta with CCT/CMR every 3–5 years (adapted to clinical status and previous imaging findings). I B Recommendations for screening and management of polyvascular disease and peripheral arterial disease with cardiac diseases In patients with PVD, an LDL-C reduction by ≥50% from baseline and an LDL-C goal of <1.4 mmol/L (<55 mg/dL) are recommended. I A In patients with stable PVD who are symptomatic in at least one territory and without high bleeding risk, treatment with a combination of rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered. IIa A © ESC 2024
AAA, abdominal aortic aneurysm; AAD, acute aortic dissection; AAS, acute aortic syndrome; AHI, aortic height index; ARB, angiotensin receptor blocker; ASI, aortic size index; BAV, bicuspid aortic valve; BB, beta-blocker; b.i.d., twice daily; BP, blood pressure; BTK, below-the-knee; BSA, body surface area; CCT, cardiovascular computed tomography; CEUS, contrast-enhanced ultrasound; CLTI, chronic limb-threatening ischaemia; CMR, cardiovascular magnetic resonance; CS, carotid artery stenosis; CV, cardiovascular; CVRFs, cardiovascular risk factors; DM, diabetes mellitus; DTA, descending thoracic aorta; DUS, duplex ultrasound; ECST, European Carotid Surgery Trial; FDR, first-degree relative; FL, false lumen; GSV, great saphenous vein; HBET, home-based exercise training; HTAD, heritable thoracic aortic disease; ICA, internal carotid artery; IMH, intramural haematoma; IC, intermittent claudication; i.v., intravenous; LDL-C, low-density lipoprotein cholesterol; MFS, Marfan syndrome; NASCET, North American Symptomatic Carotid Endarterectomy Trial; OAC, oral anticoagulation; o.d., once daily; OMT, optimal medical treatment; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease; PAU, penetrating atherosclerotic ulcer; PVD, polyvascular disease; QoL, quality of life; RAS, renal artery stenosis; SAPT, single antiplatelet therapy; SET, supervised exercise training; TAA, thoracic aortic aneurysm; TAAD, type A aortic dissection; TBAD, type B aortic dissection; TOE, transoesophageal echocardiography; TEVAR/EVAR, thoracic endovascular aortic aneurysm repair; TS, Turner syndrome; TTE, transthoracic echocardiography; vEDS, vascular Ehlers–Danlos syndrome.
Table 4 Revised recommendations
Recommendations in 2017 (PAD) and 2014 (Aortic) Class Level Recommendations in 2024 Class Level
Recommendations for abdominal aortic aneurysm screening Screening for AAA with DUS Is recommended in all men >65 years of age. I A Is recommended in men aged ≥65 years with a history of
smoking to reduce the risk of death from ruptured AAA. I A
(i) May be considered in women >65 years of age with
history of current/past smoking. IIb C May be considered in men aged ≥75 years (irrespective of
smoking history) or in women aged ≥75 years who are
current smokers, hypertensive, or both. IIb C (ii) Is not recommended in female non-smokers without familial history. III C Family AAA screening with DUS Targeted screening for AAA with ultrasound should be considered in first-degree siblings of a patient with AAA. IIa B Is recommended for FDRs of patients with AAA aged
≥50, unless an acquired cause can be clearly identified. I C
Opportunistic AAA screening with DUS Targeted screening for AAA with ultrasound should be considered in first-degree siblings of patients with AAA. IIa B Should be considered in men ≥65 years and in women aged ≥75 years during TTE. IIa B Recommendations for antihypertensive therapy in patients with peripheral and aortic disease In patients with PAD and hypertension, it is recommended to control blood pressure at <140/90 mmHg I A In patients with PAAD and hypertension an SBP target
towards 120–129 mmHg, if tolerated, is recommended. I A
ACEIs or ARBs should be considered as first-line therapy in patients with PAD and hypertension. IIa B ACEIs/ARBs may be considered in all patients with PAD, regardless of BP levels, in the absence of contraindications. IIb B Recommendations for lipid-lowering therapy for patients with peripheral arterial and aortic diseases In patients with PAD, it is recommended to reduce LDL-C to <1.8 mmol/L (70 mg/dL) or decrease it by >50% if baseline values are 1.8–3.5 mmol/L (70–135 mg/dL). I C An ultimate LDL-C goal of <1.4 mmol/L (55 mg/dL) and a
>50% reduction in LDL-C vs. baseline are recommended in patients with atherosclerotic PAAD. I A
Recommendations for carotid artery stenosis assessment DUS (as first-line imaging), CTA, and/or MRA are recommended for evaluating the extent and severity of extracranial carotid stenosis. I B It is recommended to use DUS as first-line imaging to
diagnose ICA stenosis. I C
ESC Guidelines 3555
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.19
Recommendations in patients with visceral artery stenosis In patients with acute embolic occlusion of the SMA, both endovascular and open surgery therapy should be considered. IIa B In patients with acute mesenteric ischaemia due to acute occlusion of the SMA, endovascular revascularization is
recommended. I B
Recommendations for surveillance of patients with abdominal aorta aneurysm In patients with small (30–55 mm) AAA, the following time interval should be considered: • Every 3 years for AAA of 30–39 mm diameter • Every 2 years for AAA of 40–44 mm diameter • Every year for AAA >45 mm diameter. IIa B DUS surveillance should be considered annually in women with AAA of 40–45 mm and in men with AAA of 40–
49 mm. IIa B
Recommendations for surgery in aortic root and ascending aorta dilatation associated with tricuspid aortic valve Surgery should be considered in patients who have isolated aortic arch aneurysm with a maximal diameter ≥55 mm. IIa C Surgery is recommended in patients with dilatation of the aortic root or ascending aorta with a tricuspid aortic valve
and a maximum diameter of ≥55 mm. I B
Aortic valve repair using the reimplantation technique or remodelling with aortic annuloplasty is recommended in young patients with aortic root dilation and tricuspid aortic valves. I C Valve-sparing aortic root replacement is recommended in
patients with aortic root dilatation if performed in experienced centres and durable results are expected. I B
Lower thresholds for intervention may be considered according to BSA in patients with small stature or in the case of rapid progression, aortic valve regurgitation, planned pregnancy, and patient’s preference.
IIb C Ascending aortic or root replacement may be considered at a maximum diameter of ≥50 mm in patients with
proximal aorta dilatation who can be offered surgery with low predicted risk and present with any of the following: • Growth of the aortic diameter ≥3 mm per year • Resistant hypertension • Short stature (<1.69 m) • Root phenotype • Aortic length >11 cm • Age <50 years • Desire for pregnancy • Aortic coarctation. IIb B
Recommendations for surgery in aortic arch aneurysms Aortic arch repair may be considered in patients with aortic arch aneurysm who already have an indication for surgery of an adjacent aneurysm located in the ascending or descending aorta. IIb C In patients undergoing open surgical repair of an ascending
aortic aneurysm, concomitant hemi-arch replacement should be considered if the dilatation extends into the proximal aortic arch (>50 mm). IIa C
Recommendations for follow-up after treatment of aortic aneurysms After TEVAR or EVAR, surveillance is recommended after 1, 6, and 12 months and then yearly. Shorter intervals can be proposed in the event of abnormal findings requiring closer surveillance. I C After TEVAR, follow-up imaging is recommended at 1 and
12 months post-operatively, then yearly until the fifth post-operative year if no abnormalities are documented. I B
Long-term surveillance of open abdominal aortic repair may be considered at loose (5 year) intervals using colour DUS or CCT imaging. IIb C After open repair of AAA, first follow-up imaging is
recommended within 1 post-operative year, and every 5 years thereafter if findings are stable. I A
If neither endoleak nor AAA sac enlargement is documented during first year after EVAR, then colour DUS, with or without contrast agents, should be considered for annual post-operative surveillance, with non-contrast CT imaging every 5 years. IIa C After EVAR, follow-up imaging is recommended with CCT
(or CMR) and DUS/CEUS at 1 month and 12 months post-operatively, then, if no abnormalities are documented, DUS/CEUS is recommended every year, repeating CCT or CMR (based on potential artefacts) every 5 years. I A
Recommendations for diagnostic work-up of acute aortic syndrome TTE is recommended as an initial imaging investigation. In stable patients with a suspicion of AAS, the following imaging modalities are recommended (or should be considered according to local availability and expertise): I C In patients with suspected AAS, focused TTE (with use of
contrast if feasible) is recommended during the initial evaluation. I C
MRI
I C In patients with suspected AAS, CMR should be
considered as an alternative imaging technique if CCT is not available. IIa C
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.20
TOE
IIa C In patients with suspected AAS, TOE is recommended to
guide peri-operative management and detect complications. I C
Recommendations for medical treatment in acute aortic syndromes In all patients with AD, medical therapy, including pain relief and blood pressure control, is recommended. I C Invasive monitoring with an arterial line and continuous
three-lead ECG recording, as well as admission to an intensive care unit, is recommended. I B
Recommendations for the management of patients presenting with acute type B aortic dissection In complicated TBAD, TEVAR is recommended. I C In patients with complicated acute TBAD, emergency intervention is recommended. I B In complicated TBAD, surgery may be considered. IIb C In complicated TBAD, TEVAR may be recommended. IIb C In patients with complicated acute TBAD, TEVAR is recommended as the first-line therapy. I B In complicated TBAD, surgery may be considered. IIb C Recommendations for the management of intramural haematoma In complicated type B IMH, TEVAR should be considered. IIa C In complicated type B IMH, TEVAR is recommended. I C Recommendations for the management of penetrating atherosclerotic ulcer In the case of type A PAU, surgery should be considered. IIa C In the case of type A PAU, surgery is recommended. I C In complicated type B PAU, TEVAR should be considered. IIa C In complicated type B PAU, endovascular treatment is
recommended. I C
Recommendations for traumatic aortic injury In cases of TAI with suitable anatomy requiring intervention, TEVAR should be preferred to surgery. IIa C In cases of TAI with suitable anatomy requiring intervention, TEVAR is recommended over open surgery. I A Recommendations for genetic testing and aortic screening in aortic disease It is recommended to investigate FDRs (siblings and parents) of a subject with TAAD to identify a familial form in which relatives all have a 50% chance of carrying the family mutation/disease. I C Imaging screening of family members of patients with TAD with risk factors for HTAD in whom no (likely)
pathogenic variant is identified should be considered starting at age 25, or 10 years below the youngest case, whichever is younger. If the initial screening is normal, continued screening every 5 years until the age of 60 should be considered. IIa C
Recommendations for bicuspid aortic valve-associated aortopathy management Cardiac MRI or CT is indicated in patients with BAV when the morphology of the aortic root and the ascending aorta cannot be accurately assessed by TTE. I C CCT or CMR of the entire thoracic aorta is
recommended at first diagnosis and when important discrepancies in measurements are found between subsequent TTE controls during surveillance, or when the diameter of the aorta exceeds 45 mm.
I C In the case of aortic diameter >50 mm or an increase of >3 mm per year measured by echocardiography, confirmation of the measurement is indicated, using another imaging modality (CT or MRI). I C In the case of a diameter of the aortic root or the ascending aorta >45 mm or an increase of >3 mm per year measured by echocardiography, annual measurement of aortic diameter is indicated. I C Surveillance serial imaging by TTE is recommended in BAV
patients with a maximum aortic diameter >40 mm, either with no indication for surgery or after isolated aortic valve surgery, after 1 year, then if stability is observed, every 2–3 years. I C
In cases of BAV, surgery of the ascending aorta is indicated in the case of: • Aortic root or ascending aortic diameter >50 mm in the presence of other risk factors (coarctation of the aorta,
systemic hypertension, family history of dissection, or increase in aortic diameter of >3 mm per year).
I C In patients with low surgical risk and ascending phenotype
bicuspid aortopathy, surgery should be considered at a maximum diameter ≥50 mm if any of the following is the case: • Age <50 years • Short stature • Ascending aortic length ≥11 cm • Aortic diameter growth rate >3 mm per year • Family history of acute aortic syndrome • Aortic coarctation • Resistant hypertension • Concomitant non-aortic-valve cardiac surgery • Desire for pregnancy IIa C
ESC Guidelines 3557
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.21
4 Epidemiology and risk factors
4.1 Epidemiology
Peripheral arterial disease (PAD) is prevalent worldwide and affects 113 million people aged 40 and older, of which 42.6% are in countries with a low-to-middle sociodemographic index. Global prevalence is 1.52%, increases with age (14.91% in those aged 80–84 years), and is higher in females than in males (18.03% vs. 10.56%, in the same age group).10–13 PAD prevalence rose by 72% from 1990 to 2019, considering a 45% growth rate in the world population.10,11,14 The overall global age-standardized prevalence is about 1470 per 100 000 persons (Figure 2).14 Ischaemic cerebral disease, mainly linked to carotid stenosis (65% of cases), has a prevalence of 77.19 million, marking a 95% increase from 1990 to 2019.15
The overall prevalence of aortic disease including aneurysm and dissections is estimated at around 1% to 3% in the general population, with up to 10% prevalence in older age groups. European studies show a decrease in abdominal aortic aneurysm (AAA) prevalence in screened men >65 years of age, at 1.3%–3.3%,16,17 contrasting with the United States of America’s 5% found in screened male smokers.16,17 Globally, in 2019, there were 172 000 aortic aneurysm-related deaths (82.1% increase from 1990).10
In cases of BAV, surgery of the ascending aorta is indicated in the case of: • Aortic root or ascending aortic diameter >45 mm when surgical aortic valve replacement is scheduled. I C Surgery for bicuspid aortopathy in patients undergoing
aortic valve surgery should be considered at a root or ascending diameter ≥45 mm. IIa C
Recommendations for screening and management of polyvascular disease and peripheral arterial disease with cardiac diseases In patients undergoing CABG, DUS is recommended in patients with a recent (<6 months) history of TIA/stroke. I B Carotid DUS should be considered for stable patients
scheduled for CABG with TIA/stroke within the past 6 months without carotid revascularization. IIa B © ESC 2024
AAA, abdominal aortic aneurysm; AAS, acute aortic syndrome; ACEI, angiotensin-converting enzyme inhibitor; AD, aortic dissection; ARB, angiotensin receptor blocker; BAV, bicuspid aortic valve; BP, blood pressure; BSA, body surface area; CABG, coronary artery bypass grafting; CCT, cardiovascular computed tomography; CEUS, contrast-enhanced ultrasound; CMR, cardiovascular magnetic resonance; CT, computed tomography; CTA, computed tomography angiography; DUS, duplex ultrasound; ECG, electrocardiogram; FDR, first-degree relative; HTAD, heritable thoracic aortic disease; ICA, internal carotid artery; IMH, intramural haematoma; LDL-C, low-density lipoprotein cholesterol; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease; PAU, penetrating atherosclerotic ulcer; SBP, systolic blood pressure; SMA, superior mesenteric artery; TAAD, type A aortic dissection; TAD, thoracic aortic disease; TAI, traumatic aortic injury; TBAD, type B aortic dissection; TOE, transoesophageal echocardiography; TEVAR/EVAR, thoracic endovascular aortic aneurysm repair; TIA, transient ischaemic attack; TTE, transthoracic echocardiography.
30 000
25 000
20 000
15 000
10 000
5000 0 40–44 45–49 50–54 55–59 60–64 65–69 70–74 75–79 80–84 85–89 90–94
Female Male
Age (years)
Prevalence rate (per 100 000 population)
Figure 2 Estimated specific prevalence of peripheral arterial disease, by sex, in people aged 40 years and older. Adapted from12 under the terms of the Open access Creative Commons CC-BY license. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.22
4.2 Risk factors
Main PAAD risk factors are summarized in Figure 3. Traditional risk factors in tools like Framingham, Reynolds, Atherosclerotic Cardiovascular Disease (ASCVD) risk estimator Plus (United States of America), SCORE2 (Systematic Coronary Risk Evaluation 2, age 40–69 years), SCORE2- Diabetes (Systematic Coronary Risk Evaluation 2 - diabetes), and SCORE2-OP (Systematic Coronary Risk Evaluation 2–Older Persons) (Europe)18 also contribute to PAAD’s pathophysiology and development. More details are available in Supplementary data online, Section 1.1, and the 2021 ESC Guidelines on CV disease prevention in clinical practice.19
Low-density lipoprotein cholesterol (LDL-C) is a pivotal factor in atherosclerosis,19 with diabetes and tobacco exposure significantly
A
t
h
e
r
o s c l e r o t i c P
A
A
D
Traditional risk factors
Non-traditional risk factors
Female-specific
risk factors
Non-modifiable risk factors Modifiable risk factors
Overweight
Sedentary lifestyle
Sleep disorders
Apolipoproteins
Environmental pollution
Socio-economic status
Menopause
Pregnancy-induced hypertension/ diabetes
Polygenic and family inheritance
Sex Age Tobacco Diabetes Lipids
Hypertension
Stressful lifestyle
Alcohol
Diet
Inflammation Autoimmune disease
Figure 3 Main risk factors associated with atherosclerosis in peripheral arterial and aortic diseases. PAAD, peripheral arterial and aortic diseases.
ESC Guidelines 3559
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.23
amplifying PAD risk by 2–4 times each.20 Both men and women face a similar risk of PAD, but women have distinct risk factors (Figure 3).21 Hypertension and male sex are major risk factors for AAA, whereas diabetes mellitus lowers its incidence by 25%.22–24 Thoracic aortic aneurysm (TAA) or dissection share atherosclerotic risk factors, yet monogenic or polygenic diseases like Marfan syndrome (MFS), more prevalent in younger individuals, also contribute.24,25 Inflammation as a risk factor can be observed in PAAD26 and the potential for inflammation to be a modifiable risk factor is indicated by research related to colchicine and the effects demonstrated by canakinumab (a monoclonal antibody that reduces inflammation by inhibiting interleukin-1 beta).27,28
5 Evaluation of peripheral arteries
and aorta
To be consistent with existing literature, the term PAD is used to refer to lower-extremity atherosclerotic arterial disease.
5.1 Clinical history and examination, and
laboratory assessment, in patients with peripheral arterial and aortic diseases Clinical evaluation encompassing history (including family history), review of symptoms, and physical examination are the first steps in diagnosing and assessing patients with PAAD. Pulse palpation, femoral, carotid, and abdominal bruit auscultation, heart auscultation, and observation of the legs and feet need to be part of the vascular examination. Clinical signs, beyond aiding diagnosis, offer prognostic insights. Carotid bruits double the risk of myocardial infarction (MI) and CV death,29,30 while a brachial systolic blood pressure (SBP) difference of more than 15 mmHg raises CV death risk by 50%.31 Hence, bilateral arm blood pressure (BP) measurement is recommended.32 Lab assessments should include lipid profile (including lipoprotein[a] at least once in a lifetime),33 fasting glycaemia, glycated haemoglobin (HbA1c), renal function, blood count, coagulation studies, liver function, electrolytes, and inflammatory markers (C-reactive protein [CRP] and erythrocyte sedimentation rate). Additional evaluations, like thyroid function tests, are advised as needed.
5.2 Functional and quality of life
assessment in patients with peripheral arterial and aortic diseases Patients with PAD have decreased walking performance and selfreported physical and mental health-related quality of life (HRQoL).34–40 Muscle strength and balance are also impaired,41–45 leading to a faster decline in functional (physical functioning) performance in both symptomatic and asymptomatic patients.46,47 Depression is associated with greater impairment in functional performance.48,49 Impaired functional status is related to decreased self-reported HRQoL,50,51 and predicts further mobility loss and CV mortality.52,53 Very poor HRQoL has been found in patients with chronic limbthreatening ischaemia (CLTI).54 Different questionnaires are available assessing different facets (functional, mental, and social status) of patient-reported outcome measures (PROMs).34–36,38 The Short-form 36-item health questionnaire (SF-36) (including physical- and mental health-related items) is the most used generic questionnaire in PAD.35,36,38 The Edinburgh Claudication Questionnaire is a modified version of the initially developed Rose questionnaire and has a sensitivity of 91% and a specificity of 99% in comparison with a physician-based diagnosis.55,56 The Walking Impairment Questionnaire (WIQ), the Walking Estimated Limitation Calculated by History (WELCH), and the Vascular quality of life (VascuQoL) questionnaire are the most used PAD-specific questionnaires.34–36,38
Treadmill testing, using standardized criteria, is the gold standard to assess walking performance.37,57–62 Patients are asked to walk until maximal pain levels, defining the maximal walking distance (MWD). Patients are also asked to indicate the point at which pain begins, defining the pain-free walking distance (PFWD). Constant-load protocols have poorer reliability than graded protocols.60–64 Additionally, the six-minute walk test (6MWT) should be performed to assess functional walking performance.62,65 For muscular lower-limb strength assessment,66 isokinetic dynamometry has good test–retest reliability.67 Alternatively, the Short physical performance battery (SPPB) test should be used.62,64,68,69 The SPPB has good test–retest reliability.64 Few data exist on HRQoL, functional assessment, and exercise capacity in patients with aortic diseases.70,71 Those with acute aortic dissection (AAD), as well as patients who had aortic valve or thoracic aortic surgery, may present with depression and anxiety, leading to mental health issues72,73 that can also be assessed with the SF-36 questionnaire or the hospital anxiety and depression score (HADS).72 Patients with MFS have reduced HRQoL and a significant decline over time in physical HRQoL.74,75 Assessing HRQoL in aortic disease patients is crucial for understanding well-being, disease impact, and treatment effects. This involves PROMs, including surveys, symptom assessment, functional evaluation, psychological well-being (HADS), social and occupational function, and medication/treatment side effects. It also covers healthcare utilization and patient satisfaction, informing care and enhancing aortic disease management.
Recommendation Table 1 — Recommendations for clinical and laboratory, and for functional and quality of life, assessment in patients with peripheral arterial and aortic disease (see also Evidence Table 1)
Recommendations Classa Levelb
When managing PAAD, it is recommended to adopt a comprehensive approach that addresses the entirety of the arterial circulation.76 I B To assess PAAD, it is recommended to perform thorough clinical, vascular, and CVRFs laboratory evaluation.77 I C Overall evaluation of functional (physical functioning) performance with objective tests should be considered in patients with symptomatic and asymptomatic chronic PAD.57,61,63 IIa B Overall evaluation of self-reported (i.e. by questionnaire) physical and mental/social HRQoL should be considered in patients with PAAD.34–36,38,72 IIa B © ESC 2024
CVRFs, cardiovascular risk factors; HRQoL, health-related quality of life; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.24
5.3 Vascular examination of peripheral
arteries
The ankle-brachial index (ABI)78,79 is a low-cost, easy, and largely used tool, used both at rest or after exercise80–84 for PAD diagnosis and surveillance (Figure 4). Both oscillometric and Doppler methods have shown good concordance.78 Resting ABI has a 68%–84% sensitivity and an 84%–99% specificity for PAD diagnosis (Figure 4).79 An ABI ≤0.90 confirms PAD diagnosis.79,85–87 For values >1.40, the term ‘non-compressible arteries’ should be used.
Ankle–brachial index >1.40, seen in arterial stiffness (diabetes, severe kidney failure, or advanced age), correlates with increased CV events and mortality risk.88,89 For ABI >1.40, assessing resting toe– brachial index (TBI) is recommended.79,90–95 Toe–brachial index addresses medium-calibre artery rigidity96 measuring pressure on the hallux, second, or third toe using laser Doppler probe or plethysmography.97,98 Sensitivity and specificity for PAD diagnosis
Ankle-brachial index (ABI)
Haemodynamic criteria for PAD
Haemodynamic criteria for CLTI
Higher systolic ankle pressure of target leg
(posterior tibial or dorsalis pedis artery)
Higher systolic brachial pressure,
irrespective of target leg Toe-brachial index (TBI)
Toe pressure of target leg Higher systolic brachial pressure,
irrespective of target leg
Borderline ABI
0.90 1.0 0.70
1.40 Abnormal
low ABI Abnormal
low TBI
Abnormal high ABI
Normal
ABI Normal
TBI
Ankle pressure <50 mmHg
How to measure Transcutaneous oxygen partial pressure (TcPO2)
Toe pressure <30 mmHg
TcPO2 <30 mmHg
In supine position, 5–10 min resting, constant room temperature ABI and ankle pressure: cuffs on upper arms and lower limbs (just above the ankle) TBI and toe pressure: cuffs on upper arms and photoplethysmography probe on distal pulp of first or second toe TcPO2: preferred position of measurement electrode at first intermetatarsal position
Figure 4 Haemodynamic assessment of peripheral arterial disease. ABI, ankle–brachial index; CLTI, chronic limb-threatening ischaemia; PAD, peripheral arterial disease; TBI, toe–brachial index; TcPO2, transcutaneous oxygen pressure.
ESC Guidelines 3561
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.25
range from 45% to 100% and 17% to 100%, respectively.91 The usual pathological threshold for TBI is ≤0.70 (Figure 4).99 Used within the Framingham risk score, ABI enables the upgrading of risk estimation in ‘low-risk’ women and men,77,88 it allows CV risk assessment in diverse ethnic groups independently of risk factors,77,89 and is inexpensive and minimally time-consuming.100 Trained physicians have better reproducibility than inexperienced ones.101,102 In patients with exertional limb pain relieved by rest and a resting ABI >0.90, exercise testing with post-exercise ABI measurements or exercise oximetry has been proposed to diagnose lower-limb arterial stenoses.103–105 The post-exercise ABI is determined 1 min after the cessation of a standardized treadmill exercise.106 The physician measures bilateral ankle BP, starting with the symptomatic leg, using the ankle artery used for the reference resting ABI measurement. Brachial SBP should simultaneously be measured to enable calculation of the post-exercise ABI.104 Discrepancies in PAD diagnosis exist between exercise criteria, such as a fall in absolute ankle BP >30 mmHg or a drop of >20% in the postexercise ABI.104 Recent studies identified numerous false positives in a healthy population when using a post-exercise ABI drop of >20% as the diagnostic threshold, as commonly proposed.103 Measurement of transcutaneous oxygen pressure (TcPO2) is a means of evaluating tissue viability and is proposed as a diagnostic criterion of CLTI (Figure 4).107 TcPO2 is affected by local and general factors such as skin thickness, probe temperature, inflammation, and oedema,108,109 resulting in misleading values. Resting TcPO2 >30 mmHg is a favourable indicator of wound healing;110–112 however, resting TcPO2 <10 mmHg is associated with bad prognosis for wound healing and amputation in CLTI patients treated with bone marrow-derived stem cells.107 When performed at successive levels on an ischaemic limb, TcPO2 measurement may help to determine amputation level.113–115
Exercise transcutaneous oximetry has also been proposed.116,117 This seems of interest to detect proximal (buttock) claudication105 or unsuspected exercise-induced hypoxaemia118 in patients with intermittent claudication (IC).117
5.3.1 Duplex ultrasound
Duplex ultrasound (DUS) is a first step in the vascular work-up for PAD screening and diagnosis, allowing a dynamic, non-invasive, radiation- and contrast-free examination. It localizes vascular lesions and quantifies their extent and severity through velocity criteria.119–121 In combination with ABI or TBI, DUS permits determining the haemodynamic relevance of arterial lesions122,123 and estimation of ABI.124 DUS has a sensitivity of 88% and specificity of 95% for >50% stenosis detection.125 Post-exercise DUS can reveal borderline arterial lesions if initial findings are inconclusive.122,126,127 Duplex ultrasound distinguishes atherosclerotic (even subclinical disease) from non-atherosclerotic lesions, but its reliability relies on the sonographer’s expertise.122 Cross-sectional imaging is advisable for revascularization planning. ABI and DUS are recommended for PAD patient follow-up post-revascularization.128 More recent techniques, such as flow imaging, 3D echography, ultrafast ultrasound, and shear wave elastography, as well as the use of contrast-enhanced ultrasound (CEUS), could further improve DUS performance.129 5.3.2 Digital subtraction angiography, computed
tomography angiography, and magnetic resonance angiography Detailed information about these techniques can be found in the Supplementary data online, Section 1.2 (Table S1). Digital subtraction angiography (DSA) remains mostly limited to revascularization procedures. Computed tomography angiography (CTA) offers better spatial resolution than magnetic resonance angiography (MRA) and better calcification visualization; however, it can also overestimate stenosis severity due to the blooming effect. MRA allows arterial wall and lumen assessment as well as tissue and organ perfusion distal to or surrounding the explored arterial territory.
5.4 Evaluation of the aorta
The aorta can be divided into different anatomical regions (from proximal to distal) for reporting purposes. The main anatomical aortic regions are the aortic root, ascending aorta, aortic arch, descending thoracic aorta (DTA), abdominal aorta (AA), infrarenal aorta, and the iliac arteries (Figure 5).134,135
5.4.1 Aortic measurements
The main imaging techniques used for aortic evaluation are illustrated in Table 5. Evaluating aortic dilation and progression depends on standardized measurements. In echocardiography, aortic diameters should be measured using the leading-to-leading edge method during end-diastole (as systole sees about a 2 mm aortic expansion) in all segments (Figure 6).137,138 Most studies supporting prophylactic surgery have used this approach. Furthermore, better agreement exists between echo’s leading-to-leading edge and cardiovascular computed tomography (CCT)/cardiovascular magnetic resonance (CMR)’s inner-to-inner edge during end-diastole.137,139,140 However, when the aortic wall thickens (e.g. atheroma, thrombus, intramural haematoma [IMH], or aortitis) or in cases of aortic dissection (AD), also report the outer-to-outer diameter (Figure 6).
Recommendation Table 2 — Recommendations for diagnostic tests in patients with peripheral arterial disease
Recommendations Classa Levelb
Measurement of the ABI is recommended as the first-line non-invasive test for screening and diagnosis of PAD, using an ABI ≤0.90 as a diagnostic criterion.79,90,130,131 I B In the case of non-compressible ankle arteries or ABI >1.40, additional methods such as TP, TBI or Doppler waveform analysis are recommended.90,91,124,132,133 I B © ESC 2024
ABI, ankle–brachial index; PAD, peripheral arterial disease; TBI, toe–brachial index; TP, toe pressure. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.26
Distal descending
aorta
Aortic arch
Thoracic descending aorta
Mid aortic arch
Proximal aortic arch Ascending aorta 37 mm
40 mm 34 mm
36 mm
Sinotubular junction Sinus of Valsalva (<22 mm/m2) 38 mm
40 mm 33 mm
34 mm 0 1 23 4
5
6 7 8
9 10 11
29 mm 26 mm
23 mm 20 mm
34 mm 31 mm
Abdominal
aorta 23 mm 19 mm
Proximal descending
aorta
Figure 5 Anatomy and aortic segments and upper normal values for aortic dimensions. Numbers represent the 11 aortic segments based on the Society for Vascular Surgery/Society of Thoracic Surgeons (SVS/STS) classification for surgical and endovascular purposes.136 Z-scores can be calculated for aortic root and ascending aorta. Calculation of z-scores can be performed following these links: https://www.marfan.fr/accueil/z-score-calculus/ or https://marfan.org/dx/z-score-adults.
ESC Guidelines 3563
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.27
Table 5 Main aortic imaging techniques
TTE/DUS TOE CCT CMR
Availability ++++ +++ ++ + Cost + ++ +++ ++++ Time requirement + +++ +++ ++++ Radiation 0 0 +++ 0 Spatial resolution 1 mm 1 mm 0.6 mm 1–2 mm Temporal resolution 20 msec 20 msec 80 msec 30 msec Nephrotoxicity 0 0 +++ + Accuracy ++ ++++ ++++ ++++ Serial examination ++++ ++ ++ ++++ Aortic wall visualization ++ +++ ++++ ++++ Aortic valve function +++ ++++ + ++++ RV/LV function +++ +++ +++a ++++ Aortic root assessment +++ +++ ++++ ++++ Aortic arch assessment ++ +++ ++++ ++++ Thoracic aorta assessment + ++ ++++ ++++ Abdominal aorta assessment +++ - ++++ ++++ © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; LV, left ventricle; RV right ventricle; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography. aCCT can be used to evaluate left and right ventricular function only if retrospective gating is used.
A B C
D E F
AoR ASC
Figure 6 Conventional measurements of the aorta at different levels by echocardiography or duplex ultrasound (A, B, C), cardiovascular computed tomography or cardiovascular magnetic resonance (D, E, F). (A) Echocardiographic measurements of the aortic root and ascending aorta using the leading-to-leading edge methodology. (B) The outer-to-outer convention in the abdominal aorta in cases with aortic wall disease in a longitudinal view. This method can be used in a non-circular section as an alternative. (C) The outer-to-outer antero-posterior diameter of the abdominal aorta in a cross-sectional view. Evaluation of the aortic root using the cusp-to-cusp diameter (D) and the cusp-to-commissure convention (E); (F) measurement of the ascending aorta and the descending aorta with the double-oblique technique. AoR, aortic root; ASC, proximal ascending aorta. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.28
Given the high incidence of atherosclerotic plaques/thrombi in the AA, the outer-to-outer convention should be preferred (also presenting the best agreement with CCT and CMR) (Figure 6).141,142 Regarding CCT and CMR, measurements must be performed using the inner-to-inner edge method (Figure 6) in end-diastole (fewer motion artefacts).137,143,144 The aortic root is measured in the parasternal long axis by transthoracic echocardiography (TTE),137,139,140,145 since the short axis underestimates the diameter due to possible plane obliquity. By CMR or CCT, the cusp-to-cusp diameter best correlates with echocardiography (Figure 6). A diameter difference >5 mm (among root diameters within the same imaging modality) indicates root asymmetry, frequent in bicuspid aortic valve (BAV) or genetic aortopathies, which is important to be determined since it generates underestimations.146 While 3D echocardiography is a potential surveillance alternative in these cases (especially if CMR/CCT is limited for serial follow-up), validation studies are lacking.147 In end-diastole, measure the ascending aorta by moving the transducer 1–2 intercostal spaces up in the parasternal long axis. Echocardiography provides information on aortic arch or DTA enlargement, but diagnostic certainty (precise measurement of the diameters) is lacking. CCT or CMR uses the double-oblique technique to measure aortic diameters, reporting antero-posterior and perpendicular dimensions for accurate assessment.148 It is recommended to report aortic measurements by specific segments based on anatomical landmarks and to relate the largest diameter to a nearby anatomical structure for reference. Changes in aortic diameter require a ≥3 mm increase in echocardiography, which should be confirmed with CCT/CMR and compared with baseline measurements. For accurate assessment, stick to the same imaging technique, centre, methodology, and side-by-side comparisons.137,140
5.4.2 Normal aortic values
When evaluating aortic dimensions and clinical relevance, consider factors like aortic region, anthropometric measurements, patient history, and underlying medical conditions. Factors influencing aortic and peripheral artery size in the normal population include age, sex, ethnicity, body surface area (BSA), and, particularly, height.149 Body surface area is the most used method to normalize aortic dimensions based on an individual’s body size, thus an ascending thoracic aorta >22 mm/m2 or a DTA >16 mm/m2 is considered aortic dilatation.150–152 However, extremes of low or high body weight pose limitations. In such cases, surgical thresholds may involve indexing aortic diameter by height (an aorta height index >32.1 mm/m is associated with a 12% yearly risk of aortic adverse events [AAE]),153 aortic cross-sectional area to patient height (a ratio ≥10 cm2/m implies reduced long-term survival),154 or aortic length (from the aortic annulus to the innominate artery, considering a length >11 cm a threshold for surgery).155 To correlate measured diameter with the expected one based on age, sex, and body surface, use nomograms or z-score calculation formulas, especially in heritable thoracic aortic disease (HTAD). Supplementary data online, Figure S1 and Table S2, presents nomograms developed for echocardiography, applicable also to CCT and CMR.156,157 Calculation of z-scores can be performed following these links: https://www.marfan.fr/accueil/z-score-calculus/ or https:// marfan.org/dx/z-score-adults/; reference values used for their estimation may vary depending on age and other factors. However, z-scores are limited by the fact that not all ethnic groups are equally represented (mostly white) and over- or underweight can lead to an over- or underestimation.158 Moreover, with ageing and loss of elastic properties, the aorta tends to enlarge. Aortic growth in adults is about 0.9 mm per 10 years in males and 0.7 mm per 10 years in females, which may be influenced by BP, physical activity, and genetic factors.
5.4.3 Chest X-ray and electrocardiogram
Chest X-ray obtained for other indications in asymptomatic patients or in cases of acute aortic syndrome (AAS) suspicion may detect abnormalities of aortic size/contour that need to be confirmed by another imaging technique. It presents limited sensitivity (64%) and specificity (86%) in the diagnosis of aortic diseases;162 thus, a normal chest X-ray may not rule out the diagnosis of AAS.162–164 On the contrary, chest X-ray may identify other causes of chest pain (e.g. pleural effusion or pneumothorax). Electrocardiogram (ECG) might be useful to rule out other causes of chest pain (e.g. MI) or AAS complications (coronary occlusion/dissection) but it is not useful for AAS diagnosis.
5.4.4 Echocardiography
It is considered the first-line imaging technique in the evaluation of aortic disease, assessing all echocardiographic windows and the aortic valve. It provides key anatomic information (i.e. dilatation, atherosclerotic lesions, or dissection) for the ascending aorta, arch, and AA; however, it is not useful to assess the exact diameters of the aortic arch and DTA (requiring confirmation with CCT/CMR). Also, the distal ascending aorta and proximal arch (blind spot) are inadequately visualized due to left mainstem bronchus interposition. Transthoracic echocardiography can identify AAS complications (e.g. aortic regurgitation, tamponade, or wall motion abnormalities), but its diagnostic accuracy for AAS is limited (sensitivity: 78%–100% for type A, 31%–55% for type B). Contrast enhancement improves diagnosis.165
Recommendation Table 3 — Recommendations for imaging of the aorta (see also Evidence Table 2)
Recommendations Classa Levelb
It is recommended that aortic diameters are measured at pre-specified anatomical landmarks, and the largest diameter of the section be perpendicular to the longitudinal axis.134,135 I C It is recommended in cases of serial imaging of the aorta over time to use the same imaging modality with the same measurement method.159 I C It is recommended to consider renal function, pregnancy, age, and history of allergy to contrast media to select the optimal imaging modality with minimal radiation exposure and lowest iatrogenic risk, except for emergency cases.159–161 I C Indexing aortic diameters to BSA, along with the use of nomograms, z-scores, or other indexing methods, should be considered for more accurate assessment of aortic size, especially for body sizes at the lower end of the normal distribution.156–158 IIa B © ESC 2024
BSA, body surface area. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3565
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.29
Transoesophageal echocardiography (TOE) is highly accurate (sensitivity: up to 99%, specificity: 89% for AAS), except with absolute contraindications like oesophageal issues, bleeding, recent gastro-oesophageal surgery, or respiratory distress. TOE is convenient for bedside and intraoperative use but less suitable for long-term surveillance, which requires evaluation with CCT/CMR.
5.4.5 Duplex ultrasound imaging of the abdominal
aorta After scanning both transversally and longitudinally, the anteroposterior (AP) diameter in a cross-sectional view of the AA should be measured. Ensure the DUS beam is perpendicular to the AA axis, forming a circular vessel section. If the AA is sinuous or dilated, achieving equal AP and transverse diameters may be challenging. In such instances, calculate the mean ellipse diameter or measure the AA diameter in a clear longitudinal view with a perpendicular diameter (Figure 6).122 The outer-to-outer (Figure 6) method is the one recommended by the American Institute of Ultrasound in Medicine, the American College of Cardiology/American Heart Association (ACC/AHA), and the European Society of Cardiology (ESC), since it is more reliable in cases of atherosclerotic plaque or intravascular thrombus and best correlates with CCT and CMR. However, the most effective methodology is under debate and further studies are needed to determine the best convention.169
Normal diameters of the AA are reported in Figure 5 and Supplementary data online, Section 1.3.
5.4.6 Cardiovascular computed tomography
Cardiovascular computed tomography, due to its quick acquisition, wide availability, high reproducibility, and suitability for emergency departments, is the primary imaging method for aortic disease diagnosis, prognosis, and therapy planning (sensitivity 100%, specificity 98% for AAS).170–172 ‘Double or triple rule-out’ protocols concurrently assess the aorta, pulmonary, and coronary arteries.173,174 Electrocardiogram triggering is crucial to prevent motion artefacts (especially in the aortic root and ascending aorta), which can distort measurements or resemble dissection flaps, facilitating coronary artery assessment. The standard protocol comprises non-enhanced scans (for calcification, IMH, or surgical material), contrast-enhanced CCT angiography, and a late scan (to visualize contrast leakage or aortic wall late enhancement suggestive of inflammation or infection).175 Iodinated contrast agents carry potential allergic reactions and postcontrast acute kidney injury (PC-AKI) risks.176 In these cases, opt for contrast-free CCT for accurate aortic diameter measurement (also for CMR-intolerant patients). Moreover, excessive radiation caution is crucial, particularly in young females, when performing CCT for monitoring chronic aortic diseases.177
5.4.7 Cardiovascular magnetic resonance
Cardiovascular magnetic resonance comprehensively evaluates the aorta, including shape, diameter, tissue characteristics (inflammation, infection, atheroma, bleeding),178 lesion extent, side branches, adjacent structures, and mural thrombus. It assesses ventricular and valve function, quantifies flow, and employs cine steady-state free precession (SSFP) or ECG-gated angio-CMR for the aortic root, while non-gated sequences suffice for the rest. Recently, 4D flow sequences179 have been developed to evaluate complex intravascular flows,180,181 complex flow parameters (wall shear stress, pulse wave velocity, or kinetic energy), or flow quantification at different levels in one unique acquisition (useful in AD or congenital diseases).182,183 Cardiovascular magnetic resonance obviates ionizing radiation and iodinated contrast (3D contrast CMR), making it ideal for young patients, women, and pregnancy. Caution is warranted, especially with non-macrocyclic gadolinium, for estimated glomerular filtration rate (eGFR) <30 mL/min/1.73 m2 (Supplementary data online, Section 1.2). CMR is increasingly used in patients with intracardiac devices (pacemakers/implantable cardioverter defibrillators, CMR- and non-CMR-compatible devices) with proper monitoring, but not for those with cochlear implants or intracranial clips.184,185 In the acute setting, CMR use is limited because of low availability, difficulties in monitoring unstable patients, and longer acquisition times.166,186
5.4.8 Positron emission tomography
Positron emission tomography (PET) usually uses 18F-fluorodeoxyglucose (FDG), allowing non-invasive assessments of metabolic activity
Recommendation Table 4 — Recommendations for thoracic aortic measurements
Recommendations Classa Levelb
TTE is recommended as the first-line imaging technique in evaluating thoracic aortic diseases.159,165 I B It is recommended to report aortic diameters using the leading-to-leading edge convention in end-diastole by echocardiography.137,139,140,159 I C It is recommended to report aortic diameters using the inner-to-inner edge convention in end-diastole by CCT or CMR.137,143,144,159 I C It is recommended to report aortic diameters from images obtained with the double-oblique technique (not axial images) by CCT or CMR.148 I C ECG-triggered CCT is recommended for comprehensive diagnosis, follow-up, and pre-invasive treatment assessment of the entire aorta, particularly the root and ascending aorta.159 I C CMR is recommended for diagnosis and follow-up of thoracic aortic diseases, especially when chronic follow-up is required.166–168 I C The aortic root should be measured using the cusp-to-cusp distance. Also, the presence of asymmetry (>5 mm) among distances should be reported.137,146 IIa C If an increase of ≥3 mm per year in aortic diameters by TTE is observed, confirmation by CCT/CMR should be considered.137,159 IIa C Chest X-ray may be considered in cases of low clinical probability of AAS; however, a negative exploration should not delay dedicated aortic imaging in high-risk patients.162–164 IIb C © ESC 2024
AAS, acute aortic syndrome; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; ECG, electrocardiogram; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.30
(inflammation/infection) and treatment response.187,188 Although different tracers have been tested to identify calcification, fibrosis and/or thrombus formation, most PET studies have focused on vasculitis. The relationship between FDG-PET images and AAA progression is controversial. However, fluorine-18–sodium fluoride (18F–NaF) PET-computed tomography (PET-CT), a marker of active vascular calcification and high-risk plaques, has shown a correlation between increased tracer uptake, AAA growth, and CV events.189 PET-CT has shown better diagnostic accuracy in identifying lesions and detecting graft infection or infectious aortic diseases.190–193 High radiation exposure, high costs, and limited availability are the main limitations of PET.
5.4.9 Intravascular ultrasound
Intravascular ultrasound (IVUS) provides high-resolution imaging for artery and vein diseases, aiding complex aortic disease management by distinguishing true and false lumens and guiding stent placement. It is operator-dependent, costly, and less accessible, but seems to provide better measurements for acute aortic syndromes.194
5.4.10 Digital subtraction aortography
Non-invasive imaging modalities have replaced DSA in first-line diagnostic testing, both in suspected AAS or known chronic AD; however, DSA might be useful if findings in non-invasive techniques are ambiguous or incomplete. It is primarily used for the percutaneous treatment of CAD, aortic visceral branches, or for monitoring thoracic endovascular aortic aneurysm repair (TEVAR/EVAR) implantation.
6. Screening for carotid, peripheral arterial, and aortic diseases
6.1 Screening for carotid and peripheral
arterial diseases 6.1.1. Lower-extremity peripheral arterial disease Due to elevated CV risk in chronic PAD, early diagnosis, prevention, and robust cardiovascular risk factor (CVRF) control are essential, even in asymptomatic cases. ‘Intermediary CV risk’ individuals may be reclassified as ‘high or very high risk’, prompting adapted prevention. ABI is the preferred first-line test for asymptomatic individuals aged ≥65 years,14,195 especially women.196 Screening might also be beneficial at a younger age in case of CVRFs, but data are still lacking. Clinical examination, functional status, and walking capacity assessment are recommended to detect ‘masked PAD’.77 In diabetes, early PAD (and foot neuropathy) diagnosis is crucial. Effective CVRF management and treatment can prevent CV disease, foot wounds, and amputation.197 In patients with diabetes and normal resting ABI, TBI measurement should be considered. The prevalence of popliteal aneurysms (PAs) is high in patients with AAA and subaneurysmal aortic dilatation, warranting screening. PAs are correlated with iliac and femoral artery diameters.76 In patients needing transfemoral access, screening for iliofemoral artery disease may be considered.198 6.1.2 Carotid artery stenosis
Due to the low prevalence of ≥70% asymptomatic carotid artery stenosis (CS) in the general population (0%–3.1%), widespread screening is not recommended since it does not reduce stroke risk and might lead to inappropriate stress and invasive procedures.199,200 Conversely, screening for significant CS in a highly selected population might be cost-effective, especially if prevalence is ≥20% (Table 6).201 When the degree of asymptomatic CS is ≥70%, the 5 year ipsilateral stroke risk is significantly increased (14.6%) and revascularization may be beneficial.202 Selective screening aims to prevent CV events, rather than identifying candidates for an intervention.203
6.1.3 Multisite artery disease
Multisite artery disease (MAD) is defined as the presence of atherosclerosis in two or more vascular beds.204 This is a common condition in patients with atherosclerotic diseases. Although associated with worse clinical outcomes, screening for asymptomatic disease in additional vascular sites did not seem to improve outcomes.77 More recently, screening for coronary calcifications (coronary artery calcium [CAC] score) and screening for carotid and femoral plaques have
Table 6 High-risk populations for carotid artery stenosis
Population Prevalence of carotid stenosis
(%)
>60 years + CVRFs (hypertension, CAD, current smoking, first-degree family history of stroke)210 Two CVRFs: 14%
Three CVRFs: 16% Four CVRFs: 67%
Hypertension + cardiac disease211 22% HD212 • In HD patients, prevalence of
carotid stenosis is high, and is associated with high peri-operative and long-term stroke or death rates • Carotid stenosis is a predictor of
death in patients with long-term dialysis and aged ≥70 years at time of surgery • Lower risk if previous renal
transplant.
PAD213 23.2% Severe CAD (before CABG) • Almost 20%214
• Carotid bruit and T2DM:
increased predictive value215 • Carotid stenosis = risk factors for
peri-operative stroke.215
Carotid bruit216 31% Previous neck irradiation217 21.7% (70%–99% stenosis) © ESC 2024
CABG, coronary artery bypass grafting; CAD, coronary artery disease; CVRFs, cardiovascular risk factors; HD, haemodialysis; PAD, peripheral arterial disease; T2DM, type 2 diabetes mellitus.
ESC Guidelines 3567
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.31
been shown to be of potential assistance in CV risk reclassification of ‘presumed moderate-risk patients’ into a higher-risk category, leading to more aggressive prevention strategies.205–209
6.2 Screening for aortic diseases
6.2.1. Screening for abdominal aortic aneurysm Abdominal aortic aneurysm screening by DUS is effective in reducing rupture-related mortality in populations with high AAA prevalence (especially male smokers aged ≥65 years).221–224 However, no such effect has been found in a single large study in which AAA prevalence was low (current or former smoking women aged 65–74 years, or with a history of CAD).225 Screening for AAA by non-contrast computed tomography (CT) was not found to be effective over 5 years in males aged 65–74 years in a Danish trial.226 Longer-term follow-up is planned, and as the technique involves ionizing radiation, no recommendation is made in relation to CT at present. Screening may be considered in populations at intermediate risk, such as men aged >75 years, or women aged >75 years who are hypertensive, smokers, or both, since almost all women in a contemporary population-based study who had ruptured AAA and were aged >75 years were either smokers or hypertensive.227,228 Screening for AAA is recommended in first-degree relatives (FDRs) of patients with AAA (especially siblings), as they are at increased risk of AAA when >50 years of age.229 The risk associated with family history is uncertain, but a population-based study estimated a relative risk of around 2.230 Screening should be repeated periodically if initial assessment is reassuring and performed at a relatively young age.231 Opportunistic screening (during TTE) identified AAA in about 2% of subjects, thus it may be considered in high-prevalence populations (males ≥65 or women ≥75 years of age).232 Additionally, opportunistic screening detects AAA in patients with symptomatic/asymptomatic PAD (with a 12% cumulative incidence in symptomatic PAD), making it worthwhile in this population.233 6.2.2 Screening for thoracic aortic aneurysm
Screening for TAA is described in detail in Section 10.1 and Section 10.2.
7 Optimal medical treatment
Optimal medical treatment (OMT), including lifestyle measures and pharmacological treatment, is recommended for all patients with PAAD (Figure 7).
7.1 Lifestyle, exercise, patient education
Apart from genetic-related TAA, hypertension and ASCVD are the main causative factors for PAAD. As lifestyle factors are strongly related to ASCVD,11 patients with PAAD should strive to maintain a healthy lifestyle. The 2021 ESC Guidelines on cardiovascular prevention19 give comprehensive guidance on risk factors for ASCVD and their treatment.
7.1.1 Diet
A Mediterranean diet rich in legumes, dietary fibre, nuts, fruits, and vegetables proves crucial and efficacious for primary and CV prevention in PAAD.238 It has demonstrated notable reductions in cholesterol and BP,239–247 and holds potential protective benefits against PAAD development.248,249 In a large cohort with 17.5 years of follow-up, adherence to a Mediterranean diet was associated with reduced AAA risk in current and ex-smokers.249,250 Malnutrition and metabolic disorders can complicate post-invasive procedure recovery and nutritional support may improve nutritional status and HRQoL.251
Recommendation Table 5 — Recommendations for peripheral arterial disease screening (see also Evidence Table 3)
Recommendations Classa Levelb
In patients with diabetes or chronic kidney disease, and normal resting ABI, TBI measurement should be considered. IIa B In patients ≥65 years of age with CVRFs, screening for PAD by ABI or TBI should be considered.77,218,219 IIa C In patients with AAA, femoro-popliteal aneurysm screening with DUS should be considered.76 IIa C In patients ≥65 years without CVRFs, screening for PAD by ABI or TBI may be considered.220 IIb C In patients needing intervention with transfemoral access, screening for iliofemoral artery disease may be considered.198 IIb C In patients with two or more CVRFs, screening for CS may be considered.201,203,210 IIb C © ESC 2024
AAA, abdominal aortic aneurysm; ABI, ankle–brachial index; CS, carotid artery stenosis; CVRFs, cardiovascular risk factors; DUS, duplex ultrasound; PAD, peripheral arterial disease; TBI, toe–brachial index. aClass of recommendation. bLevel of evidence. Recommendation Table 6 — Recommendations for abdominal aortic aneurysm screening
Recommendations Classa Levelb
Screening for AAA with DUS: Is recommended in men aged ≥65 years with a history of smoking to reduce the risk of death from ruptured AAA.221–224,234 I A May be considered in men aged ≥75 years (irrespective of smoking history) or in women aged ≥75 years who are current smokers, hypertensive, or both.227,228,235–237 IIb C Family AAA screening with DUS: Is recommended for FDRs of patients with AAA aged ≥50, unless an acquired cause can be clearly identified.231 I C Opportunistic AAA screening with DUS: Should be considered in symptomatic/asymptomatic PAD patients.233 IIa B Should be considered in men aged ≥65 years and in women aged ≥75 years during TTE.232 IIa B © ESC 2024
AAA, abdominal aortic aneurysm; FDR, first-degree relative; DUS, duplex ultrasound; PAD, peripheral arterial disease; TTE, transthoracic echocardiography. Smoking is defined as lifetime smoking of >100 cigarettes or equivalent. This threshold is used to distinguish between substantial exposure and occasional use. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.32
7.1.2 Physical activity
Few patients with chronic symptomatic PAD meet the physical activity guidelines252 for reducing the risk of major adverse cardiac events (MACE).253,254 Better ambulation, HRQoL, and vascular outcomes have been observed in patients meeting the physical activity time-intensity guidelines.19,255 Regular physical activity is also relevant in patients with aortic diseases70,71,256–259
and lowers resting heart rate and BP, thus decreasing the risk of aortic complications.256,259 Few data exist on the practice of exercise and sports in patients with aortic diseases.70,71,256–259 Recommendations should be individualized and based on risk stratification.71
Medications
Lifestyle Targets
Targets
Systolic blood pressure
≤120–129 mmHg
Beta-blockers ACEi or ARB Calcium channel blockers
Antiplatelet therapy
Statins Ezetimibe PCSK9i Bempedoic acid Reducing risk of atherothrombosis
Optimal glucose control (HbA1c <7%)
Educational programmes
Psychological support Genetic counselling Supervised exercise training LDL <55 mg/dL (<1.4 mmol/L)
Healthy diet BMI 20–25 kg/m2 Waist: <94 cm men; <80 cm women Low-to-moderate exercise training
Limit isometric exercise in
aortic diseases
Avoid excessive alcohol intake
Avoid smoking/smoking cessation
Avoid cocaine and stimulating drugs
Glucose-lowering agents Diastolic blood pressure
≤70–79 mmHg
Anticoagulants
Figure 7 Cardiovascular risk modification and healthy lifestyle interventions and targets in patients with peripheral arterial and aortic diseases. ACEi, angiotensin-converting enzyme inhibitors; ARB, angiotensin receptor blocker; BMI, body mass index; LDL, low-density lipoprotein; PCSK9i, proprotein convertase subtilisin/kexin type 9 inhibitor; HbA1c, glycated haemoglobin.
ESC Guidelines 3569
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.33
7.1.3 Smoking
Patients with PAAD who smoke should strongly be advised to quit (see Supplementary data online, Section 1.1.5). Complete smoking cessation and avoiding second-hand smoke or environmental particle air pollution are crucial in patients with PAAD to reduce the risk of death, AD, acute mesenteric ischaemia (AMI), AAA, and PAD.119,260–267 Smokers should be offered structural follow-up support, including nicotine replacement therapy, varenicline, and bupropion, individually or in combination.19,268,269 Smoking avoidance also includes cannabis, associated with premature ASCVD.266 Vaping and e-cigarette use has surged in the past decade, viewed by some as a healthier option than smoked tobacco, though long-term health effects remain unknown.270 E-cigarettes may be considered as an aid to quit tobacco smoking, as a recent Cochrane review found that they increase quit rates as compared with nicotine replacement therapy,271 but their use has been associated with adverse effects on CV, respiratory, immunological, and periodontal health compared with non-users, but with a milder impact than smoked cigarettes.272–274 However, their use should be brief and preferably not concurrent with traditional cigarettes.271,275 The main limitation of the evidence base remains imprecision due to the small number of randomized controlled trials (RCTs), often with low event rates and follow-up limited to 2 years.
7.1.4 Patient education
While detailed explanations of CVRFs might not always inspire lifestyle changes,276 providing plain language and visual aids is essential for patient understanding.277 Structured programmes, incorporating psychological and behavioural aspects, are pivotal in fostering desired changes.276 Engaging patients’ families, friends, and support networks significantly contributes to perpetuating these changes (particularly in self-care),276 and increases treatment compliance and self-efficacy, reducing hospitalization risk and enriching patient HRQoL.278,279 When caregivers disconnect from healthcare professionals, they should be recognised to receive better support systems.280,281 Psychosocial interventions are crucial to navigating complexities with resilience.282 Advocating active involvement, education, clear communication, and shared decision-making is key for achieving optimal patient outcomes.276–283
7.1.5 Risk scoring models in secondary prevention
Recent ESC CV prevention guidelines discuss risk models for developing vascular disease in healthy individuals and ASCVD patients.19 Several registries enabling risk prediction in ASCVD have been developed: REACH (The REduction of Atherothrombosis for Continued Health)284 and SMART (Secondary Manifestation of ARTerial disease)285 which use clinical parameters such as medical history, SBP, and common biomarkers. Addition of carotid ultrasound did not improve the model.286 A new algorithm combining the SMART and REACH models287 enables calculation of lifetime risk and treatment effects. The SMART model has recently been updated and validated288,289 with the SMART-2 algorithm. These tools are available online as clinical risk calculators (see www.u-preveotnt.com) and smartphone apps on the ESC website (https://www.escardio.org/ Education/ESC-Prevention-of-CVD-Programme/Risk-assessment/SMART- Risk-Score).
Recommendation Table 7 — Recommendations for lifestyle, physical activity, and patient education (see also Evidence Table 4)
Recommendations Classa Levelb
In patients with PAAD, cessation and abstinence from smoking of any kind is recommended to reduce the risk of AD, MI, death, and limb ischaemia.119,261–267 I A A healthy diet rich in legumes, dietary fibre, nuts, fruits, and vegetables, with a high flavonoid intake (Mediterranean diet), is recommended for CV disease prevention in patients with PAAD.239– 241,249,290–293 I A Low- to moderate-intensity (or high if tolerated)c aerobic activities are recommended in patients with PAD to increase overall and pain-free walking distance.37,294 I A In patients with PAAD, behavioural counselling to promote healthy diet, smoking cessation, and physical activity is recommended to improve the CV risk profile.241,249,253,295 I B It is recommended to promote patient and caregivers’ education and empowerment through tailored guidance on lifestyle adjustments and the importance of regular physical activity.276,277,283 I C In patients with PAAD, avoidance of exposure to second-hand smoke and air pollution should be considered.261 IIa C Physical exercise and sports activities should be considered in patients with aortic diseases based on prior risk stratification (based on the extent of the aneurysm, risk of dissection, and BP control).71 IIa C Use of web- or app-based secondary prevention risk calculators should be considered in the shared decision-making to improve patient adherence to treatment and lifestyle changes.288,289 IIa C E-cigarettes may be considered as an aid to quit tobacco smoking, but it is advisable to limit their use and avoid simultaneous use with conventional cigarettes due to unknown long-term effects.119,271,296,297 IIb C © ESC 2024
AD, aortic dissection; BP, blood pressure; CV, cardiovascular; MI, myocardial infarction; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease. aClass of recommendation. bLevel of evidence. cLow intensity refers to an exercising heart rate (HR) of 57%–63% HRmax or a rate of perceived exertion (RPE) on the Borg’s scale of 9–11. Moderate intensity refers to an exercising heart rate of 64%–76% HRmax or RPE of 12–13. Vigorous intensity refers to an exercising heart rate of 77%–95% HRmax or RPE of 14–17.298 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.34
7.2 Principles of pharmacological medical
therapy 7.2.1. Antithrombotic therapy Antithrombotic therapy is crucial for patients with symptomatic PAAD at high CV risk. While trials are fewer than in CAD, recent evidence should guide practice. In the absence of specific indications for chronic oral anticoagulation (OAC) in concomitant CV disease, a single antiplatelet agent is the primary long-term treatment for patients with symptomatic PAAD. Combining it with another antiplatelet agent or low-dose anticoagulants depends on the patient’s ischaemic and bleeding risk, as well as therapeutic paths (e.g. endovascular therapy). Recent guidelines299 propose a tool for bleeding risk assessment in PAD patients (OAC3 PAD score). Antithrombotic strategy is detailed in Sections 8 and 9 for each arterial territory.
7.2.2 Antihypertensive therapy
New 2024 ESC Guidelines on hypertension are currently published and should be reviewed for further details.300 Patients with hypertension and PAAD are considered to have target organ damage and are at high CV risk.300 Different meta-analyses showed that systolic BP treatments reduce CV risk in all ages up to 85 years down to a level of 120– 129 mmHg.301,302 There is no need to increase the BP target in healthy patients up to the age of 85 years.303,304 To reduce cardiovascular disease (CVD) risk, it is recommended that treated SBP values in most adults be targeted to 120–129 mmHg, provided the treatment is well tolerated. However, in cases where BP-lowering treatment is poorly tolerated and achieving an SBP of 120–129 mmHg is not possible, it is recommended to target an SBP level that is ‘as low as reasonably achievable’ (ALARA principle).301,302,305 To avoid overtreatment, out-of-office BP measurements may be helpful when pursuing this target. If on-treatment SBP is on target, but diastolic blood pressure (DBP) is ≥80 mmHg, intensified treatment may be considered to further reduce the CV risk.306 Because the CVD benefit of an on-treatment BP target of 120– 129 mmHg may not generalize to some groups, setting personalized and more lenient BP targets (e.g. <140/90 mmHg) has to be considered in patients with pre-treatment orthostatic hypotension, age ≥85 years, clinically significant frailty at any age, or a limited lifespan (<3 years).301 Patients with both PAAD and hypertension face a high or very high CV risk. Antihypertensive medications such as diuretics, beta-blockers (BBs), calcium channel blockers (CCBs), angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor blockers (ARBs) are all appropriate options for managing hypertension in PAAD. These agents can be used as monotherapy or in various combinations (excluding ARBs+ACEIs), considering individual patients’ conditions. It is often necessary to implement combination therapy, preferably in the form of a single pill, to effectively achieve the recommended treatment goals. However, ACEIs or ARBs should be considered as first-line antihypertensive therapy to reduce CV events.300,307–312 Regardless of BP levels and in the absence of contraindications, ACEIs/ARBs may be considered in all patients with PAD to reduce cardiovascular events.312,313 A meta-analysis suggests that antihypertensive treatment may improve mean walking distance in patients with PAD.310 Beta-blockers can be prescribed, if necessary, to patients with intermittent claudication, since they do not worsen walking capacity or limb events.314 There is some evidence suggesting a higher amputation rate315 or increased rate of re-intervention316 in patients with CLTI treated with ACEIs, although in one smaller study no effect on limb-related outcomes was observed.317 Thus, they remain a treatment option in hypertensive patients with PAD, especially in those with concomitant CAD.318 BBs were not associated with worsened clinical outcomes in a retrospective study319 on CLTI patients, but it seems prudent to avoid excessively low heart rates in these patients.
7.2.2.1 Renovascular hypertension
Angiotensin-converting enzyme inhibitors and ARBs effectively manage unilateral renal artery stenosis (RAS) by blocking the renin–angiotensin system, potentially reducing renal capillary perfusion pressure.320–322 This transiently lowers glomerular filtration rate (GFR) and raises serum creatinine. For bilateral RAS, regular follow-up assessments of renal function and kidney perfusion are advised. Angiotensin-converting enzyme inhibitors and ARBs additionally (combined with hydrochlorothiazide and/or CCBs if needed) contribute to CV risk reduction in patients with atherosclerotic disease and reduced eGFR.307,323,324
Recommendation Table 8 — Recommendations for antihypertensive therapy in patients with peripheral and aortic disease
Recommendations Classa Levelb
In patients with PAAD and hypertension an SBP target towards 120–129 mmHg, if tolerated, is recommended.301–305,325 I A In unilateral RAS patients, it is recommended that antihypertensive medication include ACEIs/ ARBs.307,320–323 I B In patients with PAAD and hypertension, ACEIs or ARBs should be considered as first-line antihypertensive therapy.307,312 IIa B In RAS-related hypertension, the combination of ACEIs/ARBs with diuretics and/or calcium channel blockers should be considered.324 IIa B An individualized, more lenient BP goal (e.g. <140/ 90 mmHg) should be considered in:301 • Age ≥85 years • Residential care • Symptomatic orthostatic hypotension IIa C An individualized, more lenient BP goal (e.g. <140/ 90 mmHg) may be considered in:301 • Clinically severe frailty at any age • Limited life expectancy (<3 years) IIb C In patients with bilateral RAS, antihypertensive medication including ACEIs/ARBs may be considered if close patient monitoring (renal function) is feasible.321 IIb B ACEIs/ARBs may be considered in all patients with PAD, regardless of BP levels, in the absence of contraindications.312,313 IIb B
Continued
ESC Guidelines 3571
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.35
7.2.3 Lipid-lowering therapy
Patients with symptomatic PAAD are at very high CV risk but are usually inadequately managed compared with patients with CAD.5,247,326–332 Both LDL-C reduction by ≥50% from baseline and an LDL-C goal of <1.4 mmol/L (<55 mg/dL) are recommended to obtain a reduction in CV death, MI, and stroke, and to improve walking distance.242,333–336
7.2.3.1 Statins
Statins demonstrate mortality and CV event reduction in RCTs for PAD, CS, and severe aortic arch plaques.243–245 Even in advanced disease stages, they are linked to lower MACE and mortality.246 Statins significantly improve CV outcomes in patients with PAD, reducing major adverse limb events (MALE).244,327–329,337,338 Meta-analyses show enhanced walking distances.244,338,339 For CS, statin pre-treatment lowers recurrent stroke risk posttransient ischaemic attack (TIA).19,340–343 While lacking RCTs in renovascular or visceral artery disease, statins benefit cardiorenal events and post-RAS stenting prognosis.344–346 Mixed evidence suggests statins may mitigate AAA and TAA growth.347–352 However, since most patients with AAA or TAA present with associated CVRFs, liberal use of lipid-lowering treatment19 should be considered, using an individualized approach with shared decision-making and considering residual CV risk.353 Pre-operative statin use links to increased 5 year survival after TEVAR.19 Statin use was associated with a mean AAA growth rate reduction and a lower rupture risk.347–349,352,354 Some evidence suggests that statins may reduce TAA growth rate and risk of rupture.350,351,355 No benefit on AAA or TAA growth rate was shown with fenofibrate therapy.356,357
7.2.3.2 Ezetimibe
Ezetimibe combined with statins benefits selected patients with PAAD, particularly when the target LDL-C level is not met.335 In an IMProved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE-IT) subanalysis, involving acute coronary syndrome (ACS) patients with PAD, ezetimibe consistently reduced CV risk, especially in high-risk subgroups.247,331
7.2.3.3 Proprotein convertase subtilisin/kexin type 9 inhibitors
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, in addition to statins, reduce CV events in symptomatic atherosclerotic disease patients with LDL-C ≥1.8 mmol/L.336 Adding them to statins further reduces MACE and MALE risk in patients with PAD and improves walking distance;333 however, their potential in TAA/AAA is an emerging area of research.247 Inclisiran, administered semi-annually, has proved a notable 26% MACE risk reduction in a pooled phase III analysis,358 but its role in PAAD is not firmly established and ongoing RCTs including PAD participants (e.g. ClinicalTrials.gov NCT05030428) aim to provide insights. 7.2.3.4 Bempedoic acid
Bempedoic acid, acting upstream of statins in cholesterol metabolism, has been shown to reduce cholesterol levels by 17%–28%359,360 and demonstrated a decrease in the incidence of MACE in statin-intolerant PAD patients.361 However, its impact on aortic diseases and AAA still requires further research.
7.2.3.5 Hypertriglyceridaemia
Beyond LDL-C, evidence shows insulin resistance, elevated triglycerides, and remnant lipoproteins are associated with ASCVD, particularly in PAD.362–365 However, in a meta-analysis and an RCT, fibrates showed no benefit over placebo in reducing MACE in patients with PAD for a composite outcome of non-fatal stroke, non-fatal MI, and vascular death.366 Fibrates showed no benefit over placebo in reducing coronary and cerebrovascular events in patients with PAD in an RCT.367 While the relationship between triglycerides and aortic diseases is complex and not fully understood, some evidence suggests that triglyceride levels may contribute to the development and progression of aortic diseases. In contrast, icosapent ethyl (IPE) demonstrated a reduction in mortality and morbidity among individuals with hypertriglyceridaemia in the Reduction of Cardiovascular Events With Icosapent Ethyl–Intervention Trial (REDUCE-IT).368 Its impact on patients with PAAD is unexplored,369 although a small pilot RCT suggested an improved ABI in hyperglycaemic haemodialysis patients.370
In cases where on-treatment SBP is at or below target (120–129 mmHg) but DBP is not at target (≥80 mmHg), intensifying BP-lowering treatment to achieve an on-treatment DBP of 70–79 mmHg may be considered to reduce CVD risk.306 IIb C © ESC 2024
ACEIs, angiotensin-converting enzyme inhibitors; ARBs, angiotensin receptor blockers; BP, blood pressure; CVD, cardiovascular disease; DBP, diastolic blood pressure; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease; RAS, renal artery stenosis; SBP, systolic blood pressure. aClass of recommendation. bLevel of evidence.
Recommendation Table 9 — Recommendations for lipid-lowering therapy in patients with peripheral arterial and aortic diseases
Recommendations Classa Levelb
In patients with atherosclerotic PAAD, lipid-lowering therapy is recommended.242,334–336 I A An ultimate LDL-C goal of <1.4 mmol/L (55 mg/dL) and a >50% reduction in LDL-C vs. baseline are recommended in patients with atherosclerotic PAAD.19,242,246,300,335 I A Statins are recommended in all patients with PAD.328,329,337,371 I A If the target LDL-C level is not achieved on maximally tolerated statins and ezetimibe, treatment with a PCSK9 inhibitor is recommended in patients with atherosclerotic PAAD, to achieve target values.372,373 I A If the target LDL-C level is not achieved, a combination of statins and ezetimibe is indicated in patients with atherosclerotic PAAD, to achieve the given target values.247 I B For statin-intolerant patients with atherosclerotic PAAD, at high CV risk, who do not achieve their LDL-C goal on ezetimibe, it is recommended to add bempedoic acid either alone or in combination with a PCSK9 inhibitor.361 I B Statins for the reduction of growth and rupture of AAA should be considered.347–349,352,354 IIa B
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.36
7.2.4 Diabetes and pre-diabetes conditions
Screening for diabetes or pre-diabetes is recommended in PAAD. Recent ESC Guidelines on diabetes and CVD374 provide detailed diagnostic criteria and underscore the importance of diagnosing diabetes in ASCVD patients and vice versa. Both Type 1 (T1DM) and Type 2 (T2DM) diabetes mellitus imply significantly increased risk of PAD, carotid stenosis, and polyvascular disease, depending on disease duration and the status of other CVRFs. Diabetes is present in 30% of patients with IC and 50%–70% of those with CLTI.375,376 Although the prevalence of PAD in patients with diabetes is 20%–30%, only half of them are symptomatic because of peripheral neuropathy with decreased pain sensitivity.377 As already detailed in Section 4, diabetes implies reduced risk of TAA, AAA, or aortic dissection. However, patients with T2DM and PAAD are in the very high-risk group for stroke, MI, and CV death,374 and for T1DM, an online risk prediction tool has recently been developed.377–380 For non-pregnant PAAD patients, aiming for an HbA1c level of <53 mmol/mol (7%) to avoid significant hypoglycaemia is appropriate. Consider a higher threshold (<69 mmol/mol [8.5%]) for limited life expectancy or when treatment risks outweigh benefits.374 In PAAD, it is recommended to aim for tight glycaemic control, preferably with agents with proven CV benefits such as sodium-glucose co-transporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA), adding metformin and other glucoselowering agents as necessary.374,381–384 The Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results (LEADER) trial and Trial to Evaluate Cardiovascular and Other Long-term Outcomes with Semaglutide in Subjects with Type 2 Diabetes (SUSTAIN-6) investigated subcutaneous GLP-1RAs liraglutide (≤1.8 mg/day) and semaglutide (0.5 or 1.0 mg/week), respectively, vs. placebo in T2DM patients with high CV risk. Overall, 12.7% of patients in LEADER and 14.0% in SUSTAIN-6 presented with PAD at baseline. Although non-statistically significant due to a lack of power, the effects on MACE showed a consistently beneficial trend in PAD: liraglutide (hazard ratio (HR), 0.77; 95% confidence interval (CI), 0.58–1.01) and semaglutide (HR, 0.61; 95% CI, 0.33–1.13).381 The (Empagliflozin) Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients (EMPA-REG OUTCOME) investigated the SGLT2i empagliflozin (10 mg or 25 mg per day) vs. placebo in patients with T2DM and high CV risk. Overall, 20.8% of patients presented with PAD at baseline. In these patients, empagliflozin reduced CV death (HR, 0.57; 95% CI, 0.37–0.88) and all-cause mortality (HR, 0.62; 95% CI, 0.44–0.88), and there was a non-significant reduction in limb amputation: 5.5% with empagliflozin vs. 6.3% with placebo (HR, 0.84; 95% CI, 0.54–1.32).382 In the Canagliflozin Cardiovascular Assessment Study (CANVAS)385 investigating canagliflozin, there was an increased risk of amputation, but this was not confirmed in the Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE) trial investigating canagliflozin in patients with T2DM and chronic kidney disease (CKD).386 Still, the use of other SLGT2is seems reasonable in PAD patients.
Patients with carotid stenosis were included in trials testing GLP-1RA and SGLT2i, but no analysis on this subpopulation was performed. A meta-analysis of eight trials investigating GLP-1RAs vs. placebo in patients with T2DM reported a reduction in all strokes (HR, 0.84; 95% CI, 0.75–0.93).387 Among patients with T2DM and prior history of MI or non-fatal stroke, GLP-1RAs reduced the incidence of recurrent MACE (HR, 0.86; 95% CI, 0.8–0.92).388 SGLT2is do not appear to reduce stroke in patients with T2DM, but patients with a stroke history experienced similar cardiorenal benefits as the rest of the population.389 Before the era of GLP-1RAs and SGLT2is, different studies (United Kingdom Prospective Diabetes Study [UKPDS] 34390 and Hyperinsulinaemia: the Outcomes of its Metabolic Effects [HOME] trials391) showed that metformin reduced the risk of MALE and MACE in patients with PAD.391,392 But a recent study with GLP-1RA dulaglutide found the same risk reduction in MACE between patients with and without baseline metformin, calling into question its add-on value.384,393 However, there are studies suggesting that metformin may reduce AAA growth (see Section 9.2.4).
Statins for the reduction of growth and rupture of TAA may be considered.350,351,355 IIb B In high-risk patients with PAAD and triglycerides >1.5 mmol/L despite lifestyle measures and statin therapy, icosapent ethyl 2 g b.i.d. may be considered in addition to a statin.368 IIb B Fibrates are not recommended for cholesterol lowering.367 III B © ESC 2024
AAA, abdominal aortic aneurysm; b.i.d., twice daily; CV, cardiovascular; LDL-C, low-density lipoprotein cholesterol; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease; PCSK9, proprotein convertase subtilisin/kexin type 9; TAA, thoracic aortic aneurysm. aClass of recommendation. bLevel of evidence.
Recommendation Table 10 — Recommendations for the medical management of patients with peripheral arterial and aortic diseases and diabetes
Recommendations Classa Levelb
It is recommended to apply tight glycaemic control (HbA1c <53 mmol/mol [7%]) to reduce microvascular complications in patients with PAAD.374,394–397 I A SGLT2i with proven CV benefit are recommended in patients with T2DM and PAAD to reduce CV events, independent of baseline or target HbA1c and concomitant glucose-lowering medication.382,386,398–402 I A GLP-1RAs with proven CV benefit are recommended in patients with T2DM and PAAD to reduce CV events, independent of baseline or target HbA1c and concomitant glucose-lowering medication.381,403–407 I A It is recommended to avoid hypoglycaemia in patients with PAAD.374,408–412 I B It is recommended to individualize HbA1c targets according to comorbidities, diabetes duration, and life expectancy.408,411 I C It is recommended to prioritize the use of glucose-lowering agents with proven CV benefits,c,d followed by agents with proven CV safety,e over agents without proven CV benefit or safety.374 I C If additional glucose control is needed, metformin should be considered in patients with T2DM and PAAD.374,384,393 IIa B © ESC 2024
CV, cardiovascular; GLP-1RAs, glucagon-like peptide-1 receptor agonists; HbA1c, glycated haemoglobin; PAAD, peripheral arterial and aortic diseases; SGLT2i, sodium-glucose co-transporter-2 inhibitors; T2DM, type 2 diabetes mellitus. aClass of recommendation. bLevel of evidence. cEmpagliflozin, canagliflozin, dapagliflozin, sotagliflozin. dLiraglutide, semaglutide subcutaneous, dulaglutide, efpeglenatide. eMetformin, pioglitazone, dipeptidyl peptidase 4 (DPP-4) inhibitor (sitagliptin, alogliptin, linagliptin), glimepiride, gliclazide, insulin glargine, insulin degludec, ertugliflozin, lixisenatide, exenatide (extended release), oral semaglutide.
ESC Guidelines 3573
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.37
7.2.5 Other pharmacological therapy
Increased attention is focused on inflammation in ASCVD,413 supported by the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS),414 which showed that canakinumab, a monoclonal antibody targeting interleukin (IL)-1β, reduced MACE in high-risk patients with previous MI and increased high-sensitivity (hs)-CRP. Data for patients with PAAD are not reported. Furthermore, low-dose colchicine (0.5 mg/day) has been shown to reduce MACE among those with stable atherosclerosis after recent MI.415 However, the effect of colchicine and other anti-inflammatory drugs in PAAD remains unproven.416
8 Peripheral arterial disease
8.1 Lower-extremity peripheral arterial
disease 8.1.1. Peripheral arterial disease syndromes 8.1.1.1. Clinical presentation and diagnosis Atheromatous lower-extremity PAD is a chronic disease with different clinical manifestations. PAD may be symptomatic or asymptomatic and may or may not be associated with limb wounds. Wound healing and amputation risk may be affected by the concomitant presence of PAD, diabetes, and/or infection;417 therefore, amputation risk assessment should be systematically performed using the Wound, Ischaemia, and foot Infection (WIfI) classification. PAD presents as: • Asymptomatic PAD: suspected by lower-limb pulse abolition or imaging studies performed for other purposes and detected by pathological ABI or TBI.418,419 These patients do not present with IC or atypical effort-related symptoms. However, attention should be paid to those with wounds, with masked effort-related symptoms due to reduced walking capacity (for reasons other than PAD), or reduced pain sensitivity. ‘Masked PAD’ is defined as PAD without provoked leg pain because of reduced walking capacity for other reasons or reduced pain sensitivity.420 • Symptomatic (effort-related) PAD: patients with pathological ABI or TBI, presenting with IC, atypical effort-related symptoms, or chronic lower-limb wounds (diabetic foot or non-healing ulceration/gangrene ≥2 weeks) without critically reduced limb perfusion.417,421 In these patients, IC is characterized by exertional muscle pain and dysfunction in the supply area of the obstructed arterial segment, which is relieved at rest.422 Some patients may present with atypical symptoms or with ‘masked PAD’.420,423 In women, the prevalence of IC is lower than in men, while atypical symptoms are more common.424
• CLTI represents the more severe chronic PAD presentation and underlies poor limb outcomes without intervention. In addition to common signs of chronic PAD, patients with CLTI present with a critical haemodynamic status (ankle pressure <50 mmHg, toe pressure [TP] <30 mmHg, or TcPO2 <30 mmHg) responsible for ischaemic rest pain, non-healing chronic (>2 weeks of duration) ulceration, or foot gangrene.425,426
PAD syndromes can be categorized according to their clinical presentation (Table 7).
The 5 year cumulative incidence of clinical deterioration from asymptomatic PAD to IC is 7%, and 21% from IC to CLTI.427 All patients with PAD are at high risk of MACE, cerebrovascular disease, and MALE (Figure 8).428–430 The 5 year cumulative incidence of CV mortality is 9% in asymptomatic PAD and 13% in symptomatic patients. In comparison with symptomatic PAD, CLTI further increases all-cause mortality risk (relative risk [RR] 2.26) and the risk of MACE (RR 1.73).431 Health insurance data reveal a major amputation rate of 9% in patients with CLTI and 1% in patients with IC, while considerably higher amputation rates were reported in trials and registries data focusing on patients with CLTI.432–435 Among patients with PAD, development of MALE is associated with poor prognosis, with a three-fold increase in death and a 200-fold increase in subsequent lower-extremity amputation.429 Prevention of MALE is crucial, and the risk of MACE/MALE increases with the increased number of arterial beds involved.
Table 7 Peripheral arterial disease categorized according to clinical presentation
Clinical characteristics of PAD Rutherford classification Fontaine classification
Category Signs and symptoms Stage Signs and symptoms
Asymptomatic PAD 0 Asymptomatic I Asymptomatic Symptomatic (effort-related) PAD 1 Mild claudication IIa Non-disabling intermittent claudication
2 Moderate claudication IIb Disabling intermittent claudication
3 Severe claudication
Chronic limb-threatening Ischaemia 4 Ischaemic rest pain III Ischaemic rest pain
5 Minor tissue loss IV Ischaemic ulceration or gangrene
6 Major tissue loss © ESC 2024
PAD, peripheral arterial disease. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.38
8.1.1.1.1. Diagnostic tests. Vascular assessment: ABI, TBI, TcPO2 measurements (refer to Section 5.3) Ankle–brachial index is the proposed initial non-invasive diagnostic test to confirm lower-limb decreased perfusion status90,436,437 and needs to be reported separately for each leg (see Recommendation Table 2). An ABI ≤0.90 confirms PAD diagnosis.90,436,437 In cases of an ABI >0.90 and clinical suspicion of PAD, post-exercise ABI measurements should be considered, along with imaging studies (preferably by treadmill). A post-exercise ABI decrease of >20% may serve as a PAD diagnostic criterion.438,439 In cases of abnormally high ABI values (ABI >1.4; see Recommendation Table 2) and patients with CLTI and diabetes440
(see Recommendation Table 11), TP measurements, the calculation of TBI and TcPO2, as well as pulse volume recordings or analysis of distal arterial Doppler waveforms, should be considered,90,91,132,133,441 and ABI can be estimated from distal Doppler waveforms independent of diabetes and media sclerosis.124 Apart from the assessment of limb perfusion, ABI serves as a surrogate marker for CV and all-cause mortality.88,442,443 A diagnostic PAD algorithm is depicted in Figure 9.
4–5x increased risk of CV events compared with
patients without PAD Cardiac disease (MACE):
Cerebrovascular disease
Lower limb disease (MALE):
CV mortality Myocardial infarction Coronary revascularization Hospitalization for heart failure
Amputation Chronic or acute lower limb ischaemia Lower limb revascularization Increased death and vascular amputation risk
Figure 8 Cardiovascular risk in patients with peripheral arterial disease. CV, cardiovascular; MACE, major adverse cardiac event; MALE, major adverse limb event; PAD, peripheral arterial disease.
ESC Guidelines 3575
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.39
Walking impairment questionnaires, assessment of functional and walking capacity Determining walking impairment, capacity, and functional status in all patients with PAD is mandatory (refer to Section 5.2). Assessment of amputation risk In patients with PAD and chronic lower-limb wounds (diabetic foot ulcer, non-healing lower-limb ulceration, or gangrene of ≥2 weeks of duration), even without haemodynamic parameters of critical limb perfusion, the additional presence of comorbidities such as diabetes and/or wound infection may contribute to an increased risk of amputation. The WIfI classification system takes the patients’ limb perfusion, wound size, and the extent of foot infection into account to determine the amputation risk (Table 8).417,444–446
8.1.1.1.2 Imaging methods. Duplex ultrasound is recommended as
the first-line imaging method for PAD screening and diagnosis. CTA and/or MRA are recommended as adjuvant imaging. For details refer to Supplementary data online, Section 1.4.
Suspicion of PAD
Clinical assessment (personal history, physical examination), walking impairment assessment (questionnaire, treadmill),
and functional assessment (6MWT, SPPB)
Haemodynamic/vascular assessment
(ABI, AP, TP, TcPO2, DUS), wound assessment (WIfl)
PAD
Y
Typical symptoms
Y
N
Ischaemic rest pain or gangrene or non-healing chronic wound and critical limb perfusion
(AP <50 mmHg, TP <30 mmHg or TcPO2 <30 mmHg)
N Masked PAD N Asymptomatic PAD with or without wound
N Symptomatic PAD with or without wound
Y
Chronic limb-threatening ischaemia
Other diagnosis
Figure 9 Diagnostic algorithm for peripheral arterial disease. 6MWT, six-minute walk test; ABI, ankle–brachial index; AP, ankle pressure; DUS, duplex ultrasound; PAD, peripheral arterial disease; SPPB, short physical performance battery; TcPO2, transcutaneous oxygen pressure; TP, toe pressure; WIfI, Wound, Ischaemia, and foot Infection classification. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.40
Table 8 Assessment of the risk of amputation: the Wound, Ischaemia, and foot Infection classification
Component Score Description
W (Wound) 0 No ulcer (ischaemic rest pain)
1 Small, shallow ulcer on distal leg or foot without gangrene
2 Deeper ulcer with exposed bone, joint or tendon ± gangrenous changes limited to toes
3 Extensive deep ulcer, full thickness heel ulcer ± calcaneal involvement ± extensive gangrene
I (Ischaemia) ABI Ankle pressure (mmHg) Toe pressure or TcPO2 0 ≥0.80 >100 ≥60
1 0.60–0.79 70–100 40–59 2 0.40–0.59 50–70 30–39 3 <0.40 <50 <30
fl (foot infection) 0 No symptoms/signs of infection
1 Local infection involving only skin and subcutaneous tissue
2 Local infection involving deeper than skin/subcutaneous tissue
3 Systemic inflammatory response syndrome
Ischaemia – 0 Ischaemia – 1 Ischaemia – 2 Ischaemia – 3
W–0 VL VL VL VL VL L L M L L M M M H H H W–1 VL VL VL VL L M M M M H H H H H H H W–2 VL VL VL VL M M H H H H H H H H H H W–3 VL VL VL VL M M M H H H H H H H H H
fl–0 fl–1 fl–2 fl–3 fl–0 fl–1 fl–2 fl–3 fl–0 fl–1 fl–2 fl–3 fl–0 fl–1 fl–2 fl–3 © ESC 2024
Very low (green) = VL = clinical stage 1; low (yellow) = L = clinical stage 2; moderate (orange) = M = clinical stage 3; high (red) = H = clinical stage 4. ABI, ankle–brachial index; TcPO2, transcutaneous oxygen pressure. The Wound, Ischaemia and foot Infection (WIfI) classification allows the assessment of the individual risk of amputation in PAD patients: it comprises scores for wound size (W), degree of ischaemia (I), as assessed by the ABI, ankle pressure, and toe pressure or TcPO2, and extent of foot infection (fI) as depicted in the respective table. The combination of all three components results in the amputation risk stratification (VL = very low, L = low, M = moderate, H = high). Table reproduced with permission from.417
Recommendation Table 11 — Recommendations for diagnostic tests in patients with peripheral arterial disease and diabetes, renal failure, and wounds
Recommendations Classa Levelb
Measuring TP or TBI is recommended in patients with diabetes or renal failure if resting ABI is normal.90,91,94,440 I C In patients with PAD and chronic wounds, the WIfI classification system should be considered to estimate individual risk of amputation.417,444–446 IIa C © ESC 2024
ABI, ankle–brachial index; PAD, peripheral arterial disease; TBI, toe–brachial index; TP, toe pressure; WIfI, Wound, Ischaemia, and foot Infection classification. aClass of recommendation. bLevel of evidence. Recommendation Table 12 — Recommendations for imaging in patients with peripheral arterial disease
Recommendations Classa Levelb
DUS is recommended as the first-line imaging method to confirm PAD lesions.122,123,447 I C In symptomatic patients with aorto-iliac or multisegmental/complex disease, CTA and/or MRA are recommended as adjuvant imaging techniques for preparation of revascularization procedures.448,449 I C Analysis of anatomical imaging tests in conjunction with symptoms and haemodynamic tests prior to an invasive procedure is recommended.426 I C © ESC 2024
CTA, computed tomography angiography; DUS, duplex ultrasound; MRA, magnetic resonance angiography; PAD, peripheral arterial disease. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3577
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.41
8.1.1.2 Medical treatment
Patients with PAD should receive comprehensive OMT, including supervised exercise training and lifestyle modification (Figures 10– 12). A personalized programme of guidelines-guided pharmacotherapy to reduce MACE and MALE should be prescribed and tightly followed. Patients with PAD are less likely to receive OMT than patients with CAD.450–452 For general lifestyle and pharmacological therapy see Section 7.
8.1.1.2.1 Exercise therapy. A consensus document on exercise and
PAD has been published recently.62 Symptomatic patients should be medically screened before any supervised exercise training (SET) programme initiation.37,62 In patients with symptomatic PAD, SET is safe and improves treadmill PFWD, MWD, functional walking as measured by six-minute walking distance (6MWD), HRQoL, and cardiorespiratory fitness (Figure 13).294,453–463 Exercise has not been found to improve ABI.457,458 Ideally, SET should be co-ordinated by vascular physicians, and training sessions supervised by clinical exercise physiologists or physiotherapists.62 In Europe, SET is usually underused.464,465
When SET is not available, home-based exercise training (HBET) should be proposed (Figure 13), although it is inferior with regard to improving walking performance.466–469 HBET is safe and its inferiority is reduced if monitoring is implemented.469,470 Compared with no exercise, HBET improves walking performance.471 SET training frequency should be at least three times per week, for 30–60 min, and the programme last for at least 12 weeks.37,58,59,454,472,473 Patients should exercise to moderate-severe claudication pain to improve walking performance.37,294,453,454,456–458,474 However, prescribing high-pain exercise may hinder programme uptake and adherence. Additionally, it has been reported that improvements in walking performance may be obtained with less severe claudication pain.455,460 Therefore, a flexible approach is recommended, considering the patient’s needs
Optimal
medical treatment Address lower limbs-related symptoms Improve quality of life
Address general CV risk prevention
Smoking cessation
Weight loss
Healthy diet
Supervised exercise training Antihypertensive drugs
Optimal glucose control in diabetics
Cholesterol-lowering drugs
Antithrombotic drugs
+
Figure 10 Optimal medical treatment in patients with peripheral arterial disease. CV, cardiovascular. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.42
and preferences.62 Alternative training modalities, such as strength training, arm cranking, cycling, and combinations of different modes, have proven effective in improving walking performance compared with traditional walking training, with limited evidence for HRQoL.475 However, this evidence is low due to small sample size and risk of bias.475 Vigorous intensity exercise training (77%–95% of maximal heart rate or 14–17 on the rate of perceived exertion on Borg’s scale) has been shown to induce the best walking and cardiorespiratory fitness improvements.294,457 Training programmes should begin at low-to-moderate intensity, gradually advancing to vigorous exercise if well tolerated.62 This approach assesses patient response and minimizes complications.37,62
N
N
Chronic PAD syndromes (without wounds)
Vascular follow-up (clinical, physical, functional, vascular assessment)
Asymptomatic PAD Symptomatic PAD CLTI
Optimal medical treatment Optimal medical treatment Optimal medical treatment
Vascular team assessment
Revascularization feasible
Supervised or structured
home-based exercise training Vascular team assessment
Improved PAD-related
symptoms Revascularization indicated
and reasonable
Revascularization indicated
and reasonable
Revascularization and supervised or structured
home-based exercise training Supervised or structured
home-based exercise training Evaluate alternative treatment
strategy (pharmacological,
amputation)
Revascularization feasible
Revascularization
Y Y
Y N
N
Y
Y
N
Figure 11 Treatment algorithm in peripheral arterial disease without wounds. CLTI, chronic limb-threatening ischaemia; PAD, peripheral arterial disease.
ESC Guidelines 3579
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.43
N
N N
N
N
N
N Chronic PAD syndromes (with wounds)
Vascular follow-up (clinical, physical, functional, vascular assessment)
Asymptomatic PAD Symptomatic PAD CLTI
Optimal medical treatment Optimal medical treatment Optimal medical treatment
Wound care Wound care
Wound care
Healing Healing
Vascular team assessment
Revascularization feasible
Supervised or structured
home-based exercise training
Vascular team assessment Vascular team assessment
Improved PAD-related
symptoms Revascularization indicated
and reasonable
Revascularization indicated
and reasonable
Revascularization and
Wound care Revascularization and
Wound care
Evaluate alternative treatment strategy (pharmacological,
amputation)
Revascularization and supervised or structured home-based exercise training
Supervised or structured home-based exercise training Revascularization feasible
Revascularization indicated
and reasonable
Y
Revascularization feasible
Y
Y
Y
Y
Y
Y
Y N
N
Y
Figure 12 Treatment algorithm in peripheral arterial disease with wounds. CLTI, chronic limb-threatening ischaemia; PAD, peripheral arterial disease. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.44
Data on the efficacy of exercise therapy in women compared with men are scarce. Women may respond less well than men,476,477 although discrepancies among studies exist.478–481 SET combined with endovascular revascularization significantly improves walking performance, HRQoL, and reduces future revascularization.482,483
An exercise therapy algorithm in PAD has been recently described.62
Supervised hospital-based
exercise programmes Supervised home-based
exercise programmes
Training characteristics
Training benefits
Potential involved mechanisms
Mitochondrial content/function
Symptoms Quality
of life Walking performance Patient awareness CVR Functional
status
Arteriogenesis Endothelial
function Myofibre size Inflammation
Supervised group sessions
Different training modes Remote monitoring, logbook and connected devices
At least three times per week
Different levels of elicited pain
Low-to-moderate exercise intensity (or high if tolerated)
Session duration of at least 30 min. Programmes duration of at least 12 weeks.
Figure 13 Exercise training characteristics and benefits in patients with peripheral arterial disease. CVR, cardiovascular risk.
ESC Guidelines 3581
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.45
8.1.1.2.2 Pharmacological treatment. Antithrombotic therapy
Asymptomatic PAD Although patients with PAD are at very high CV risk,404,484 a trial evaluating the effect of antiplatelet agents in asymptomatic patients with an ABI ≤0.95 did not show an effect on MACE or revascularization.485 Another trial on patients with an ABI ≤0.99 and diabetes also failed to show any difference in MACE or amputation.486 However, these data were not powered to analyse subgroups and do not rule out the possibility that aspirin could provide a benefit in subjects at increased risk of CV events. In a randomized trial evaluating aspirin in the prevention of cancer and CVD in patients with diabetes without known arterial disease, MACE occurred in a significantly lower percentage of participants in the aspirin group than in the placebo group, with more major bleeding events in the aspirin group.487 The effect of antithrombotics in patients with higher-risk PAD (i.e. ABI <0.90 and other CV risk factors) has not been evaluated in randomized trials. Antithrombotic therapy should not be systematically administered in patients with asymptomatic PAD.
Symptomatic PAD In patients with symptomatic PAD, antithrombotic therapy improves CV prognosis.488–492 Clopidogrel may have a modest advantage over aspirin (Figure 14).493,494 In the Examining Use of tiCagreLor In peripheral artery Disease (EUCLID) trial, single antiplatelet therapy (SAPT) with ticagrelor showed no superior benefit in the reduction of MACE or major bleeding compared with clopidogrel.495–497 Dual antithrombotic therapy with aspirin and vascular-dose rivaroxaban (2.5 mg b.i.d.) in patients with PAD is more effective than aspirin alone, reducing MACE, MALE, and preventing acute limb ischaemia (ALI), but with increased major bleeding risk.429,430,498,499 Patients with high-risk limb presentation (CLTI, previous amputation, or revascularization) or high-risk comorbidities (heart failure [HF], diabetes, or polyvascular disease [PVD]) benefit the most.498 After endovascular therapy, dual antiplatelet therapy (DAPT) for 1–3 months is supported by rare randomized studies.500,501 DAPT is not associated with reduced CV mortality or MACE,501 but seems to improve patency without increasing bleeding (Figure 15).502–504 The combination of aspirin 100 mg and vascular-dose rivaroxaban (2.5 mg b.i.d.), started post-revascularization, showed a moderate but significantly lower incidence of MALE and MACE compared with aspirin alone,490,505 without an increase in thrombolysis in myocardial infarction (TIMI) major bleedings, but with an increase in International Society on Thrombosis and Haemostasis (ISTH) major bleedings, especially when clopidogrel was given for >1 month.506
Patients with CLTI are at high risk of MACE and MALE.429,431,507 Among CLTI patients, there is no robust evidence favouring a specific antithrombotic strategy for vein graft maintenance. DAPT with clopidogrel and aspirin is not superior to aspirin alone in below-the-knee (BTK) bypass grafts.508–510 Vitamin K antagonists (VKAs) may be considered for high-risk conduits with low bleeding risk.509 Dual antiplatelet therapy could confer benefit for prosthetic conduit (occlusion, revascularization, amputation, or death), without increasing major bleeding.510 VKAs with an international normalized ratio (INR) of 3–4.5 are slightly beneficial in venous conduits, but with a 1.9-fold and 1.3-fold increase in major and fatal bleedings, respectively.509 A study suggested that VKAs could be associated with prolonged patency of at-risk prosthetic grafts due to poor run-off.511 In patients with another indication for OAC (such as atrial fibrillation [AF] or mechanic valve replacement) and PAD, anticoagulation is warranted.512 Additional SAPT post-endovascular therapy should be brief.
Recommendation Table 13 — Recommendations for exercise therapy in patients with peripheral arterial disease (see also Evidence Table 5)
Recommendations Classa Levelb
In patients with symptomatic PAD, SET is recommended.294,453,456–458,462 I A In those patients undergoing endovascular revascularization, SET is recommended as an adjuvant therapy.482,483 I A When SET is not available or feasible, a structured and monitored (calls, logbooks, connected devices) HBET programme should be considered.468,469,471 IIa A Walking should be considered as a first-line training modality. When walking exercise is not an option, alternative exercise modes (strength training, arm cranking, cycling, and combinations of different training modes) should also be considered.475 IIa A Walking training performed at high intensity (77%– 95% of maximal heart rate or 14–17 self-perceived exertion on Borg’s scale) should be considered to improve walking performance,294 and high-intensity exercise training (various aerobic training modes) should be considered to improve cardiorespiratory fitness.294,457 IIa A Training frequency of at least three times per week, training session duration of at least 30 min, and training programme duration of at least 12 weeks should be considered.472 IIa B In patients with PAD, exercise training to moderate-severe claudication pain may be considered to improve walking performance.37,454,456,458 However, improvements are also achievable with lesser claudication pain severities (low-mild pain or pain-free).455,460 IIb B Based on patient’s tolerance, a progressive increase (every 1–2 weeks) in exercise training load may be considered.37,62 IIb C © ESC 2024
HBET, home-based exercise training; PAD, peripheral arterial disease; SET, supervised exercise training. aClass of recommendation. bLevel of evidence.
Recommendation Table 14 — Recommendations for antithrombotic therapy in patients with peripheral arterial disease (see also Evidence Table 6)
Recommendations Classa Levelb
Use of antiplatelet therapy with aspirin alone (range 75–160 mg o.d.) or clopidogrel alone (75 mg o.d.) is recommended for the reduction of MACE in patients with symptomatic PAD.488–490 I A Treatment with combination rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered for patients with PAD, high ischaemic risk,c and non-high bleeding risk.d,429,498,499 IIa A
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.46
Pharmacotherapy to decrease walking impairment Verapamil,516 statins,517,518 antiplatelet agents, and prostanoids (prostaglandins I2 and E1)519 can alleviate walking impairment in patients with symptomatic PAD. However, drugs like cilostazol, naftidrofuryl, pentoxifylline, buflomedil, carnitine, and propionyl-L-carnitine are suggested to increase walking distance in patients with IC without impacting CV health.339,520 Their objective benefit is generally limited, ranging from mild to moderate, with considerable variability.339 The additional benefit of these drugs alongside antithrombotics, antihypertensives, and statins remains unknown. Cilostazol, a phosphodiesterase type III inhibitor, improved MWD compared with placebo and pentoxifylline.520–522 In a Cochrane analysis, 100 mg twice daily increased MWD by 76%,521 while another review reported a 25% average improvement.520 Cilostazol also has antiplatelet effects, requiring cautious combination with other anticoagulant and antiplatelet treatments.522 Notably, it increases bleeding complications.523 Naftidrofuryl oxalate, tested for IC,524 demonstrated a 74% average increase in MWD and improved HRQoL.524,525 In a systematic review, the average MWD improvement was 60% compared with placebo.520 However, inconsistent results for other medications, such as prostanoids, pentoxifylline, L-arginine, buflomedil, or Gingko biloba, preclude their recommendation for patients with IC.519,526,527
8.1.1.2.3 Aorto-iliac lesion revascularization. Aorto-iliac lesions can
be treated by either an endovascular or a surgical approach according to the lesion morphology and patient risk. Long-term patency with a low risk of complications can be achieved by balloon angioplasty with or without stenting in external iliac arteries or primary stenting in common iliac arteries.528 A meta-analysis evaluated outcomes of open surgery vs. an endovascular approach in aorto-iliac lesions (TASC II C-D) and found that short-term morbidity and mortality favours the endovascular approach, but early and mid-term primary patency favours open surgery; however, secondary patency is comparable in all groups.
Treatment with combination rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered for patients with PAD and non-high bleeding risk following lower-limb revascularization.490,505 IIa B Use of antiplatelet therapy with clopidogrel alone (75 mg o.d.) may be considered over aspirin to reduce MI, stroke, and vascular death.493,494 IIb B Aspirin (75–100 mg) for primary prevention may be considered in patients with asymptomatic PAD and DM, in the absence of contraindications.419,487 IIb A DAPT for at least 1 month after revascularization may be considered to reduce limb events.500,501,503,513,514 IIb B Long-term DAPT in patients with PAD is not recommended.489 III A Oral anticoagulant monotherapy for PAD (unless for another indication) is not recommended.515 III A The routine use of ticagrelor in patients with PAD is not recommended.495 III A It is not recommended to systematically treat patients with asymptomatic PAD without any sign of clinically relevant ASCVD with antiplatelet drugs.485 III B © ESC 2024
ASCVD, atherosclerotic cardiovascular disease; DAPT, dual antiplatelet therapy; DM, diabetes mellitus; MACE, major adverse cardiovascular events; MI, myocardial infarction; o.d., once daily; PAD, peripheral arterial disease. aClass of recommendation. bLevel of evidence. cHigh ischaemic risk: previous amputation, critical limb threatening ischaemia, previous revascularization, high-risk comorbidities (heart failure, diabetes, vascular disease in two or more vascular beds), eGFR <60 mL/min/1.73 m2.498 dHigh bleeding risk: dialysis or renal impairment GFR <15 mL/min/1.73 m2, acute coronary syndrome <30 days, history of intracranial haemorrhage, stroke or TIA, active or clinically significant bleeding.
Patients with chronic symptomatic PAD
Assess risk level at every follow-up
High-risk limb presentation or high-risk comorbiditiesa without high bleeding risk
Non high-risk limb presentation
or high-risk comorbiditiesa
Single antiplatelet therapy
(ASA or clopidogrel)
(Class I) ASA and 2.5 mg rivaroxaban b.i.d.
(Class IIa) Single OAC monotherapy
(Class IIb)
Patients requiring long-term anticoagulation
Figure 14 Long-term antithrombotic therapy in patients with symptomatic peripheral arterial disease. b.i.d., twice daily; OAC, oral anticoagulant; PAD, peripheral arterial disease; ASA, aspirin aHigh-risk limb presentation: previous amputation, chronic limb-threatening ischaemia, previous revascularization, high-risk comorbidities: heart failure, diabetes, vascular disease in two or more vascular beds, moderate kidney dysfunction; eGFR <60 mL/min/1.73 m2.
ESC Guidelines 3583
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.47
8.1.1.2.4 Femoro-popliteal lesion revascularization. If revasculariza-
tion is indicated, endovascular therapy should be the first choice even for complex lesions, especially in surgical high-risk patients.119,529–531 Endovascular therapy faces the challenge of sustaining long-term patency and durability in the femoro-popliteal region, particularly post-stent placement in a highly mobile artery. Drug-eluting balloons have improved long-term patency in complex patient cohorts and lesions.532 With regard to paclitaxel-coated devices, a meta-analysis caused a decline in their usage, especially as the United States Food and Drug Administration (FDA) reacted and restricted their use.533 Consequently, data from large national databases were evaluated and the mortality signal could not be confirmed. The FDA revised its position, and drug-eluting treatment is now deemed to be a safe and efficient treatment strategy for femoro-popliteal lesions.534–538 An open surgical approach in femoro-popliteal lesions should be considered when an autologous vein (e.g. great saphenous vein [GSV]) is available and the patient shows low surgical risk, and in complex lesions after an interdisciplinary team discussion.
8.1.1.2.5 Below-the-knee artery revascularization. In patients with
severe IC in whom endovascular femoro-popliteal treatment is performed, BTK arteries can be treated in the same intervention if there is substantially impaired outflow.539
N Y
Patients with chronic symptomatic PAD after endovascular revascularization
Long-term anticoagulation required
Bleeding risk
No high bleeding risk High bleeding riska No high bleeding risk High bleeding riska
Bleeding risk
ASA and 2.5 mg rivaroxaban
b.i.d. +/- clopidogrel
for 1 month (Class IIa)
ASA + 2.5 mg rivaroxaban b.i.d.
(Class IIa) OAC monotherapy
(Class IIa) OAC monotherapy
(Class IIa)
SAPT (ASA or clopidogrel)
(Class I)
DAPT 1–3 months (Class IIa) SAPT 1–3 months
and OAC (Class IIa)
Figure 15 Patients with chronic symptomatic PAD after endovascular revascularization. b.i.d., twice daily; DAPT, dual antiplatelet therapy; OAC, oral anticoagulant; PAD, peripheral arterial disease; ASA, aspirin; SAPT, single antiplatelet therapy aHigh bleeding risk: dialysis or a renal impairment glomerular filtration rate <15 mL/min/1.73 m2, acute coronary syndrome <30 days, history of intracranial haemorrhage, stroke or TIA, active or clinically significant bleeding.
Recommendation Table 15 — Recommendations for interventional treatment of asymptomatic and symptomatic peripheral arterial disease (general)
Recommendations Classa Levelb
In patients with symptomatic PAD, after a 3 month period of OMT and exercise therapy, PAD-related QoL assessment is recommended.119 I B It is recommended to adapt the mode and type of revascularization options to anatomical lesion location, lesion morphology, and general patient condition.119 I C In patients with symptomatic PAD and impaired PAD-related quality of life after a 3 month period of OMT and exercise therapy, revascularization may be considered.465,540 IIb B In patients with PAD, revascularization is not recommended if the reason is to solely prevent progression to CLTI.541–544 III B In patients with asymptomatic PAD, revascularization is not recommended.119,529 III C © ESC 2024
CLTI, chronic limb-threatening ischaemia; OMT, optimal medical treatment; PAD, peripheral arterial disease; QoL, quality of life. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.48
8.1.1.3 Follow-up
Asymptomatic and symptomatic PAD are at increased risk of leg symptom worsening427 and of CV mortality and morbidity.419,431,551 Follow-up post-revascularization is crucial to ensure perfusion improvement, address CVRFs, optimize pharmacological treatment adherence, identify disease progression, and evaluate mental health and functional capacity. Experienced vascular care physicians should conduct follow-up, although specific protocols are currently undefined.128,552 Data on asymptomatic PAD follow-up are limited.553 For symptomatic PAD or postintervention, annual follow-up are advised, including ABI/TBI measurement and DUS for new or worsening symptoms.
8.1.2 Chronic limb-threatening ischaemia
8.1.2.1. Clinical presentation and diagnosis Chronic limb-thretening ischaemia describes chronic lower-limb hypoperfusion responsible for ischaemic rest pain, or non-healing ulceration or gangrene (typically in distal segments).555,556 Ischaemic rest pain primarily affects the patient’s forefoot and aggravates in a supine position, while lowering of the affected leg eases ischaemic symptoms.
8.1.2.1.1 Definition. Chronic limb-thretening ischaemia should be
considered in the presence of one of the following lower-limb clinical signs or symptoms: • Ischaemic rest pain • Non-healing lower-limb wound of ≥2 weeks’ duration • Lower-limb gangrene
The following haemodynamic criteria may be used to guide diagnosis in patients with suspicion of CLTI: • Ankle pressure <50 mmHg • TP <30 mmHg • TcPO2 <30 mmHg
8.1.2.1.2 Initial assessment and risk of amputation. For patients
with CLTI, initial diagnostic steps involve clinical examination and limb perfusion assessment through haemodynamic measurements. Regarding haemodynamic assessment in CLTI, standard ABI may be normal or falsely elevated due to non-compressible arteries related to medial sclerosis (common in diabetes or CKD),557 which can be overcome by estimation of ABI based on Doppler waveforms.124 Therefore, standard ankle pressure alone may not be reliable in estimating limb loss risk.441,558 In addition, a large proportion of patients with ulcers may have below-the-ankle lesions.440 In patients with CLTI, TP, TBI, or TcPO2 should additionally be obtained.90,441,559 Particularly in patients with CLTI, the WIfI classification system should be applied. In addition to patients’ limb perfusion, the WIfI classification considers the wound size and the extent of foot infection to determine the individual risk of amputation.417,444–446
8.1.2.1.3 Imaging. In all patients with CLTI, comprehensive vascular
imaging is mandatory to evaluate revascularization options. CLTI commonly affects more than one arterial segment of the lower limbs, involving infra-popliteal arteries (BTK and below-the-ankle arteries) in most cases. While non-invasive imaging (DUS, CTA, MRA) provides reliable results for above-the-knee arteries, imaging of BTK arteries, especially below the ankle, may be hampered by severe calcification.448,560,561 Therefore, in CLTI additional DSA with dedicated views of the foot should be considered for the assessment of BTK arteries.560 Even in patients who are not candidates for revascularization, DSA should be obtained to prevent unnecessary amputation or to minimize amputation extent.560,562
8.1.2.1.4 Mortality risk assessment. All-cause mortality and event
rates of MI are more than two-fold higher in CLTI patients than in unselected patients with an ABI ≤0.90.431 In CLTI patients undergoing revascularization, the post-revascularization period is particularly associated with an increased risk of MALE and MACE.563 The management of patients with CLTI should therefore include an individual peri-procedural risk assessment. Referring to the periprocedural risk patients can be categorized as average procedural risk (peri-procedural mortality <5% and 2 year survival >50%) or high procedural risk (peri-procedural mortality ≥5% and 2 year survival ≤50%).564,565 Besides revascularization, it also needs to be considered that lowerlimb amputation is associated with 30 day mortality rates of up to 22%.566
Recommendation Table 16 — Recommendations for interventional treatment of patients with symptomatic peripheral arterial disease (per arterial bed)
Recommendations Classa Levelb
In femoro-popliteal lesions, drug-eluting treatment should be considered as the first-choice strategy.534–537 IIa A In iliac lesions, balloon angioplasty with or without stenting in external iliac arteries, or primary stenting in common iliac arteries, should be considered.545–548 IIa B In femoro-popliteal lesions, if revascularization is indicated, endovascular therapy should be considered.119,529–531 IIa B In femoro-popliteal lesions, if revascularization is indicated, an open surgical approach should be considered when an autologous vein (e.g. GSV) is available in patients with low surgical risk.119,529 IIa C In patients with severe IC undergoing endovascular femoro-popliteal revascularization, treatment of BTK arteries may be considered in the same intervention.549,550 IIb C © ESC 2024
BTK, below-the-knee; GSV, great saphenous vein; IC, intermittent claudication. aClass of recommendation. bLevel of evidence.
Recommendation Table 17 — Recommendations in patients with peripheral arterial disease: follow-up of patients with peripheral arterial disease
Recommendations Classa Levelb
It is recommended to regularly, at least once a year, follow up patients with PAD, assessing clinical and functional status, medication adherence, limb symptoms, and CVRFs, with DUS assessment as needed.553,554 I C © ESC 2024
CVRFs, cardiovascular risk factors; DUS, duplex ultrasound; PAD, peripheral arterial disease. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3585
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.49
8.1.2.2 Medical treatment
Chronic limb-thretening ischaemia is associated with a high risk of ischaemic events,429,431 thus management of patients with CLTI must include OMT. In addition, rest pain, optimal wound care, and infection control should be managed. A vascular team, including at least a vascular physician, a vascular surgeon, and a radiologist, should be involved to prevent amputation.568 Lower-limb exercise training is contraindicated until ulcers are healed and aggressive offloading should be ensured to allow healing. Depending on infection extent, oral antibiotics may suffice, however, if extensive with systemic signs of inflammation, admission for intravenous (i.v.) antibiotic administration may be required.569,570 Good-quality evidence on the advantages of one type of wound dressing over others is lacking, while in selected patients individualized treatments with antimicrobial dressing,571 silver dressing,572 collagen dressing,573 honey- or iodine-based dressings,574 platelet-rich plasma, or negative pressure therapy575,576 may accelerate wound healing, shorten hospital stay, and prevent amputations. If deep-seated infection is suspected, X-ray or MRA are required to diagnose osteomyelitis, in which case a longer course of antibiotics may be necessary.577 Antibiotics for osteomyelitis treatment may be empirical, however, they should be adapted according to (preferably tissue) cultures.578–581 Ulcers require assessment of venous aetiology and potential for endovenous therapy, while mixed ulcers require compression therapy after revascularization.582 8.1.2.3 Interventional treatment
8.1.2.3.1. Revascularization. In CLTI, revascularization should be attempted to rapidly restore an inline direct blood flow to the foot.585–588 Three RCTs compared endovascular therapy with open surgery in infra-inguinal arteries. In the Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial, no significant difference was found regarding mortality or amputation-free survival at 2 years.589 However, surgery was associated with a significantly reduced risk of amputation, death, or both after 2 years.564,589 In the Best Endovascular versus Best Surgical Therapy for Patients with Critical Limb Ischemia (BEST-CLI) trial (median follow-up of 2.7 years), the incidence of MALE or death was lower in patients in which one segment of the GSV was available for surgical revascularization than in patients who underwent endovascular revascularization. In the same trial, outcomes of patients for whom an alternative bypass conduit was needed for surgical revascularization were similar to those of patients who underwent endovascular revascularization.567 In the BASIL-2 trial, which included patients requiring infra-popliteal, with or without additional further proximal infra-inguinal, revascularization procedures, endovascular revascularization was associated with better amputation-free survival than surgical revascularization, which was primarily due to fewer deaths in this group.590 It is important to consider591 both revascularization options individually in each patient, considering the complexity of the diseased anatomical region.
Multilevel disease Patients with CLTI commonly present with multilevel disease.592 Especially for complex lesions, comprehensive patient assessment, including the individual patient’s clinical presentation, the lesion morphology, and the peri-procedural risk, needs to be undertaken by a multidisciplinary vascular team to weigh the risks against the benefits of the respective methods of revascularization (endovascular vs. surgical).590,593–596 A structured approach is essential to achieve rapid and durable restoration of an inline flow to the foot. When possible, the angiosome concept can be considered, targeting the most affected ischaemic area.597 When CLTI leaves no viable revascularization options, transcatheter arterialization of deep veins may be considered.598 Aorto-iliac disease An endovascular approach is the first choice, commonly employing bare metal or covered stents.599–603 Surgery is reserved for extensive obstructions and lesions treated unsuccessfully with an endovascular procedure.604 Hybrid revascularization should be considered in occlusion of the common femoral artery or profunda femoris artery requiring endarterectomy, in addition to inflow and/or outflow disease amenable to endovascular therapy. Hybrid procedures should be encouraged in a one-step modality.605 Femoro-popliteal disease Chronic limb-threatening ischaemia is unlikely to be related to isolated superficial femoral artery lesions; femoro-popliteal involvement in combination with aorto-iliac or infra-popliteal disease is frequently found. In 40% of cases, inflow treatment of femoro-popliteal disease is necessary.606 The revascularization strategy should be selected according to lesion complexity.422 If endovascular therapy is chosen, landing zones for potential bypass grafts should be preserved. When bypass surgery is decided, the bypass should be as short as possible, using the saphenous veins.567 Infra-popliteal disease Extended infra-popliteal disease is mainly seen in patients with diabetes607–610 and CKD,611,612 often being associated with superficial femoral artery lesions. In short infra-popliteal lesions, endovascular
Recommendation Table 18 — Recommendations for the management of chronic limb-threatening ischaemia
Recommendations Classa Levelb
For limb salvage in patients with CLTI, revascularization is recommended.564,567 I B Early recognition of CLTI and referral to the vascular team are recommended for limb salvage.417,560 I C In patients with CLTI, imaging of the entire affected limb should be considered.560 IIa C © ESC 2024
CLTI, chronic limb-threatening ischaemia. aClass of recommendation. bLevel of evidence.
Recommendation Table 19 — Recommendations for medical treatment in patients with chronic limbthreatening ischaemia (see also Evidence Table 7)
Recommendations Classa Levelb
It is recommended that patients with CLTI are managed by a vascular team.568 I C In patients with CLTI and ulcers, offloading mechanical tissue stress is recommended to allow wound healing.583,584 I C It is recommended to treat infection with antibiotics.569,570 I C Lower-limb exercise training is not recommended in patients with CLTI and wounds.584 III C © ESC 2024
CLTI, chronic limb-threatening ischaemia. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.50
therapy is the first choice.593 Drug-eluting balloons607 and bare metal stent implantation613 have shown no superiority over plain balloon angioplasty, although drug-eluting stents may be used for relatively short proximal lesions.614–616
8.1.2.3.2 Spinal cord stimulation. Spinal cord stimulation (SCS) may
be considered in treating patients with CLTI and no viable revascularization options. SCS offers modest pain relief and an 11% reduction in amputation rate compared with conservative management at 1 year. No effect was seen in ulcer healing and benefits should be weighed against the high cost and possible complications.617 Recent technological advances in neuromodulation may improve the treatment value of this modality.618
8.1.2.3.3. Amputation. Minor amputation, usually up to the forefoot, is often needed for necrotic tissue removal with minor impact on patient mobility. Pre-amputation revascularization enhances wound healing. In cases of extensive necrosis or infectious gangrene, primary major amputation without revascularization may be preferable to avoid complications. Secondary amputation is indicated when revascularization fails, re-intervention is not possible, or limb deterioration persists despite a patent graft and optimal management. BTK amputation allows better mobility with a prosthesis. For bedridden patients, above-the-knee amputation may be the preferred choice.
8.1.2.4 Follow-up
In patients with CLTI, the incidence of CV events is increased.619,620 Follow-up should focus on general clinical CV condition, prevention of revascularization failure, wound healing, and contralateral limb status. After revascularization, at least an annual appointment with a vascular physician expert in CLTI management is warranted. Due to the lack of evidence, recommendations are largely based on consensus and expert opinions.128
First-year incidence of vein graft stenosis is 20%;621 however, if uneventful for 12 months, late issues are scarce.622 Clinical examination, ABI (or TBI) measurement, and DUS should be performed within 4– 6 weeks and thereafter at 3, 6, 12, and 24 months after bypass surgery.128 After endovascular treatment, restenosis and occlusion ranges from 5% in the pelvic region to >50% in the infra-popliteal arteries.623,624 Unlike after surgery, no plateau phase is seen, and the failure rate is constant for at least 5 years. Surveillance includes clinical assessment looking for recurrent symptoms or signs, ABI measurement, and DUS based on the first check-up: if normal, DUS is recommended if symptoms reappear; if abnormal, initial DUS, re-intervention, or closer DUS follow-up on a case-by-case basis are recommended.128 Post-procedural ankle duplexbased estimated ABI of <0.90 predicts suboptimal wound healing, clinically driven target lesion revascularization (cdTLR), and MALE.625 After revascularization, closer follow-up and wound care are recommended until healing. Thereafter, annual appointments with vascular physicians with expertise in CLTI management should be scheduled to check for symptoms, foot condition, ABI, and CVRFs, including availability for TP and TcPO2 if needed. Recurrence of symptoms may also be due to the progression of atherosclerotic disease above or below the bypass or angioplasty site.427
8.1.3 Acute limb ischaemia
8.1.3.1. Clinical presentation and diagnosis Acute limb ischaemia is caused by an abrupt decrease in arterial limb perfusion. Potential causes are PAD progression, cardiac/aortic embolization, AD, graft thrombosis, aneurysm thrombosis, popliteal artery entrapment syndrome, trauma, phlegmasia cerulea dolens, ergotism, hypercoagulable states, and iatrogenic complications related to vascular procedures. ALI is a medical emergency and timely recognition is crucial to successful treatment.629–632 Patients should be rapidly evaluated by a vascular specialist633 or rapidly transferred to a facility with such resources. The time constraint is due to the period that skeletal muscle and nerves will tolerate ischaemia—roughly 4–6 h.634 Lower-extremity symptoms can include both pain and loss of function. The longer and the stronger these symptoms are, the less likely the possibility of limb salvage.
Recommendation Table 20 — Recommendations for interventional treatment of chronic limb-threatening ischaemia
Recommendation Classa Levelb
In CLTI patients, it is recommended to perform revascularization as soon as possible.564 I B In CLTI, it is recommended to use autologous veins as the preferred conduit for infra-inguinal bypass surgery.567,593 I B In multilevel vascular disease, it is recommended to eliminate inflow obstructions when treating downstream lesions. I C An individual risk assessment (weighing the patient’s individual procedural risk of endovascular vs. surgical revascularization) by a multidisciplinary vascular team is recommended. I C In CLTI patients with good autologous veins and low surgical risk (<5% peri-operative mortality, >50% 2 year survival), infra-inguinal bypass may be considered.564,567,590 IIb B In CLTI patients, endovascular treatment may be considered as first-line therapy, especially in patients with increased surgical risk or inadequate autologous veins.564,567,590 IIb B © ESC 2024
CLTI, chronic limb-threatening ischaemia. aClass of recommendation. bLevel of evidence. Recommendation Table 21 — Recommendations for follow-up in patients with chronic limb-threatening ischaemia
Recommendations Classa Levelb
In patients with CLTI, following revascularization it is recommended to follow up patients on a regular basis.552,626,627 I C At follow-up, it is recommended to assess clinical, haemodynamic and functional status, limb symptoms, treatment adherence, and CVRFs.552,625–628 I C © ESC 2024
CLTI, chronic limb-threatening ischaemia; CVRFs, cardiovascular risk factors. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3587
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.51
8.1.3.1.1 Clinical examination. The emergency level and the choice
of therapeutic strategy depend on the clinical presentation, mainly according to neurological deficits. Clinical assessment must include symptom duration as well as sensory and motor deficit severity to distinguish a threatened from a non-viable extremity. Neurological deficits (sensory loss or especially motor deficit) are signs of limb threat and require emergency imaging and revascularization.635 Severe sensory deficit and paralysis suggest the limb may be unsalvageable. Clinical ALI categories are presented in Table 9.
8.1.3.1.2 Imaging and functional tests. The imaging method de-
pends on availability and aims to diagnose clot presence and assess haemodynamic severity. DSA, CTA, DUS, and contrast-enhanced (CE)-MRA are options based on local expertise, availability, and preference.636 DUS helps determine treatment urgency when assessing neurological deficit is challenging. Loss of arterial signal suggests limb threat, while a present signal may indicate the limb is not immediately threatened, allowing for ABI measurement. The absence of both arterial and venous Doppler signals, coupled with extensive motor deficit, suggests the limb may be irreversibly damaged (non-salvageable).637 In addition, biomarkers of muscle damage such as creatinine kinase (CK) or myoglobin may be useful as high levels indicate rhabdomyolysis, risk of amputation,638 kidney failure, and mortality.639 In limb ischaemia, CK and myoglobin elevations may be lower in chronic cases, possibly due to ischaemic pre-conditioning and collateral development.640
8.1.3.2 Medical treatment
Upon clinical diagnosis, initiate analgesia, anticoagulation, and i.v. fluids. Addressing acidosis and hyperkalaemia may be necessary. Administer i.v. unfractionated heparin (bolus 5000 IU or 70–100 IU per kg body weight, followed by continuous infusion with dose adjustment based on patient response, monitored by activated clotting time or activated partial thromboplastin time) or subcutaneous low molecular weight heparin (e.g. enoxaparin 1 mg per kg twice daily) to prevent further embolization and thrombus propagation.
8.1.3.3 Surgical and interventional treatment
For a salvageable limb, urgent revascularization is essential. Diagnostic imaging, if it will not delay treatment, is recommended to guide therapy. If the limb is deemed unsalvageable, primary amputation or comfort care is indicated.
Different revascularization modalities can be applied, including percutaneous catheter-directed thrombolytic therapy, percutaneous mechanical thrombus extraction or thrombo-aspiration (with or without thrombolytic therapy), or surgical thrombectomy, bypass, and/or arterial repair.642 Moreover, these modalities can be combined, with the strategy determined by factors such as neurological deficit, ischaemia duration, localization, size, aetiology, comorbidities, type of conduit (artery or graft), and therapy-related risks and outcomes. Current endovascular approaches to ALI boast high technical success rates.626 To reduce morbidity and mortality, an endovascular-first approach is often preferred, especially in patients with severe comorbidities. Thrombus extraction, thrombo-aspiration, and surgical thrombectomy are indicated in cases of neurological deficit, while catheter-directed thrombolytic therapy is more appropriate in less severe cases without neurological deficit. Modern catheter-based thrombectomy (CDT) is associated with 12-month amputation rates of <10% in Rutherford IIB.643 A meta-analysis showed that although CDT in the treatment of not immediately threatening ALI showed high angiographic success, the long-term outcomes were relatively poor, with low patency and a substantial risk of major amputation.644 Systemic thrombolysis has no role in the treatment of patients with ALI. A meta-analysis showed that CDT and surgery have similar limb salvage rates.645 Recent analyses indicate benefits of endovascular approaches in terms of mortality at similar amputation rates.646,647 A comparison of percutaneous thrombectomy vs. ultrasoundaccelerated thrombolysis for the initial management of ALI showed no difference in terms of amputation, bleeding, clinical success, and adverse events, with primary patency at 30 days of 82% and 71%, respectively.629,648,649 After thrombus removal, in cases of pre-existing arterial lesions, these should be treated by endovascular therapy or open surgery. If surgical treatment is required, it should be ideally performed in a hybrid room with capacity to allow sufficient completion angiographic imaging and initiation of local lysis if any remaining clot is visualized. Lower-extremity four-compartment fasciotomies should be performed in patients with long-lasting ischaemia to prevent postreperfusion compartment syndrome.637 The management of ALI is summarized in Figure 16.
Table 9 Clinical categories of acute limb ischaemia
Grade Category Sensory
loss Motor deficit Arterial
Doppler
signal Venous
Doppler
signal Capillary
refill Biomarkers Prognosis
I Viable None None Yes Yes Yes Not elevated No immediate
threat
IIA Marginally
threatened None or
minimal (toes) None No Yes Salvageable if
promptly treated
IIB Immediately threatened More than toes Mild-moderate No Yes Salvageable if promptly
revascularized
III Irreversible Profound,
anaesthetic Profound
paralysis (rigor) No No No Massively
elevated Major tissue loss,
permanent nerve damage inevitable © ESC 2024
Adapted with permission from.641 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.52
Neurological function
No sensory loss Normal motor function Sensory loss limited to toes No muscle weakness Sensory loss more than toes and rest pain Mild-to-moderate muscle weakness Complete sensory loss and loss of motor function Capillary refill
Intact Slow-intact Slow-absent Absent Arterial Doppler
Audible Inaudible Venous Doppler
Audible
I: Viable IIA: Marginally threatened IIB: Immediately threatened III: Irreversible
Inaudible
Muscle biomarkers
Elevated
Suspected ALI
Acutely cold and painful leg
Pain management
Medical management and follow-up
Imaging (DUS, CTA, DSA, MRA) Imaginga
(DUS, CTA, DSA, MRA)
Urgent revascularization
AND anticoagulation unless contraindicated Emergency revascularization
AND anticoagulation unless contraindicated Primary amputation
or palliative care
Clinical evaluation by experienced clinician
Figure 16 Management of acute limb ischaemia. ALI, acute limb ischaemia; CTA, computed tomography angiography; DSA, digital subtraction angiography; DUS, duplex ultrasound; MRA, magnetic resonance angiography. aShould not delay treatment.
ESC Guidelines 3589
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.53
8.1.3.4 Follow-up
After revascularization or amputation, haemodynamic success should be established, aetiology of ALI investigated, and OMT ensured. Statins improve outcomes after revascularization.552,630 Since ALI is frequently caused by thrombo-embolism, Holter-ECG, echocardiogram, and aortic imaging are useful to allow initiation of appropriate therapy, in particular anticoagulation.650 Additionally, consider other prothrombotic syndromes, such as antiphospholipid syndromes and vasculitis, if clinically suspected. While there is only sparse evidence, the inclusion of PAD patients after revascularization into structured follow-up may improve their functional outcomes.627 8.2 Extracranial carotid and vertebral
artery disease 8.2.1. Clinical presentation and diagnosis 8.2.1.1. Clinical presentation Atherosclerotic CS represents one of the major causes of acute ischaemic stroke (20%).657
CS may be revealed by a cervical bruit, but also by a TIA or stroke.
8.2.1.2 Diagnosis
Atherosclerotic lesions are primarily located in specific arterial segments, including the carotid bifurcation, siphon, M1 segment of the middle cerebral artery, brachiocephalic trunk, subclavian artery, first and fourth segments of the vertebral artery, or first segment of the basilar artery. Carotid plaques (CP), originating in the intima, offer a better representation of the atherosclerotic process than carotid intima-media thickness (cIMT). CP may be diffuse or focal (protuberant). According to the Mannheim carotid plaque consensus, a CP is defined as a focal structure encroaching into the arterial lumen by ≥0.5 mm or ≥50% of the surrounding vessel.658 The American Society of Echocardiography (ASE) recently proposed a definition that includes any focal thickening considered atherosclerotic in origin and encroaching into the lumen of any carotid artery segment (protuberant-type plaque) or, in the case of diffuse vessel wall atherosclerosis, when cIMT measures ≥1.5 mm in any carotid artery segment.659 Plaques can progress to CS, defined as ≥50% narrowing of the extracranial internal carotid artery (ICA), with stenosis severity estimated using the North American Symptomatic Carotid Endarterectomy Trial (NASCET) method or its non-invasive equivalent assessed by DUS (Figure 17).122,660 Other methods are described in the Supplementary data online, Section 1.5. The European Carotid Surgery Trial (ECST) and the area methods overestimate the severity of the CS and are not recommended.77 Carotid DUS is safe, accurate, and reliable if performed by a skilled vascular specialist. It is the first-line imaging modality for screening, diagnosis, and surveillance of extracranial carotid arteries.77 The degree of stenosis is mostly based on Doppler analysis of blood flow in the common carotid artery (CCA), ICA, and external carotid artery (Table 10).661,662 Vertebral and subclavian arteries must also be checked. In some cases, indirect signs of severe stenosis have to be evaluated by transcranial and/or ophthalmic artery Doppler. Severe arterial calcification can decrease DUS accuracy.122
Recommendation Table 22 — Recommendations for the management of patients presenting with acute limb ischaemia (see also Evidence Table 8)
Recommendations Classa Levelb
In patients with ALI, it is recommended that an urgent evaluation is performed by a vascular clinician with sufficient experience to assess limb viability and implement appropriate therapy.635 I C In cases of neurological deficit, urgent revascularization is recommended; diagnostic imaging is recommended to guide treatment, provided it does not delay treatment, or if the need for primary amputation is obvious.422,635,651,652 I C In the absence of severe neurological deficit, revascularization is recommended within hours of initial imaging in a case-by-case decision.422,635,652 I C Treatment with analgesics is recommended as soon as possible for pain control. I C It is recommended to monitor for compartment syndrome after revascularization and treat (fasciotomy).637,652 I C It is recommended to assess clinical and haemodynamic success following revascularization.627 I C In patients with ALI, it is recommended to obtain a comprehensive medical history and determine the cause of thrombosis and/or embolization.650 I C In patients with ALI, following revascularization if not on anticoagulation for other reasons, DAPT or rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered.514,653 IIa C Upon confirmation of ALI diagnosis, treatment with heparin may be considered.635,654–656 IIb C © ESC 2024
ALI, acute limb ischaemia; b.i.d., twice daily; DAPT, dual antiplatelet therapy; DPI, dual pathway inhibition; o.d., once daily. aClass of recommendation. bLevel of evidence. Recommendation Table 23 — Recommendations for carotid artery stenosis assessment
Recommendations Classa Levelb
It is recommended to use the NASCET method or its non-invasive equivalent to assess ICA stenosis.77,122,660 I B It is recommended to use DUS as first-line imaging to diagnose ICA stenosis.77,663 I C It is not recommended to use the ECST method for ICA stenosis assessment.77,122,660 III C © ESC 2024
DUS, duplex ultrasound; ECST, European Carotid Surgery Trial; ICA, internal carotid artery; NASCET, North American Symptomatic Carotid Endarterectomy Trial. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.54
8.2.2 Asymptomatic carotid artery stenosis
8.2.2.1. Medical treatment Optimal medical treatment is based on CVRF correction through lifestyle intervention and pharmacological treatment, with the goal of reducing cerebrovascular and global CV events.19 Concerning hypertension, similar target values as those presented in the general section are recommended for patients with asymptomatic CS.
8.2.2.1.1. Lipid-lowering therapy. See Section 7. 8.2.2.1.2. Antihypertensive therapy. See Section 7. 8.2.2.1.3. Glucose-lowering therapy. See Section 7. 8.2.2.1.4. Antithrombotic therapy. The clinical benefit of antithrombotic treatment in patients with asymptomatic CS remains unproven.664 The only RCT (the Asymptomatic Cervical Bruit Study [ACB]) addressing the issue enrolled only 188 patients per arm, and failed to show superiority of aspirin vs. placebo in reducing TIA, stroke, MI, or death.665 In observational studies, SAPT (mainly low-dose aspirin) was associated with reduced risk of MACE, although data were conflicting for moderate stenosis (i.e. 50%– 75%);664 DAPT, combining aspirin and clopidogrel, has no benefit over SAPT.496,497
The Cardiovascular Outcomes for People Using Anticoagulation Strategies (COMPASS) trial reported a non-significant decrease in MACE in patients with either history of carotid revascularization or asymptomatic patients with >50% CS and CVRFs allocated to dual antithrombotic therapy (aspirin 100 mg o.d. and rivaroxaban 2.5 mg b.i.d.)
NASCET (% stenosis) ECST (% stenosis)
50 75
60 80
70 85
80 91
90 97
A C
B Carotid artery stenosis
equivalents between NASCET and ECST criteria
ECST method
C
NASCET method
x 100% (C-A)
B x 100% (B-A)
Figure 17 North American Symptomatic Carotid Endarterectomy Trial/European Carotid Surgery Trial methods. ECST, European Carotid Surgery Trial; NASCET, North American Symptomatic Carotid Endarterectomy trial.
Table 10 Peak systolic velocity criteria for grading internal carotid artery stenosis
% stenosis Reference 50%–69% (moderate stenosis) ≥70% (severe stenosis) PSV threshold SRUCC662
------------------------- Gornik et al.661 125–230 cm/s
------------------------- ≥180 cm/s or ≥125 cm/s + PSV ICA/CCA ≥2 >230 cm/s
------------------------- Overestimation with SRUCC criteria but no consensus © ESC 2024
CCA, common carotid artery; ICA, internal carotid artery; PSV, peak systolic velocity; SRUCC, Society of Radiologists in Ultrasound.
ESC Guidelines 3591
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.55
vs. aspirin alone or rivaroxaban 5 mg b.i.d. alone. However, specific data on asymptomatic CS were not reported. Since these patients present a two times higher risk of MI,30 lifelong low-dose aspirin should be considered in asymptomatic CS patients at increased risk for CV events (i.e. diabetic patients) and low bleeding risk497 to reduce stroke and CV risk.19,299,488,666
8.2.2.2 Interventional treatment
8.2.2.2.1. Open surgery vs. medical therapy. The rationale for carotid endarterectomy (CEA) in asymptomatic CS stems from two trials that were published some time ago. The Asymptomatic Carotid Atherosclerosis Study (ACAS) and the Asymptomatic Carotid Surgery Trial 1 (ACST-1) compared CEA with medical therapy in asymptomatic patients with 60%–99% CS.672–674 In ACAS, 5 year rates of ipsilateral stroke/death under CEA vs. medical therapy were 5.1% vs. 11.0%. ACST-1 reported 5 year rates of any stroke of 6.4% vs. 11.8%, respectively. In a combined analysis of both trials, CEA conferred less benefit in women at 5 years.675 At 10 years, however, ACST-1674 reported that females benefit following CEA (absolute risk reduction [ARR] 5.8%) to the same extent as men (ARR 5.5%). Medical treatment has advanced following the recruitment of patients in these trials.672–676 A 60%–70% decline in annual stroke rates was also observed in medically treated patients in both trials over 1995 to 2010.676 This reduction was attributed to better medical treatment and lower smoking incidence. The Stent Protected Angioplasty versus Carotid Endarterectomy study (SPACE-2) compared OMT alone against OMT plus CEA/carotid artery stenting (CAS) in asymptomatic patients with CS ≥70% according to ECST criteria. Due to slow recruitment, the study was underpowered. The 1 year rate of the major secondary endpoint was 2.5% after CEA, 3.0% after CAS, and 0.9% after OMT.677 Incidence of any stroke or death from any cause within 30 days or any ipsilateral ischaemic stroke within 5 years (primary efficacy endpoint) was 2.5% with CEA plus OMT, 4.4% with CAS plus OMT, and 3.1% with OMT alone. Results from the Carotid Revascularization Endartectomy vs. Stenting Trial 2 (CREST-2) are awaited to clarify whether intervention is beneficial in the treatment of asymptomatic CS compared with modern OMT. The ARR in stroke favouring surgery over OMT was only 4.6% at 10 years in ACST-1, indicating that 95% of asymptomatic patients ultimately underwent unnecessary interventions.674,678
A recent meta-analysis confirmed the role of modern OMT in reducing major stroke, combined stroke, and mortality in asymptomatic patients, suggesting that OMT has the potential to reduce the requirement for surgical intervention in patients with asymptomatic carotis stenosis.679 In conclusion, for invasive treatment of asymptomatic carotid stenosis, the overall risk reduction is low compared with OMT. Current data are not available to assess subgroups that may still benefit from intervention. However, there is a need to target revascularization in a subgroup of patients with clinical and/or imaging features that increase the risk for stroke on OMT (Table 11).678,680 Importantly, ACST-1 found no evidence that age >75 years at baseline was associated with any ipsilateral stroke reduction at 5–10 years.676–678,696 Neither the ACAS nor ACST-1 studies found any evidence that stenosis severity or contralateral occlusion increased late stroke risk.672,674,697 In a recent meta-analysis, increasing stenosis was associated with late ipsilateral stroke only in the presence of concomitant high-risk features.698 The general algorithm of CS management is presented in Figure 18.552
8.2.2.2.2 Carotid revascularization: surgery vs. stenting. In a recent
meta-analysis update on RCTs in asymptomatic patients comparing CEA vs. CAS, including altogether 7092 patients, CAS was associated with significantly higher rates of 30 day ‘any’ stroke and 30 day death/ any stroke, while CEA was associated with significantly higher rates of 30 day MI. No significant differences were seen in 30 day death, 30 day disabling stroke, 30 day death/disabling stroke, or 30 day death/any stroke/MI when CAS was compared with CEA.699 In the largest RCT, ACST-2, post-operative death and major stroke were similar (1.0%) between groups.700,701 No significant difference was found in the 5 and 10 year incidence of ipsilateral stroke and any stroke between CEA and CAS.696,702,703 The 5 year non-procedural stroke rate in ACST-2 was 2.5% in each group for fatal/disabling stroke, and 5.3% with CAS vs. 4.5% with CEA for any stroke.700,701
Recommendation Table 24 — Recommendations for antithrombotic treatment in patients with carotid stenosis
Recommendations Classa Levelb
Carotid artery disease In patients with symptomatic CS, not undergoing carotid endarterectomy or stenting, DAPT with low-dose aspirin and clopidogrel (75 mg) is recommended for the first 21 days or longer, followed by clopidogrel 75 mg or long-term aspirin to reduce the risk of stroke.667–669 I A In patients with asymptomatic >50% CS, long-term antiplatelet therapy (commonly low-dose aspirin) should be considered if bleeding risk is low.488,497,670,671 IIa C © ESC 2024
CS, carotid artery stenosis; DAPT, dual antiplatelet therapy. aClass of recommendation. bLevel of evidence. Table 11 High-risk features associated with increased risk of stroke in patients with asymptomatic internal carotid artery stenosis on optimal medical treatment
Clinicala Contralateral TIA/stroke681,682 Cerebral imaging Ipsilateral silent infarction683–685 Ultrasound/CT imaging Stenosis progression (>20%)340,684,685
Spontaneous embolization on transcranial Doppler (HITS)341,686 Impaired cerebral vascular reserve687,688 Large plaques689,690 Echolucent plaques136,691 Increased juxta-luminal black (hypoechogenic) area689,690
MRAb Intraplaque haemorrhage692,693
Lipid-rich necrotic core694,695 © ESC 2024
CT, computed tomography; HITS, high-intensity transient signal; MRA, magnetic resonance angiography; TIA, transient ischaemic attack. aAge is not a predictor of poorer outcome. bMore than 40 mm2 on digital analysis. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.56
Duplex ultrasound
Individual risk assessmenta
Average-to-high surgical risk
<60% carotid stenosis 60–99% carotid stenosis 100% carotid occlusion
Asymptomatic patient
OMT (Class I)
Revascularization
(Class III)
Revascularization
(Class IIb)
CTA and/or MRA (incl. aortic arch)
CEA or CAS/TCAR decision by vascular team based on an individual patient approach
Surgical/endovascular risk assessmenta Routine revascularization
(Class III)
OMT (Class I)
Revascularization
(Class III)
OMT (Class I)
Vascular team and neurologist
N Y
Duplex ultrasound CTA and/or MRA (incl. aortic arch)
<50% carotid stenosis 50–69% carotid stenosis 100% carotid occlusion
Symptomatic patient
OMT (Class I)
Routine revascularization
(Class III) OMT (Class I)
Revascularization
(Class III)
OMT (Class I)
Revascularization
(Class IIa) 70–99% carotid stenosis
OMT (Class I)
Revascularization
(Class I)
CEA or CAS/TCAR decision by vascular team based on an individual patient approach
Figure 18 Algorithm of carotid artery stenosis management. CAS, carotid artery stenting; CEA, carotid endarterectomy; CTA, computed tomography angiography; MRA, magnetic resonance angiography; OMT, optimal medical treatment; TCAR, transcarotid artery revascularization; TIA, transient ischaemic attack. aAssess presence of high-risk features according to Table 11. If surgery/revascularization is considered, assess the overall risk related to surgery according to Table 12.
ESC Guidelines 3593
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.57
The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial randomized symptomatic and asymptomatic patients deemed ‘high-risk for surgery’ to either CEA or CAS (using embolic protection devices).704 Overall, 71% of SAPPHIRE patients were asymptomatic, and in these patients the 30 day rate of death/stroke after CAS was 5.8% vs. 6.1% after CEA704— both beyond the recommended 3%. If these procedural risk levels reflect contemporary practice, most ‘high-risk for surgery’ asymptomatic patients would be better treated medically. A small sample size RCT has provided evidence that the use of a double-layer mesh stent can reduce the occurrence of peri-procedural diffusion-weighted imaging (DWI)-detected ischaemic lesion after carotid stents, when compared with conventional stents. At 1 year followup the use of a double-layer mesh stent was associated with a significant reduction in the composite endpoint of MACE and in-stent restenosis or occlusion. The clinical benefit of these findings has to be proven.705,706 Transcarotid artery revascularization (TCAR) has been introduced recently. Although no RCTs are available, large registry-based analyses report a 99.7% technical success rate and low 30 day complication rates (<3% in 30 day stroke/death and <1% MI).681 In a large-scale registry the 1 year rate of stroke or death was 6.4% for TCAR, 5.2% for CEA, and 9.7% for transfemoral carotid artery stenting (TFCAS).707 Properly conducted RCTs comparing TCAR with CEA in asymptomatic patients are required to establish the true place of TCAR in carotid revascularization.708 8.2.3 Symptomatic carotid artery stenosis
8.2.3.1. Medical treatment 8.2.3.1.1. Lipid-lowering therapy. See Section 7. 8.2.3.1.2. Antihypertensive therapy. See Section 7. 8.2.3.1.3. Glucose-lowering therapy. See Section 7. 8.2.3.1.4. Antithrombotic therapy. Symptomatic CS is associated with a high risk of early recurrence of cerebrovascular ischaemic events.667–669,683 DAPT with low-dose aspirin and clopidogrel is recommended for all patients with symptomatic CS for at least 3 months.669 Those undergoing surgical revascularization can stop clopidogrel after surgery.711 Those undergoing endovascular revascularization should continue DAPT with clopidogrel and low-dose aspirin for 4 weeks after the procedure.488,666,711,712 In patients with stroke related to extracranial arterial disease, aspirin was more effective than VKAs in reducing recurrencies.687,713 Subgroup analysis from the Acute Stroke or Transient Ischaemic Attack Treated with Aspirin or Ticagrelor and Patient Outcomes (SOCRATES) trial suggested a lower rate of MACE in patients receiving ticagrelor vs. aspirin;689 however, this analysis was underpowered to make any conclusions regarding the benefit of ticagrelor. A combination of aspirin and clopidogrel in the early phase of symptomatic carotid stenosis reduces asymptomatic cerebral embolization and stroke.692,694,714 It also reduces stroke recurrence after a minor stroke/TIA.667,668 Recently, the Acute Stroke or Transient Ischaemic Attack Treated with Ticagrelor and acetylsalicylic acid for Prevention of Stroke and Death (THALES) trial showed a 17% reduction in the risk of death or stroke when using ticagrelor and aspirin vs. aspirin alone in patients with minor stroke or high-risk TIA;715 however, bleeding events occurred more frequently in the ticagrelor plus aspirin group.700,716 Of note, COMPASS data cannot be applied to symptomatic carotid stenosis since these patients were excluded because of intracranial bleeding risk.499
Recommendation Table 25 — Recommendations for interventional treatment in patients with asymptomatic carotid artery stenosis
Recommendations Classa Levelb
When ICA revascularization is considered, documented peri-operative stroke/death rates should be <3% and the patient’s life expectancy should be considered >5 years after careful consideration of the risks and benefits by a vascular team. 674,709 IIa B In ‘average surgical risk’ patients over 75 years of age with a CS of 60%–99%, in the presence of high-risk features, CEA, in addition to OMT, should be considered.674,709 IIa B In ‘high surgical risk’ patients with a CS of 60%–99%, in the presence of high-risk features, CAS, in addition to OMT, may be considered.699,701,704 IIb B In ‘average surgical risk’ patients with a CS of 60%– 99%, in the presence of high-risk features, CAS, in addition to OMT, may be considered as an alternative to CEA.696,701,702,710 IIb B In asymptomatic patients with ICA stenosis, in the absence of high-risk features and with a life expectancy <5 years, routine revascularization is not recommended.674 III A © ESC 2024
CAS, carotid artery stenting; CEA, carotid endarterectomy; CS, carotid artery stenosis; ICA, internal carotid artery; OMT, optimal medical treatment. aClass of recommendation. bLevel of evidence. Recommendation Table 26 — Recommendations for evaluation and medical treatment in patients with symptomatic carotid artery stenosis
Recommendations Classa Levelb
DAPT is recommended in the early phase of minor strokes in patients with ICA stenosis, if not revascularized, for at least 21 days, considering the bleeding risk.667,668 I A It is recommended that symptomatic ICA stenosis patients are assessed by a vascular team including a neurologist.667,668 I C Long-term treatment with SAPT should be considered following ICA revascularization.667,668 IIa C DAPT may be considered in the early phase of minor stroke in patients with ICA stenosis for up to 90 days, considering the bleeding risk.667,668 IIb B © ESC 2024
DAPT, dual antiplatelet therapy (aspirin and clopidogrel); ICA, internal carotid artery; SAPT, single antiplatelet therapy. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.58
8.2.3.2 Interventional treatment
8.2.3.2.1. Open surgery. Optimal medical treatment is recommended for all symptomatic patients with CS. In recently symptomatic patients with <50% stenosis, CEA (plus OMT) did not prevent stroke. However, surgery reduced stroke risk in patients with moderate (50%–69%) and severe (70%–99%) stenosis. The benefit from surgery increased with increasing severity of stenosis, except for ‘nearocclusion’ lesions (95%–99% stenosis with distal ICA collapse or a narrow calibre lumen with ‘trickle flow’).660,717–720 Some features are associated with a higher increase of stroke in symptomatic patients (50%–99% stenosis) medically treated: age (>75 years), symptoms within 14 days, male sex, hemispheric (vs. retinal) symptoms, cortical (vs. lacunar) stroke, increasing comorbidities, irregular stenosis, stenosis severity, contralateral occlusion, tandem intracranial stenosis, and failure to recruit intracranial collaterals.721 Large-scale registries suggest that CEA can be performed safely in the first 7 days after TIA/minor stroke.722–724 However, not all patients benefit from urgent revascularization, and controversy exists over the safety of performing CEA within the first 48 h after symptom onset due to an increased risk of haemorrhagic transformation. Higher-risk patients include those with acute carotid occlusion, a persisting major neurological deficit, an area of middle cerebral artery infarction exceeding one-third, evidence of pre-existing parenchymal haemorrhage, and signs of impaired consciousness.724,725 The choice to perform carotid revascularization within 48 h from symptom onset is still debatable.726
8.2.3.2.2 Endovascular therapy vs. open surgery. Contemporary
RCTs comparing CEA with CAS in symptomatic patients reported a significantly higher risk of 30 day ‘any stroke’ and ‘death/stroke’ following CAS. This is mainly due to higher rates of minor stroke, which were non-disabling and resolved within 6 months.711,727 However, the occurrence of a peri-operative stroke is associated with three-fold poorer long-term survival,727 similar to a postprocedural MI (which was more frequent after CEA).728 In CAS patients, the risk increased in those aged >60 years, especially for those aged >80 years, who are four times more likely to experience a procedural stroke/death. When comparing CAS with CEA, the age-related effect became apparent in patients aged 60–65 years, and CEA is superior to CAS in patients aged >70 years.729,730 Elderly CAS patients may experience more peri-operative strokes, mainly minor ipsilateral strokes, possibly due to a higher burden of aortic arch disease. In these cases, operator/institution experience may play a role in determining peri-procedural outcomes. CAS is associated with significantly lower risks for MI, transient cranial nerve injury, and haematoma.731,732 Beyond the 30 day peri-operative period, long-term data suggest that outcomes after CAS are similar to those with CEA.703,733 The predicted magnitude of 30 day risk (according to clinical/anatomical characteristics and operator/centre experience) will thus largely determine whether CEA or CAS is preferable in individual patients. Post-hoc trial analysis revealed enhanced benefits of CEA when performed within 2 weeks of the ischaemic event,734 with reduced complications compared with CAS performed within 1 week of stroke/TIA. The Carotid Stenosis Trialists’ Collaboration found a higher stroke/ death rate (8.3% with CAS vs. 1.3% with CEA) for CAS in patients treated within 1 week of the last symptomatic event.735 These findings support a preference for early CEA in symptomatic patients. However, these trials, initiated over 30 years ago, lack evaluation of current OMT. Initially designed as an alternative for high surgical risk (HSR) patients,704,736 carotid stenting’s efficacy needs consideration in contemporary practice (Table 12).735
In conclusion, CEA is still the treatment choice for patients with symptomatic carotid stenosis. However, in patients eligible for carotid revascularization but deemed high surgical risk by a multidiscliplinary team, CAS may be preferred over CEA—the patient must be a suitable candidate for CAS, and the complication rate should not surpass 6%. At present, TCAR results have been analysed in registries only. In these studies, in-hospital stroke/death has been significantly lower after TCAR compared with transfemoral CAS.707,737 Similar to the previous results established for CEA, symptomatic patients undergoing TCAR demonstrate similar outcomes if the procedure is performed >48 h after the neurological event.738 However, TCAR has not yet been evaluated in RCTs and has not been compared with CEA or OMT.
8.2.3.2.3 Vertebral arteries. The evidence on the use of lifestyle
modifications and medical therapy in cases of symptomatic vertebral artery stenosis is lacking, but their use is reasonable given the overall CV risk in these patients. Evidence on the use of preventive strategies and antithrombotic agents is lacking, but their use is reasonable in the presence of other CVRFs. Surgery on extracranial vertebral stenosis (with transposition to CCA, trans-subclavian vertebral endarterectomy, distal venous bypass) can be performed with low stroke/death rates in experienced centres.739,740 However, with limited expertise in complex vertebral artery reconstructions, open surgery has been mostly replaced by endovascular interventions. In a combined analysis of the the Vertebral Artery Ischaemia Stenting Trial (VIST), the Vertebral Artery Stenting Trial (VAST), and the Stenting and Aggressive Medical Management for Preventing
Table 12 High-risk peri-operative features for carotid endarterectomy Clinical Congestive heart failure (NYHA functional class III/IV) Unstable angina (CCS III/IV) CAD with LM or >1 vessel with 70% stenosis Recent MI (<30 days) Planned open heart surgery (<30 days) LVEF <30% Severe pulmonary disease Severe renal disease Anatomical Surgically inaccessible lesions • At or above C2 • Below the clavicle Ipsilateral neck irradiation Spinal immobility of the neck Contralateral carotid artery occlusion (increases risk for stroke) Contralateral laryngeal palsy Tracheostomy © ESC 2024
CAD, coronary artery disease; CCS, Canadian Cardiovascular Society; LM, left main; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NYHA, New York Heart Association.
ESC Guidelines 3595
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.59
Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) trial,741 no clear benefit was shown for extracranial vertebral artery stenting. Randomized controlled trials have not assessed surgical techniques like vertebral artery endarterectomy or transposition. While case series exist, they often lack a control group following a consistent medical treatment protocol.742 As a result, the effectiveness of these procedures remains uncertain.
8.2.3.3 Follow-up
Peri-operative and post-procedural medical management after carotid revascularization should include OMT. Post-operative hypertension is a risk factor for stroke and TIAs, wound bleeding, and intracranial haemorrhage.743 Therefore, proper pharmacological BP control is important in optimizing outcomes.744 Fluctuations of hypertension and hypotension are not uncommon and should be treated promptly.744,745 An intensive lipid-lowering therapy (ILT) aiming at >50% LDL-C reduction and LDL-C <1.4 mmol/L (55 mg/dL) is also recommended.19 Antiplatelet therapy should be tailored according to type of intervention. In CEA, the reduction in peri-procedural and long-term ischaemic events under low-dose aspirin has been demonstrated.746,747 After carotid stenting, DAPT (aspirin and clopidogrel) is recommended, while optimal duration is debated.748 In the peri-operative period after CAS, DAPT should be prescribed and continued for at least 30 days post-procedure.77,749,750 Ticagrelor, when included in DAPT following CAS/TCAR, presents a drawback due to its elevated bleeding risk compared with clopidogrel.751–753 Duplex ultrasound is the first-line technique to evaluate patients after CEA or CAS. CTA and MRA are alternative methods for determining restenosis.749,754
After CEA or CAS, DUS is recommended at baseline (<3 months) and annually thereafter until the patient is stable (i.e. until no restenosis is observed in two consecutive annual scans). Regular surveillance (e.g. every 2 years) can be performed based on the stenosis of the contralateral ICA, risk profile, and patient’s life expectancy.749,754 For patients combining multiple CVRFs after the procedure, DUS may be beneficial every 6 months until a stable clinical pattern is established, and annually thereafter.749,754 Early surveillance, especially within 1–3 months and particularly in cases where intraoperative completion imaging is absent (e.g. after CEA), aids in detecting technical errors and setting a baseline for future comparisons. Follow-up enables the identification of ipsilateral carotid restenosis and contralateral disease progression, offering a chance for timely intervention to minimize the risk of stroke. Nevertheless, this concept is facing growing challenges due to a reduced and selective role for intervention in asymptomatic patients. A surveillance protocol holds significance when anticipated outcomes are expected to costeffectively influence a medical or interventional treatment plan.749,754
8.3 Other arterial locations
8.3.1. Subclavian artery disease 8.3.1.1. Clinical presentation and diagnosis Atherosclerotic upper-limb artery disease (UEAD) is most frequently located in the subclavian artery.755,756 Digital ischaemia is most frequently caused by non-atherosclerotic aetiologies, including thromboembolism, systemic sclerosis, idiopathic, thromboangiitis obliterans, iatrogenic, or cancer.757 Isolated subclavian stenosis (SS) is often asymptomatic and may be suspected because of an absolute inter-arm SBP difference >10–15 mmHg.758 In the Multi-Ethnic Study of Atherosclerosis (MESA), prevalence of asymptomatic SS was approximately 4.5% (male: 5.1%, female: 3.9%) in adults and more frequent in patients with PAD (11.4%).759 In patients attending CV clinics, a
Recommendation Table 27 — Recommendations for interventions in patients with symptomatic carotid artery stenosis
Recommendations Classa Levelb
It is recommended to perform CEA of symptomatic 70%–99% ICA stenosis provided a documented 30 day risk of procedural death/stroke is <6%.660,719 I A If indicated, it is recommended to perform CEA within 14 days in symptomatic ICA stenosis patients.734 I B OMT is recommended for all symptomatic ICA stenosis patients.19 I A CEA of symptomatic 50%–69% ICA stenosis should be considered provided a documented 30 day risk of procedural death/stroke is <6%.660,719 IIa A For symptomatic patients at high risk for CEA with a 70%–99% ICA stenosis, CAS should be considered provided a documented 30 day risk of procedural death/stroke is <6%.703 IIa B For symptomatic patients <70 years of age with a 70%–99% ICA stenosis, CAS may be considered provided a documented 30 day risk of procedural death/stroke is <6%.703 IIb A Revascularization is not recommended in patients with ICA lesions <50%.660,719 III A © ESC 2024
CAS, carotid artery stenting; CEA, carotid endarterectomy; ICA, internal carotid artery; OMT, optimal medical treatment. aClass of recommendation. bLevel of evidence. Recommendation Table 28 — Recommendations for follow-up in patients with carotid artery stenosis
Recommendations Classa Levelb
Once-yearly follow-up is recommended to check for CVRFs and treatment compliance.754 I A After ICA stent implantation, DAPT with aspirin and clopidogrel is recommended for at least 1 month.77,749,750 I A After ICA revascularization, long-term aspirin or clopidogrel is recommended.746,747 I B During follow-up, it is recommended to assess neurological symptoms, CVRFs, and treatment adherence at least yearly in patients with CS.754 I C After ICA revascularization, surveillance with DUS is recommended within the first month.749,754 I C © ESC 2024
CS, carotid artery stenosis; CVRFs, cardiovascular risk factors; DAPT, dual antiplatelet therapy; DUS, duplex ultrasound; ICA, internal carotid artery. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.60
>25 mmHg SBP difference doubles prevalence and independently predicts mortality.32,758 As obstructive disease progresses, particularly affecting vertebral vessels, the risk of ischaemia or steal symptoms significantly rises. Visual disturbances, syncope, ataxia, vertigo, dysphasia, dysarthria, and facial sensory deficits during arm movements may indicate subclavian steal syndrome, correlating with inter-arm BP difference.760 Brachiocephalic occlusive disease can lead to stroke or TIA in carotid and vertebral territories, manifesting as exercise-induced fatigue, pain, and arm claudication. Severe cases, especially with distal disease, may result in rest pain and digital ischaemia with necrosis. Duplex ultrasound assessment of subclavian arteries enables the detection of SS via intrastenotic high-velocity flows (50% stenosis: peak systolic velocity [PSV] ≥230 cm/s, PSV ratio [PSVr] ≥2.2; 70% stenosis PSV ≥340 cm/s and PSVr ≥3.0) or monophasic post-stenotic waveforms.761 The majority of patients (>90%) with at least 50% proximal SS have either intermittent or continuous flow reversal in the vertebral artery, though not all will be symptomatic.760,762 When subclavian steal syndrome is suspected, flow reversal should be assessed in the ipsilateral extracranial vertebral artery by hyperaemia testing and if available transcranial Doppler.762 Severe stenosis or occlusion of the right brachiocephalic trunk is associated with reduced flow velocities in the ipsilateral subclavian artery and the CCA. Abnormal or doubtful DUS should lead to anatomic imaging (CTA/MRA).763 CTA is excellent for supra-aortic lesions and can provide extravascular information, especially when thoracic outlet syndrome is a differential diagnosis. MRA provides both functional and morphological information useful to distinguish antegrade from retrograde perfusion and to estimate stenosis severity.764 DSA is performed if endovascular therapy is indicated. PET is useful for the diagnosis of arteritis but not for assessment of atherosclerotic lesions in clinical practice.
8.3.1.2 Treatment strategy (medical and interventional)
Optimal medical treatment is recommended in all patients with symptomatic UEAD to reduce CV risk.32 Revascularization is indicated in symptomatic patients with TIA/stroke, coronary subclavian steal syndrome, ipsilateral haemodialysis access dysfunction, or impaired HRQoL. Revascularization should be considered in asymptomatic patients with planned coronary artery bypass grafting (CABG) using the internal mammary artery and those with ipsilateral haemodialysis access, as well as asymptomatic patients with significant bilateral SS/occlusion for adequate BP surveillance. For revascularization, both endovascular and surgical procedures are available. There are no RCTs comparing endovascular vs. open repair but individual studies, including the Danish Vascular Registry, indicate similar long-term symptom resolution but higher general complication rates and hospital length of stay for open surgery.765 The risk of severe complications, including vertebrobasilar stroke, is low with both approaches. The post-procedural stroke rate is reported at 1.3% for endovascular therapy765 and 0.9%–2.4% after open surgery.765–767 Percutaneous angioplasty for subclavian arterial stenosis is often used with stenting. There is no conclusive evidence to determine whether stenting is more effective than balloon angioplasty.768 Similar results were reported for endovascular therapy of the innominate artery.769 In heavily calcified ostial lesions, balloon-expandable stents give more radial force than nitinol stents. An endovascular approach is often the default strategy. However, in selected patients with low operative risk, with subclavian artery occlusion or after endovascular therapy failure, surgical subclavian–carotid transposition is safe with excellent long-term patency results (5 year patency 96%).766 Carotid–subclavian bypass surgery with a prosthetic graft showed long-term benefit with low operative mortality and morbidity, especially in patients with extensive disease or re-occlusion after stenting (5 year patency 97%).770 Other options are extrathoracic extra-anatomic bypass procedures (axillo-axillary, carotid–axillary, or carotid–carotid bypass);771,772 however, axillo-axillary bypasses may occlude at 1 year in 14% of cases.773 The transthoracic approach is an option in patients with multivessel disease involving the aortic arch and several supra-aortic vessels.767
While critical hand ischaemia owing to below-the-elbow atherosclerotic occlusive disease is relatively uncommon, interventions are associated with a high rate of success, major amputations are rare, and many can be treated non-operatively.756 In appropriately selected patients, both endovascular and open interventions have a high rate of success.755,756 In symptomatic patients with contraindications for endovascular therapy or open surgery, prostanoid infusion or thoracic sympathectomy may be considered.774
8.3.1.3 Follow-up
Patients with UEAD should be followed up to ensure optimal CV prevention. Tighter follow-up is required in symptomatic patients to reassess indication for revascularization as a large proportion of symptoms resolve spontaneously.775 After revascularization, patients should be followed up to allow early detection and treatment of impending late procedural failure.
Recommendation Table 29 — Recommendations for the management of subclavian artery stenosis (see also Evidence Table 9)
Recommendations Classa Levelb
Bilateral arm BP measurement is recommended for all patients with PAAD.32,758 I B In symptomatic patients with atherosclerotic subclavian artery disease (TIA/stroke, coronary subclavian steal syndrome, ipsilateral haemodialysis access dysfunction, severe ischaemia), both revascularization options (endovascular ± stenting or surgery) should be considered and discussed case by case by a vascular team.776 IIa B Endovascular revascularization may be considered over surgery, despite similar long-term outcomes, due to lower complication rates.765 IIb B In patients with atherosclerotic subclavian artery disease, revascularization: Should be considered in cases of proximal stenosis in patients undergoing CABG using the ipsilateral internal mammary artery.777–781 IIa C Should be considered in cases of proximal stenosis in patients who already have the ipsilateral internal mammary artery grafted to coronary arteries with evidence of myocardial ischaemia.777,778,780 IIa C Should be considered in cases of ipsilateral haemodialysis arteriovenous access.778 IIa C Routine revascularization in patients with atherosclerotic subclavian artery disease is not recommended.776 III C © ESC 2024
BP, blood pressure; CABG, coronary artery bypass grafting; PAAD, peripheral arterial and aortic diseases; TIA, transient ischaemic attack. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3597
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.61
8.3.2 Renal artery disease
8.3.2.1. Clinical presentation and diagnosis 8.3.2.1.1. Epidemiology. In >90% of cases, RAS is caused by atherosclerosis and typically involves the ostial renal arterial segment (Table 13).782 Above 65 years of age, overall prevalence of ≥60% RAS is 6.8%, with a higher prevalence in men (9.1%) than in women (5.5%).783 In patients with PAD, RAS prevalence ranges between 7% and 42%, influenced by diagnostic criteria.784
8.3.2.1.2 Clinical presentation. Clinical presentation comprises reno-
vascular hypertension, renal function impairment and eventually, flash pulmonary oedema (Table 13). RAS reduces the filtration capacity of the affected kidney, which activates the renin–angiotensin–aldosterone pathway, potentially resulting in renovascular hypertension.782,785 In unilateral RAS, the functioning contralateral kidney may increase sodium excretion to prevent sodium retention and volume overload. In high-grade bilateral RAS or in unilateral RAS without a functioning second kidney, the risk of cardiorenal deterioration is higher than in unilateral disease.786
8.3.2.1.3 Diagnosis of renal artery disease. First diagnostic steps in-
clude laboratory tests to examine renal function, analysis of office and out-of-office BP recordings (ambulatory BP monitoring or home BP monitoring, as recommended by [upcoming] ESC/European Society of Hypertension [ESH] Guidelines for arterial hypertension), and noninvasive haemodynamic assessment of renal arteries by DUS.787 Renal artery PSV >200 cm/s measured by DUS allows the diagnosis of a >50% RAS (sensitivity 95%, specificity 90%).788 A renal-aortic peak flow velocity ratio (RAR = renal artery PSV/aortic PSV) >3.5 has 84%–91% sensitivity and 95%–97% specificity for the detection of ≥60% RAS.789 A side-to-side difference of the intrarenal resistance index ≥0.5 between both kidneys may serve as an additional haemodynamic criterion for haemodynamically relevant RAS.787,790 Other DUS criteria (acceleration time, acceleration index) have lower diagnostic accuracy.791 Sensitivity and specificity of contrast-enhanced MRA in the diagnosis of RAS is 88% and 100%, respectively;789 however, MRA overestimates the degree of RAS by 26%–32%.789 The advantages of MRA are the possibility of assessing renal parenchymal blood flow and freedom from radiation and iodinated contrast agents. Spiral multidetector CTA allows renal artery diameter measurements and provides information on vessel wall calcification and mural plaques. RAS diagnosis by CTA presents 64%–100% sensitivity and 92%–98% specificity.789 CTA drawbacks include radiation exposure, the need for contrast media in patients with impaired renal function, and limited haemodynamic assessment of RAS. Catheter angiography is the gold standard for diagnosing RAS, enabling additional haemodynamic measures (Figure 19).792 Considering the potential risks of invasive procedures, DUS and other non-invasive modalities (CTA or MRA) should precede catheter angiography and invasive haemodynamic measurements (Figure 19). Renal scintigraphy, plasma renin measurements before and after ACEI provocation, and venous renin measurements are not considered for RAS evaluation.
8.3.2.1.4 Prognosis. Atherosclerotic RAS progresses with respect to
the degree of stenosis, while total renal artery occlusions occur less frequently.793 The presence of significant RAS is a strong predictor for mortality794 and renovascular disease is an important risk factor for the development of end-stage renal disease (ESRD).795 The risk of RASrelated ESRD is higher in men than in women and increases with age.795
8.3.2.2 Treatment strategy (medical and interventional)
8.3.2.2.1. Medical therapy. Optimal medical treatment is recommended in RAS patients.785 Data on antithrombotic therapy in patients with atherosclerotic RAS are scarce and retrospective.796 However, the use of an antiplatelet agent is reasonable in atherosclerotic RAS. No prospective study has specifically examined antithrombotic therapy post-RAS stenting, and information from existing RAS stenting trials is limited.797 Following the antithrombotic treatment approach in non-coronary arterial beds, it is suggested to use DAPT for at least 1 month after RAS stent implantation.666
8.3.2.2.2 Revascularization. Revascularization in atherosclerotic RAS
Prospective RCTs comparing endovascular revascularization with OMT in atherosclerotic RAS favoured renal artery stenting over balloon angioplasty.792 However, renal artery stenting showed no superiority over OMT in reducing BP, CV events, renal events, or mortality in unilateral atherosclerotic RAS.788,798,799 A trial suggested a potential benefit of renal artery angioplasty for BP in bilateral RAS, but subsequent RCTs did not confirm this.800–802 Data on the benefit of renal artery stenting in sparing antihypertensive drugs are inconsistent.324,800,801,803,804 In specific circumstances or RAS aetiologies, revascularization should be considered (Figure 19). Open surgical renal artery revascularization appears comparable to endovascular treatment regarding BP and renal function.805,806 Thus, open surgery can be an alternative approach in cases with a revascularization indication and complex anatomy or failed endovascular repair.
Table 13 Clinical signs suggestive of renal artery disease
Hypertension onset before 30 years of age Severe hypertension after the age of 55 years, when associated with CKD or heart failure Hypertension and abdominal bruit Rapid and persistent worsening of previously controlled hypertension Resistant hypertension • Three antihypertensive drugs including a diuretic agent or • ≥4 antihypertensive drugs
and • Other secondary form unlikely
Hypertensive crisis (i.e. acute renal failure, acute heart failure, hypertensive encephalopathy, or grade 3–4 retinopathy) New azotaemia or worsening of renal function after treatment with RAAS blockers Unexplained atrophic kidney or discrepancy in kidney size, or unexplained renal failure Flash pulmonary oedema © ESC 2024
CKD, chronic kidney disease; RAAS, renin–angiotensin–aldosterone system. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.62
N
N N
N N
N Patient with suspicion of RAS
Duplex ultrasound
Renal artery revascularization
(Class III)
Diagnostic
Kidney viablea
Catheter-based angiography
>70% RAS or haemodynamically relevant 50–70% RASc
Evaluation of high-risk
features after confirmed OMTb Presence of high-risk featuresb
Kidney viablea Kidney viablea
No RAS
RAS exclusion
RAS exclusion
PSV ≥200 cm/s (>50% RAS), RAR >3.5 (≥60%) side-to-side difference of intrarenal resistance index ≥0.5
Morphologically significant RAS
Bilateral high-grade atherosclerotic
RAS (>70%) Non-atherosclerotic RAS and
special populations Unilateral atherosclerotic
RAS (>70%)
Inconclusive DUS or suspicion of haemodynamically
significant RAS
MRA/CTA (Class I)
OMT (Class I) OMT (Class I)
Renal artery revascularization
(Class III)
Renal artery revascularization
(Class IIa) OMT (Class I)
Y
Y
Y
Y Y Y
Figure 19 Diagnostic and treatment algorithm for renal artery stenosis. CTA, computed tomography angiography; MRA, magnetic resonance angiography; OMT, optimal medical treatment; Pd/Pa, distal coronary pressure to aortic pressure ratio; PSV, peak systolic velocity; RAR, renal-aortic peak flow velocity ratio; RAS, renal artery stenosis. asee table below
aKidney viability in RAS
Signs of viability Signs of non-viability
Renal size >8 cm <7 cm Renal cortex Distinct cortex (>0.5 cm) Loss of corticomedullar differentiation Proteinuria Albumin-creatinine ratio <20 mg/mmol Albumin-creatinine ratio >30 mg/mmol Renal resistance index <0.8 >0.8 © ESC 2024 bRapidly progressive, treatment-resistant arterial hypertension; rapidly declining renal function; flash pulmonary oedema; solitary kidney. cResting mean pressure gradient >10 mmHg; systolic hyperaemic pressure gradient >20 mmHg; renal PdPa ≤ 0.9 (or 0.8).
ESC Guidelines 3599
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.63
8.3.2.3 Follow-up
Following the diagnosis of significant RAS and the implementation of OMT and/or renal artery revascularization, regular follow-up exams are crucial. Monitoring should encompass laboratory tests to assess renal function, analysis of office and out-of-office BP recordings (ambulatory or home BP monitoring per upcoming ESC/ESH Guidelines for arterial hypertension), and renal artery DUS. DUS, comprising renal PSV, RAR, side-to-side difference of the resistance index, and kidney size, is the preferred imaging modality during follow-up.787 In conservatively managed RAS patients, follow-up assessment should re-evaluate potential indications for renal artery revascularization (Figure 19). After renal artery stenting, the initial follow-up is recommended at 1 month and subsequently every 12 months or when new signs or symptoms arise.807 Re-intervention may be considered for in-stent restenosis ≥60% detected by DUS, recurrent signs and symptoms (diastolic BP >90 mmHg on >3 antihypertensive drugs, or a >20% increase in serum creatinine).787,808
8.3.3 Visceral artery disease
8.3.3.1. Acute mesenteric ischaemia Acute mesenteric ischaemia can be caused by arterial embolism or thrombosis in situ, non-occlusive mesenteric ischaemia (usually due to superior mesenteric artery [SMA] vasoconstriction), and venous thrombosis. In recent decades, embolism decreased from 46% to 35%, while arterial thrombosis increased from 20% to 35%.815–817 Acute thrombo-embolic occlusion most frequently affects the SMA. Due to extensive collaterals, it infrequently leads to intestinal infarction.
8.3.3.1.1 Clinical presentation and diagnosis. Clinical examination
Early diagnosis of AMI is based on high clinical suspicion. Embolic AMI typically manifests as sudden onset intense abdominal pain, accompanied by minimal physical findings, bowel emptying (vomiting, diarrhoea), and a common embolic source (primarily AF).818–820 Emboli may also lodge in other locations, aiding diagnosis. Acute arterial thrombosis tends to occur in areas with pre-existing atherosclerotic disease, resulting in a less dramatic clinical presentation. Patients may have previous symptoms of chronic mesenteric ischaemia (CMI) or other atherosclerotic manifestations.821 Laboratory tests are unreliable for the diagnosis of AMI, although elevated levels of l-lactate, leucocytosis, and D-dimer (DD) may exist.822–825 Imaging Computed tomography angiography is the gold standard for diagnosis,826,827 allowing the detection of thrombi and/or emboli in the SMA trunk or its branches together with the recognition of intestinal ischaemic signs. A plain abdominal X-ray lacks specificity. A normal result does not rule out the diagnosis.828
8.3.3.1.2 Treatment strategy. Most patients require immediate re-
vascularization to survive. There are no RCTs comparing surgical vs. endovascular intervention in AMI. Two meta-analyses found endovascular revascularization to be superior to surgical intervention in terms of inhospital mortality and rates of bowel resection.829,830 An open surgical approach is most appropriate in centres where endovascular interventions are less available and in patients with peritonitis.831 Retrograde open mesenteric stenting (ROMS) is an alternative that offers shorter operative time; the SMA is punctured in the open abdomen, followed by stenting.832
Recommendation Table 30 — Recommendations for diagnostic strategies for renal artery disease
Recommendations Classa Levelb
DUS is recommended as the first-line imaging modality in patients with suspicion of RAS.787,789–791 I B In cases of DUS-based suspicion of RAS or inconclusive DUS, MRA, or CTA are recommended.789,791 I B In patients with atherosclerotic RAS, it is recommended to assess clinical high-risk features and kidney viability when evaluating renal artery revascularization.809,810 I B © ESC 2024
CTA, computed tomography angiography; DUS, duplex ultrasound; MRA, magnetic resonance angiography; RAS, renal artery stenosis. aClass of recommendation. bLevel of evidence.
Recommendation Table 31 — Recommendations for treatment strategies for renal artery disease (see also Evidence Table 10)
Recommendations Classa Levelb
Medical therapy In patients with atherosclerotic RAS the use of low-dose aspirin may be considered.811 IIb C Revascularization In patients with atherosclerotic unilateral >70% RAS, concomitant high-risk features, and signs of kidney viability, renal artery revascularization should be considered after OMT has been established.798,809,810 IIa B In patients with atherosclerotic bilateral (>70%) RAS or RAS in a solitary kidney, concomitant high risk features, and signs of kidney viability, renal artery revascularization should be considered.800–802 IIa B
Continued In patients with hypertension and/or signs of renal
dysfunction due to RAS caused by fibromuscular dysplasia, concomitant high-risk features, and signs of kidney viability, revascularization with primary balloon angioplasty and bailout stenting should be considered.812,813 IIa B In patients with an indication for renal artery revascularization and complex anatomy, or after failed endovascular revascularization, open surgical revascularization should be considered.805,806 IIa B In patients with atherosclerotic unilateral RAS, routine revascularization is not recommended.324,800–804,814 III A © ESC 2024
RAS, renal artery stenosis. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.64
8.3.3.1.3 Follow-up. Most patients treated for AMI require lifelong
anticoagulant/antiplatelet therapy to prevent recurrence. Patients undergoing revascularization should have surveillance with CTA or DUS within 6 months,833 as recurrent AMI after mesenteric revascularization accounts for 6%–8% of late deaths.834 Current Society for Vascular Surgery (SVS) Guidelines recommend DUS at 1, 6, and 12 months after the intervention, and then annually thereafter.754
8.3.3.2 Chronic mesenteric artery disease
Occlusive CMI is mostly caused by atherosclerosis and more frequently affects females (65%–72%).835,836 Symptoms typically manifest when at least two mesenteric vessels are involved due to extensive collaterals. Prevalence of asymptomatic coeliac artery and/or SMA stenosis is 3% in patients under 65 years of age and 18% in those aged >65.837
However, inadequate anastomoses can result in symptomatic ischaemia even with a single-vessel atherosclerotic occlusion.838,839
8.3.3.2.1 Clinical presentation and diagnosis. Clinical examination
Like AMI, early diagnosis of CMI relies on clinical suspicion. Classic symptoms include post-prandial abdominal pain, weight loss, and gastrointestinal disturbances like diarrhoea or constipation. Patients may develop food aversion to avoid pain, but their appetite remains
Patient with suspected CMI
Exclude other causes
Diagnosis
Functional test Confirmed
Isolated CA or SMA stenosis No stenosis
Chronic NOMI MALS Atherosclerosis
Multidisciplinary meeting for
consensus treatment
Endovascular or surgical revascularization
Secondary prevention
of atherosclerosis Therapy of underlying condition
Multi-vessel stenosis
CTA (Class I)
Figure 20 Algorithm of chronic mesenteric ischaemia management. CA, coeliac artery; CMI, chronic mesenteric ischaemia; CTA, computed tomography angiography; MALS, median arcuate ligament syndrome; NOMI, non-occlusive mesenteric ischaemia; SMA, superior mesenteric artery.
ESC Guidelines 3601
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.65
unaffected, distinguishing them from individuals with malignancies. An abdominal examination might reveal a bruit. Lactate, lactate dehydrogenase, and/or leucocyte count are unhelpful in CMI diagnosis.840,841 Functional testing (tonometry, visible light spectroscopy) is applicable in patients with symptomatic mesenteric stenosis and single-vessel disease.842 Imaging Duplex ultrasound is valuable due to its low costs, absence of the need for contrast agents, and no radiation. However, skilled investigators in specialized centres are required for the examination. Despite suggested diagnostic criteria, consensus is lacking.843,844 Anatomical mapping for treatment planning typically involves CTA or MRA, 845,846 with DSA reserved only for therapeutic purposes (Figure 20).
8.3.3.2.2 Treatment strategy. Optimal medical treatment is the basis
of CMI management. Prophylactic revascularization is not recommended for asymptomatic CMI. In symptomatic cases, a meta-analysis favoured endovascular over open surgery due to fewer complications and a trend towards lower 30 day mortality.835 However, open surgery showed superior long-term results, with fewer symptom recurrences and higher 1 and 5 year primary patency rates in two additional meta-analyses.847,848 Despite the growing use of endovascular therapy, open surgery remains indicated after failed endovascular therapy without the option for repeat intervention, and in cases with extensive occlusions, calcifications, or technical challenges.
8.3.3.2.3 Follow-up. Following CMI revascularization, lifelong medical
treatment, including lifestyle changes and OMT for atherosclerosis, is recommended. SVS guidelines propose mesenteric DUS surveillance for recurrent stenosis. A potential follow-up schedule involves controls within 1 month post-procedure, biannually for the first 2 years, and annually thereafter.849
9 Aorta
9.1 Atheromatous disease of the aorta
9.1.1. General concepts Atheromatous disease of the aorta has an estimated incidence of 40%–51.3%, being complicated in 7.6% of cases.850–853 Earlier stages of atherosclerosis, presenting as plaque inflammation, can be present in 48% of asymptomatic individuals.850 Atherosclerotic plaque classification is based on plaque thickness and the presence of ulceration or mobile components (Table 14).159,171,854 This classification is crucial because severe or complex atherosclerotic plaques in the aortic arch or ascending aorta are strongly linked to cerebrovascular events (odds ratio [OR] 4–9.1 for plaques ≥4 mm).855–860 Additionally, the annual incidence of stroke recurrence remains high (up to 16%) despite antiplatelet or anticoagulant therapy.855,861
9.1.2 Treatment
9.1.2.1. Primary prevention Asymptomatic non-severe/non-complex aortic plaques (Table 14) should not mandate antiplatelet therapy. Nonetheless, in severe/complex plaques, statins should be indicated to decrease plaque progression or CV events,862 and SAPT with clopidogrel or low-dose aspirin should be considered after risk/benefit evaluation.493,666,861,863 However, in this scenario, anticoagulation861 or DAPT (low-dose aspirin and clopidogrel) are not indicated.666,863 Floating aortic thrombi and complex mobile plaques are rare, with limited large-scale trials on their management. Guidance relies on case reports, observational studies, and expert opinions, yet there is evidence favouring anticoagulation, particularly for symptomatic cases.864
9.1.2.2 Secondary prevention
Secondary prevention with antiplatelet therapy after an embolic event is recommended to prevent recurrences.666,865,866 While the value of DAPT vs. SAPT remains uncertain, recent studies indicate that prolonged DAPT raises bleeding risk without added antithrombotic benefits.667,863,867 Treatment duration is unclear and must strike a balance between early benefit (notably within 7 days post-emboli) and steady bleeding risk. Statins (LDL target below 1.4 mmol/L [55 mg/dL]) prove effective in preventing strokes regardless of the aetiology.862,865,868 Additionally, a healthy lifestyle is crucial for improving CV health and reducing complications.
Recommendation Table 32 — Recommendations in patients with visceral artery stenosis
Recommendations Classa Levelb
In patients with acute mesenteric ischaemia due to acute occlusion of the SMA, endovascular revascularization is recommended.829–831 I B In patients with suspected acute or chronic mesenteric ischaemia, CTA is recommended.826,827,845,846 I C In patients with acute or chronic mesenteric ischaemia, assessment by a vascular team is recommended. I C Revascularization of asymptomatic atherosclerotic visceral artery stenosis is not recommended. III C © ESC 2024
CTA, computed tomography angiography; SMA, superior mesenteric artery. aClass of recommendation. bLevel of evidence. Recommendation Table 33 — Recommendations for primary and secondary prevention in aortic atheromatous plaques
Recommendations Classa Levelb
Primary prevention In patients with severe/complex aortic atheromatous plaques, statins should be considered to decrease progression and risk of CV events.862 IIa C SAPT with clopidogrel or low-dose aspirin should be considered in severe/complex plaques.493,666,861,863 IIa C Anticoagulation861 or DAPT863 are not recommended in aortic plaques since they present no benefit and increase bleeding risk.666 III C Secondary prevention after an embolic event related to aortic atherosclerosis In patients with an embolic event and evidence of an aortic arch atheroma, intensive lipid management to an LDL-C target <1.4 mmol/L (<55 mg/dL) is recommended to prevent recurrences.242,862,865,868 I A In patients with an embolic event and evidence of an aortic arch atheroma, SAPT is recommended to prevent recurrences.666,865,866 I C © ESC 2024
CV, cardiovascular; DAPT, dual antiplatelet therapy; LDL-C, low-density lipoprotein cholesterol; SAPT, single antiplatelet therapy. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.66
9.2 Aortic aneurysms
9.2.1. General concepts 9.2.1.1. Definitions Aortic dilatation, the second most frequent aortic disease after atherosclerosis, is defined as an aortic diameter >2 standard deviations of the predicted mean diameter depending on age, sex, and body size (z-score >2). However, in clinical practice, aortic root dilatation can be suspected in male adults when aortic diameter is >40 mm and in females at >36 mm,138,149,869 or with an indexed diameter/BSA (aortic size index [ASI]) >22 mm/m2. In extreme BSA and age values, use of z-scores is recommended (see Section 5.4 for their calculation). Arterial aneurysm is defined as a diameter >1.5 times (>50%) larger than the predicted one. This definition, as well as the use of z-scores, introduces the need for normal values and correction for age, sex, and body size. However, correcting for BSA can lead to underestimation in overweight patients,870 therefore a correction for height (aortic height index [AHI]) is becoming more popular.153 In terms of clinical risk, both ASI and AHI have been shown to improve risk stratification for AAE.153,871 Since in many cases of aortic dilatation the surgical indication is established before achieving this aneurysmal diameter, we strongly recommend the use of significant aortic dilation specifying the diameter or the indexed diameter value rather than the term ‘aneurysm’. Thoracic aortic aneurysms (TAAs) are more prevalent in men than in women (ratio 4:1);872 however, the growth rate is greater in women (0.96 ± 1.00 mm per year) than in men (0.45 ± 0.58 mm per year), and thus the risk of AAE.873 Aneurysms can be fusiform or saccular based on morphology. Saccular aneurysms relate to infection, penetrating atherosclerotic ulcer (PAU), trauma, or inflammatory diseases, while fusiform aneurysms connect with degenerative and connective tissue conditions. Although evidence about their natural course is limited, saccular aneurysms are considered more malignant in terms of AAE. Based on location, aortic aneurysms are classified into TAA and abdominal aortic aneurysm (AAA) (Figure 21). They differ in treating specialists, causes, age at onset, risk factors, and complications. However, this binary classification is artificial due to the prevalence of thoracoabdominal aortic aneurysms (TAAA) and tandem lesions (20%–30% of AAA patients also have TAA),874,875 emphasizing the importance of comprehensive aortic and vascular assessments at diagnosis. When detecting an aortic aneurysm at any site, it is advisable to conduct a thorough evaluation of the entire aorta initially and during subsequent follow-ups. Specifically, when diagnosing a TAA, it is crucial to assess the aortic valve, particularly in cases of BAV. Data on peripheral aneurysms in TAA, particularly in femoro-popliteal segments, is less clear compared with AAA. However, cerebral aneurysms, notably prevalent in women and those with HTAD, warrant thorough screening, particularly in symptomatic cases.876–878
9.2.2 Thoracic aortic aneurysms
9.2.2.1. Aetiology, risk factors, and natural history Thoracic aortic aneurysms occur in 5–10/100 000 person-years,884 with an approximate predominance of root and/or ascending aorta of ∼60%, arch of ∼10%, and descending aorta of ∼30%.885,886 Hypertension is the main risk factor (80%); however, genetics may be involved in 20% of cases.887 The decision to refer patients for genetic evaluation should consider age, family history, and presence of syndromic features,25,888 as reported in more detail in Section 10.1.
9.2.2.2 Ascending thoracic aorta and arch aneurysms
(1) Aortic root aneurysms (including sinuses of Valsalva: annuloaortic ectasia). They can be idiopathic, associated with HTAD (syndromic/non-syndromic), or found in 20%–30% of BAV patients (see Section 10).879,880 Patients are usually younger (30–50 years of age), with aortic regurgitation, and with a 1:1 sex ratio. (2) Supra-coronary aortic aneurysms (above sinuses of Valsalva). Caused by atherosclerosis in relation to hypertension affecting older patients (59–69 years) and males (ratio 3:1),880 or related to medial degeneration (isolated or associated with aortic valve disease, including BAV) (see Section 10). Primary bacterial infection or syphilis are uncommon. Arteritis is rare, but Takayasu’s and giant cell arteritis can lead to aneurysm formation. (3) Aortic arch aneurysms. Often accompanying adjacent ascend-
ing or descending aorta aneurysms, aortic arch aneurysms present surgical challenges due to potential neurological and CV risks. They are typically linked to atherosclerosis, with cystic medial degeneration primarily affecting ascending aorta-related arch aneurysms. Deceleration injuries or coarctation may extend into the aortic arch.889
Recommendation Table 34 — Recommendations for initial evaluation of thoracic aortic aneurysm and abdominal aortic aneurysm
Recommendations Classa Levelb
When an aortic aneurysm is identified at any location, assessment of the entire aorta is recommended at baseline and during follow-up.874,875 I C When a TAA is identified, assessment of the aortic valve (especially for BAV) is recommended.879,880 I C When an AAA is identified, evaluation of the presence of aneurysm in the femoro-popliteal arterial segment should be considered.876–878,881 IIa C Patients with aortic aneurysm are at increased risk of CVD, thus general CV prevention should be considered.26,882,883 IIa C © ESC 2024
AAA, abdominal aortic aneurysm; BAV, bicuspid aortic valve; CV, cardiovascular; CVD, cardiovascular disease; TAA, thoracic aortic aneurysm. aClass of recommendation. bLevel of evidence.
Table 14 Grading of atherosclerotic aortic plaques
Grade Severity (atheroma
thickness) Description
1 Normal Intimal thickness <2 mm
2 Mild Intimal thickening of 2 to <3 mm
3 Moderate Atheroma ≥3 to <4 mm (no
mobile/ulcerated components)
4 Severe Atheroma ≥4 mm (no mobile/
ulcerated components)
5 Complex Grade 2, 3, or 4 atheroma plus
mobile/ulcerated components © ESC 2024
ESC Guidelines 3603
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.67
Thoracic aortic aneurysm patients are usually asymptomatic, diagnosed incidentally during unrelated imaging or screenings. Symptoms such as chest pain, aortic regurgitation, and compression-related issues may occur.890 Patients with aortic root involvement (as seen in HTAD) are more prone to suffer from AAE.891,892 Thoracic aortic aneurysm growth rate is variable, associated with aetiology, location, and baseline aortic diameter.893–895 Degenerative TAAs grow faster in women than men and are associated with a threefold higher risk of AAE.24,873,896 When the aorta reaches 57.5 mm in size, reported yearly rates of rupture, dissection, and death are 3.6%, 3.7%, and 10.8%, respectively.897–899 9.2.2.3 Descending thoracic aorta and thoracoabdominal aorta
aneurysms They can involve different parts of the DTA and may extend to the AA: TAAA. TAAAs are divided into five groups900 according to the modified TAAA classification scheme (Figure 22), which is crucial for risk stratification. By classifying aneurysm extent, surgeons can anticipate procedure complexity, select suitable techniques, and reduce risks during surgical planning. Most DTA aneurysms and TAAA are degenerative with calcification, although other causes include trauma, infection, inflammation, or genetic factors901,902 (Figure 21). Patients with HTAD rarely develop
Media degeneration Inflammation Genetic disorders Infection
Thoracic aortic aneurysm (TAA)
Aetiology
Screening
Diagnostic TTE
TTE or TOE plus CCT or CMR
Root and ascending aorta
Descending aorta
HTAD BAV Sporadic TAA
Atherosclerosis Aortitis (infectious or not) Trauma
Abdominal aortic aneurysm (AAA)
Aetiology
Screening
Diagnostic DUS
DUS or CEUS, CCT or CMR
Atherosclerosis
Coarctation
Atherosclerosis
Figure 21 Thoracic and abdominal aortic aneurysms: aetiology, screening and diagnostic methods. AAA, abdominal aortic aneurysm; BAV, bicuspid aortic valve; CCT, cardiovascular computed tomography; CEUS, contrast-enhanced Doppler ultrasound; CMR, cardiovascular magnetic resonance; DUS, Doppler ultrasound; HTAD, heritable thoracic aortic disease; TAA, thoracic aortic aneurysm; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.68
Suprarenal AAA Pararenal AAA Juxtarenal AAA Infrarenal AAA
Type I Type III Type IV Type V Type II
SMA
IMA Left renal artery
Coeliac trunk
Innominate
artery Left carotid artery
Left subclavian artery
Classification of thoracoabdominal aortic aneurysms
Classification of abdominal aortic aneurysms
Figure 22 Classification of thoracoabdominal900 and abdominal aortic aneurysms. AAA, abdominal aortic aneurysm; IMA, inferior mesenteric artery; SMA, superior mesenteric artery.
ESC Guidelines 3605
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.69
thoracoabdominal aortic aneurysms without dissection. Mean age at diagnosis is 59–69, with a male predominance of 2–4:1. Aneurysm growth rate is 1.9–3.4 mm per year,902,903 but tends to increase notably with diameters over 50 mm or post-proximal aorta surgery in patients with MFS. In this population, debate continues as to whether this reflects a more vulnerable aorta associated to the genetic disease or haemodynamic changes post-surgery. For untreated DTA aneurysm patients, 5 year survival is about 54%, with aortic rupture as the leading cause of death.904 Rupture risk factors include HTAD, a diameter over 50 mm, hypertension, smoking, chronic obstructive pulmonary disease (COPD), symptoms, chronic aortic dissection, and age. A significant rise in AAE risk occurs at a 60 mm diameter. Although dissection can occur in smaller aortas, the individual risk is low.899 High-risk features for rupture are represented in Figure 23.
High-risk features for TAAA rupture beyond aortic diameter
Aortic root and ascending aorta
Thoracoabdominal aorta
Radiological signs of AAA rupture
Retroperitoneal haematoma Contrast extravasation High crescent sign Paraortic fat stranding Tangential calcification Calcification discontinuity Thrombus fissuration Draped aorta sign
Relation with patient’s height Upper normal limits of
aortic diameter by age
Uncontrolled resistant
hypertension Saccular aneurysm
associated to PAU Uncontrolled resistant
hypertension
COPD
Aortic length measurement
Yearly rate of diameter growth Root vs ascending phenotype
Genetic predisposition
Aortic growth rate: Ascending aorta and arch ≥ 3mm/year DTAA ≥ 10mm/year (or ≥ 5mm/6 months) AAA ≥ 10mm/year (or ≥ 5mm/6 months)
Symptoms
Descending thoracic aorta
Figure 23 Risk factors for thoracic and abdominal aneurysm rupture. AAA, abdominal aortic aneurysm; COPD, chronic obstructive pulmonary disease; DTAA, descending thoracic aorta aneurysm; PAU, penetrating atherosclerotic ulcer; TAAA, thoracoabdominal aortic aneurysm.905–908 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.70
9.2.2.4 Surveillance
Patients with TAA who do not meet surgical criteria require chronic follow-up that includes clinical evaluation and imaging techniques. The best imaging modality depends on aneurysm location: TTE, CCT, or CMR when affecting the aortic root and the ascending aorta; CMR and CCT when involving the distal ascending aorta, the aortic arch, or the DTA.159,171 Follow-up should be conducted with the same imaging technique and in the same centre.909 If a TAA is only moderate in size and remains relatively stable over time, CMR rather than CCT is reasonable to minimize radiation exposure.172,910 Follow-up for aortic aneurysms associated with HTAD is described in Section 10.1.3.2. Figure 24 proposes a follow-up algorithm for patients with TAA. In cases of aortic root or proximal ascending aorta dilatation, after initial diagnosis by TTE the basal diameter and extension must be confirmed by CMR or CCT. If there is agreement between techniques, TTE can be used for follow-up; however, if there is a difference of ≥3 mm, surveillance must be performed by CMR or CCT. After the initial diagnosis, imaging is required at 6–12 months, depending on aetiology and baseline diameter (Figure 24); see Sections 5.4.2 and 9.2.1 about indexed values of aortic dimensions, to ensure stability.159,911 Subsequently, imaging can be performed annually if there is no expansion/extension or customized according to the underlying condition. If the aorta shows rapid expansion (≥3 mm per year) or approaches the surgery/endovascular repair threshold, a closer evaluation is recommended every 6 months. In contrast, stability in aortic diameters over years could lengthen these intervals (especially in non-genetic aneurysms and those <45 mm). In cases of dilatation of aortic arch or DTA, diameters obtained by TTE are deemed less precise and need confirmation by CMR or CCT. In those types of aneurysms, follow-up frequency will depend on the baseline diameter and aetiology and will follow the same criteria established in the algorithm in Figure 24 for the 40–49 mm range. However, for the 50–55 mm range, the aorta should be re-imaged every 6 months until the threshold for intervention is reached (see Sections 9.2.5.3 and 9.2.5.4). 9.2.3 Abdominal aortic aneurysms
9.2.3.1. General concepts An AAA is defined as a focal dilation at least 1.5 times its normal diameter, generally ≥30 mm. Most AAAs are fusiform, and many are lined with laminated thrombi.916 Their prevalence increases with age, with a 4:1 male/female ratio.872 They are commonly classified based on their relation to renal arteries (Figure 22) because of the complexity of surgical treatment. AAA extends to the common iliac arteries in 25% of cases and in up to 20% of patients is associated with peripheral femoral and/or popliteal artery aneurysm.876–878
9.2.3.2 Aetiology, risk factors, and natural history
Smoking, age, male sex, and familial history of aneurysmal disease are major risk factors,917–921 whereas diabetes is associated with a decreased risk922,923 and slower growth rate924 (Figure 21, see also Section 5). Other aetiologies include inflammation (5%–10% of all AAA),925 genetic disorders, and infection. The mean growth rate is around 3 mm per year (1–6 mm)906,926 and depends on sac diameter, presence of genetic disorders, continuous smoking, metabolism (presence of inflammation), and aortic wall calcification.927–929 Risk of rupture rises exponentially depending on diameter, being higher in women.930,931 AAAs are asymptomatic in two-thirds of cases and if they become symptomatic, rupture is the main manifestation. They often represent incidental imaging findings, as the sensitivity of clinical examination— especially palpation of an abdominal mass—is generally poor. Symptoms may include acute abdominal or back pain, and in some cases, hypovolaemic shock. However, contained rupture may present with atypical low flank or abdominal pain (see Figure 23 for high-risk factors and radiological signs or AAA rupture).932–935 Independently of risk of rupture, patients with AAA have impaired survival: the 5 year mortality rate is higher (×4 in women, ×2 in men) despite AAA repair, likely due to the presence of cardiovascular disease in other areas.936
9.2.3.3 Surveillance
Those with an aortic diameter <25 mm present low risk of developing large AAA in 10 years, whereas a diameter of 25–29 mm deserves reassessment after 4 years.937,938 DUS is the standard imaging technique for surveillance; however, CCT provides superior visualization of the AA and its branches, especially for pre-operative planning. CMR is reasonable in selected patients (young and female) when a long follow-up is considered, to avoid radiation.
Recommendation Table 35 — Recommendation for the surveillance of patients with thoracic aortic aneurysms (non-heritable thoracic aortic disease)
Recommendations Classa Levelb
In thoracic aortic dilatation, TTE is recommended at diagnosis to assess aortic valve anatomy and function, aortic root, and ascending aorta diameters. Additionally, a global aortic evaluation using all echocardiographic views is recommended.159 I C CMR or CCT is recommended for surveillance of patients with aneurysm at the distal ascending aorta, aortic arch, DTA, or TAAA.70,159,172,912–915 I C In thoracic aortic dilatation, CCT or CMR is recommended to confirm TTE measurements, rule out aortic asymmetry, and determine baseline diameters for follow-up.137,143,144 I C
Continued Follow-up imaging with TTE, CCT, or CMR (based
on aneurysm location) should be considered annually if there is no expansion/extension or customized according to baseline aortic diameter and the underlying condition.70,159,172 IIa C TTE is not recommended for the surveillance of aneurysms in the distal ascending aorta, aortic arch, or DTA.159,171 III C © ESC 2024
CCT, Cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; DTA, descending thoracic aorta; TAAA, thoracoabdominal aortic aneurysm; TTE, transthoracic echocardiography. See proposed algorithm in Figure 24. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3607
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.71
Surveillance of AAA
N
Y
Root or ascending dilatation with TAV or BAV (and normal valve function)
at first or susbsequent echocardiography
40–44 mma 45–49 mm 50–52 mm
Ascending Ascending
53–54 mm ≥55 mm
<3 mm/y ≥3 mm/y
<3 mm/y ≥3 mm/y
Surgery if low operative risk
(Class IIb)
Otherwise Surgery if low operative risk
(Class IIa)
Otherwise
Confirm by CCT or CMR
Confirm by CCT or CMR
Baseline CCT/CMR
and reimage by TTE in one year
Reimage by CCT/ CMR 6 months later to define projected growth rate
Reimage by TTE yearly (or every 6 months if growth rate ≥3 mm/y)
Reimage by TTE
every 2 or 3 years Reimage every 6 months
Confirm by CCT or CMR Confirm by CCT or CMR
Aortic diameter
Phenotype
High-risk featuresb Root
TAV
BAV
Growth rate
Growth rate Phenotype
TAV/BAV
Every 4 years
Every 4 years
Consider follow-up Follow-up
Every 3 years
Every 3 years Every 12
months
Every 12 months
Every 6 months Consider intervention
(Class I)
Every 6 months
Surgery (Class I) Surgery (Class I)
AAA size
(mm) Women
Men 25 30 35 40 45 50 55 Consider intervention
(Class I)
Figure 24 Surveillance of patients with non-heritable thoracic aortic disease and abdominal aortic aneurysms. AAA, abdominal aortic aneurysm, BAV, bicuspid aortic valve; CCT, cardiovascular computed tomography; HTAD, heritable thoracic aortic disease; CMR, cardiovascular magnetic resonance; TAV, tricuspid aortic valve; TTE, transthoracic echocardiography. a36–44 mm in women. bFor TAV and BAV: age <50 years; height <1.69 m; ascending length >11 cm; uncontrolled hypertension; and, for BAV: coarctation; family history of acute aortic events. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.72
A meta-analysis advises follow-up intervals for AAAs based on size: 3 years for 30–39 mm, 1 year for 40–44 mm, and 6 months for 45– 54 mm in men, with <1% rupture risk.938 Women have similar growth rates but a four-fold higher rupture risk.938 A proposed follow-up algorithm is displayed in Figure 24. Consider shorter intervals for rapid growth (≥10 mm per year or ≥5 mm per 6 months), in which case repair may be considered.
9.2.4 Optimal medical treatment of aortic aneurysms
In patients with aortic aneurysms, the role of antithrombotic therapy is uncertain. In complicated aortic atherosclerotic plaques, concomitant CAD is common (OR 2.99) and SAPT should be considered (see Section 9.1). In patients with AAA, results of observational studies are conflicting in relation to aneurysm growth. Low-dose aspirin is not associated with a higher risk of AAA rupture but could worsen prognosis in cases of rupture.944 In an RCT of patients with AAA (35–44 mm), ticagrelor did not reduce growth rate.945 Optimal medical treatment for aortic aneurysms aims to lower CV morbidity, slow growth rate, delay surgery, reduce peri-operative risk, and prevent AAE. Aneurysm patients face elevated CV risk due to common CVRFs, and the 10 year CV event mortality risk (heart attacks or strokes) is 15 times higher than AAE risk, even after repair.882,883 According to the SMART risk score algorithm, optimal implementation of risk management guidelines would reduce the 10 year risk of MACE from 43% to 14% in patients with AAA.936 Thus, lifestyle modification, exercise, smoking cessation, and treatment of risk factors are crucial (see Section 7). Risk factors and possible drug treatment to reduce AAA growth and/ or the risk of rupture have been thoroughly discussed in a recent review paper.946 Their meta-analysis suggested a possible effect of ACEIs (but not ARBs) on the risk of rupture, whereas another meta-analysis947 did not indicate an effect of ACEIs on AAA growth. A reduction of AAA growth by statins is indicated in a recent meta-analysis.352 Furthermore, reduced AAA growth by the antidiabetic drug metformin has been suggested in several meta-analyses352,948,949 and there are several ongoing RCTs to explore this. For BP, follow general hypertension guidelines. Aim for BP below 140/90 mmHg, with a target of 120/80 mmHg, if tolerated.300,302,305 Data on the specific positive effects of beta-blockers and ARBs in TAA and AAA are limited (mostly derived from MFS populations). However, it is reasonable to use BBs and/or ARBs as first-line antihypertensive drugs in TAA and AAA.
Consider moderate/high-intensity statins in TAA patients but skip for those with low CV risk and non-atherosclerotic (HTAD). In AAA, consider statins to reduce aneurysm risks, including growth, rupture, and peri-operative mortality.330,347,348 Low-dose aspirin is debated but may be reasonable given elevated CV risk factors in TAA and AAA patients.666,950 Additionally, apply all CVD secondary prevention measures to these patients (see Section 7). Some evidence suggests that fluoroquinolones could be associated with an increased risk for aneurysm progression and dissection,951–956 but conflicting analyses do not support this association. The cautious use of fluoroquinolones should not be discouraged when there is a clinical indication, even considering concerns regarding aortic aneurysm and dissection (AA/AD). Note that AA/AD risk (both thoracic and abdominal) may increase due to infection itself, regardless of the antibiotic chosen. Infectious disease specialists discourage routine fluoroquinolone use as a first-line antibiotic if equally effective alternatives exist. Hence, do not withhold this therapy in aortic disease cases when clinically necessary. All medical and lifestyle recommendations are summarized in Figure 7.
9.2.5 Surgical management of aortic aneurysms
9.2.5.1. Surgical treatment of aortic root and ascending aorta In isolated dilatation of the ascending tubular (supra-coronary) aorta, a supra-commissural tubular graft is inserted with the distal anastomosis just before the aortic arch. For aneurysms extending proximally below the sinotubular junction (STJ) with involvement of aortic sinuses, the surgical approach depends on the aortic annulus and valve condition. If the aortic valve cusps are pliable, experienced centres may recommend aortic valve-sparing techniques,961–965 such as David’s procedure (reimplantation) or the Yacoub technique (remodelling).890,966–968
Recommendation Table 36 — Recommendations for surveillance of patients with abdominal aortic aneurysm
Recommendations Classa Levelb
DUS surveillance is recommended every 6 months in men with AAA of 50–55 mm and in women with AAA of 45–50 mm.938 I B CCT or CMR is recommended if DUS does not allow adequate measurement of AAA diameter.148,939–942 I B DUS is recommended for AAA surveillance.943 I C DUS surveillance every 3 years should be considered in patients with AAA of 30–<40 mm.938 IIa B DUS surveillance should be considered annually in women with AAA of 40–<45 mm and in men with AAA of 40–<50 mm.938 IIa B DUS surveillance should be considered every 4 years in patients with aortic diameter ≥25 mm and <30 mm and life expectancy >2 years.937,938 IIa C © ESC 2024
AAA, abdominal aortic aneurysm; CCT, Cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; DUS, duplex ultrasound. aClass of recommendation. bLevel of evidence. Recommendation Table 37 — Recommendations for medical treatment in patients with thoracic aorta or abdominal aortic aneurysms
Recommendations Classa Levelb
In patients with aortic aneurysm (TAA and/or AAA), optimal implementation of CV risk management and medical treatment (see detailed recommendations in dedicated Tables of Recommendationsc) are recommended to reduce MACE.936 I C Fluoroquinolones, while generally discouraged for patients with aortic aneurysms, may be considered if there is a compelling clinical indication and no other reasonable alternative.951–960 IIb B © ESC 2024
AAA, abdominal aortic aneurysm; CV, cardiovascular; MACE, major adverse cardiovascular events; TAA, thoracic aortic aneurysm. aClass of recommendation. bLevel of evidence. csee Tables of Recommendations 7 to 10.
ESC Guidelines 3609
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.73
Otherwise, composite replacement of the aortic root and valve with the Bentall procedure is indicated. Pre-operative evaluation890 and initial follow-up of patients is defined in Figure 25. Patients with a bioprosthetic valve should be monitored by TTE annually. However, in patients with mechanical prosthesis or native aortic valve, clinical evaluation and TTE should be performed as soon as possible if new heart symptoms develop.969 SAPT with low- dose aspirin (75–100 mg per day) should be considered for the first 3 months after conservative aortic valve surgery if there are no indications for OAC. Lifelong OAC with a VKA is recommended for all patients with a Bentall mechanical prosthesis.970,971 However, in patients with no baseline indications for OAC, low-dose aspirin (75– 100 mg/day) or OAC using a VKA should be considered for the first 3 months after Bentall surgery with a bioprosthesis.972,973
TTE and TOE Aortic valve assessment
CCT or CMR Annulus/root/ ascending aorta
assessment Supracommisural
tubular graft Aortic valve
sparing Annuloplasty Bentall procedure
Pre-surgery STJ dilatation
(Ia) STJ and aortic root
dilatation (Ib) Annulus dilatation
(Ic) Aortic valve
disease
TTE Immediate cardiac complications
(i.e. pericardial effusion...)
CCT or CMR Rule out aortic complications Before discharge
1 month
From 1 year TTE Aortic valve function and gradients
Aortic root and proximal ascending aorta assessment
TTE Aortic valve function and gradients
Aortic root and proximal ascending aorta assessment
Mechanical prosthesis
or native valve:
Bioprosthesis:
TTE/year CCT or CMR Evaluation of aortic disease
progression and rule out complications
Aorta totally repaired: Follow-up at 2 years and then every 5 years
link with aneurysm follow-up algorithm TTE based on gradients, symptoms or residual AR
Aorta not fully
repaired:
Figure 25 Peri-operative algorithm for the management of patients with surgically treated aortic root and ascending aortic aneurysm. AR, aortic regurgitation; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; STJ, sinotubular junction; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.74
Although many risk factors associated with AAE have been described (such as elongation, angulation, and unfavourable biomechanics), aortic diameter is still the main determinant of aortic complications and death.974–976 AAE rates decreased with prophylactic aortic surgery over a decade,977 and additionally, surgical risk for ascending aortic/aortic root surgery dropped significantly.978–980 Now, experienced cardiac surgery centres report <1% mortality with elective surgery.980,981 Most acute type A aortic dissections (acute TAAD) occur at diameters below 55 mm. However, the risk exceeds 1% between 50 and 54 mm,982 with a critical point at 52–53 mm.153,981,983 Pre-dissection aortic diameter at the tubular level is 25%–30% smaller than post-dissection. Over 60% of non-MFS, non-BAV acute TAAD patients have a nondilated ascending aorta before dissection.984,985 Additionally, the ‘root phenotype’ has been reported to be more malignant than those with ascending phenotype, with higher velocity of progression and AAE risk.154,891,892,986 Novel parameters, like ascending aortic length (AAL) and the ascending-arch angle, correlate with acute TAAD risk.155,976 AAL ≥13 cm links to nearly five-fold higher yearly AAE rates compared with AAL <9 cm, with a threshold of >11 cm as a risk indicator.155 Indexing aortic diameters to anthropometric parameters has been suggested and a proportional increase in the risk of AAE has been retrospectively demonstrated for increasing diameter indexed to BSA,904 diameter indexed to patient height,153 or cross-sectional area indexed to patient height.154 However, these diameter-based indexing methods share the same limitations in risk prediction as the absolute diameter in the general population,984,985 whereas they can be advantageous in patients with small body size.153,154 These additional risk factors (beyond the diameter) are summarized in Figure 23.
9.2.5.2 Surgical treatment of aortic arch aneurysms
Surgery for arch aneurysms is challenging, primarily due to risks like hypothermic circulatory arrest and the need for brain protection, resulting in higher mortality and stroke rates. Isolated aortic arch surgery is appropriate for asymptomatic degenerative aortic arch aneurysms ≥55 mm in diameter or symptoms or signs of local compression. Hemi-arch or total arch replacement are frequently required in patients who have an indication for surgery on an adjacent aneurysm of the ascending aorta. In specific cases, supra-aortic vessel transposition via offpump debranching followed by TEVAR of the arch can be an alternative to traditional surgery, particularly when avoiding hypothermic circulatory arrest is a concern.992–996 When the disease involves the proximal descending aorta or future need for treatment of the descending aorta is anticipated, the frozen elephant trunk (FET) technique is a good option.997 Assessment of patency and morphology of the circle of Willis is recommended when treatment involves the aortic arch.998,999
Recommendation Table 38 — Recommendations for surgery in aortic root and ascending aorta dilatation associated with tricuspid aortic valve (see also Evidence Table 11)
Recommendations Classa Levelb
Surgery is recommended in patients with dilatation of the aortic root or ascending aorta with a tricuspid aortic valve and a maximum diameter of ≥55 mm.172,894,899,904 I B Valve-sparing aortic root replacement is recommended in patients with aortic root dilatation if performed in experienced centres and durable results are expected.961–965 I B VKAs are recommended lifelong for all patients with a Bentall procedure with an MHV prosthesis.970,971 I B In patients with dilatation of the tubular ascending aorta who can be offered surgery with low predicted risk,c ascending aortic replacement should be considered at a maximum diameter >52 mm.153,981,983 IIa B In patients undergoing surgery for tricuspid aortic valve disease who have concomitant dilatation of the aortic root or ascending tubular aorta, and low predicted surgical risk, ascending aorta or root replacement should be considered at a maximum diameter ≥45 mm, otherwise ≥50 mm.70,987–989 IIa B
Continued SAPT with low-dose aspirin (75–100 mg per day)
should be considered for the first 3 months after valve-sparing aortic surgery when there are no other baseline indications for OAC. IIa C In patients undergoing non-aortic-valve cardiac surgery who have concomitant dilatation of the ascending aorta or aortic root with a maximum diameter ≥50 mm, concomitant aortic surgery should be considered.70,990,991 IIa C Ascending aortic or root replacement may be considered at a maximum diameter of ≥50 mm in patients with proximal aorta dilatation who can be offered surgery with low predicted riskc and present with any of the following:153–155,891,892 • Growth of the aortic diameter ≥3 mm per year • Resistant hypertensiond • Short stature <1.69 m • Root phenotype • Aortic lengthe >11 cm • Age <50 years • Desire for pregnancy • Aortic coarctation IIb B © ESC 2024
MHV, mechanical heart valve; OAC, oral anticoagulation; SAPT, single antiplatelet therapy; VKA, vitamin K antagonist. For heritable thoracic aortic disease and bicuspid aortic valve-related thoracic aortic aneurysm refer to Section 10. aClass of recommendation. bLevel of evidence. cIndividual patient’s risk <3%. dHypertension that cannot be adequately controlled despite use of three or more agents recommended by a physician with expertise in the management of hypertension. eCurvilinear distance at aortic centreline between the ventriculo-aortic junction and the origin of the innominate artery.
Recommendation Table 39 — Recommendations for surgery in aortic arch aneurysms
Recommendations Classa Levelb
In patients with low or intermediate operative risk with an aortic arch aneurysm and recurrent episodes of chest pain not attributable to non-aortic causes, open surgical replacement of the arch is recommended.70,172 I C
Continued
ESC Guidelines 3611
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.75
9.2.5.3 Surgical treatment of the thoracic descending aorta
9.2.5.3.1. General considerations. At 60 mm diameter, a DTA aneurysm has a 10% annual rupture risk, justifying intervention at ≥55 mm.902,1002 Intervention at a diameter <55 mm may not bring any further survival benefit except for women,904,1003 patients with connective tissue disorders,904 or rapid growth (≥10 mm per year or ≥5 mm every 6 months),1004 (for high-risk factors see Figure 23). This threshold may be increased in high surgical risk patients.1005 It is advisable to centralize complex procedures in centres with expertise in aortic diseases and a multidisciplinary team for effective patient management.
9.2.5.3.2 Open repair. Thoracic endovascular aortic aneurysm
repair is recommended as first-choice intervention for DTA aneurysms,1006–1010 thus open repair is limited to patients with unsuitable anatomy for TEVAR1011 or connective tissue disorders.1012 The early mortality benefit of TEVAR seems to decrease after 1 year, and thereafter long-term survival (10 years) seems better with open repair.1013 Therefore, open repair is advisable for young, healthy patients with unsuitable TEVAR anatomy and prolonged life expectancy, particularly when symptoms from aneurysm rupture or compression arise. However, open repair involves significant post-operative risks, necessitating thorough pre-operative evaluations for cardiac, pulmonary, renal function, carotid, and peripheral arterial diseases. Risks include stroke, mesenteric and renal ischaemia due to clamping duration,1014,1015 and paraplegia tied to the extent of aneurysmal disease.1016,1017 Outside experienced centres, outcomes have shown minimal improvement in recent years, with mortality rates around 10% and spinal cord ischaemia rates at 11%–15%.1016,1018
9.2.5.3.3 Endovascular repair. Comparative studies favour TEVAR
over open repair, showing lower mortality (6%) and morbidity.1006,1019,1020 However, TEVAR’s survival advantage is balanced by an increased risk of follow-up re-intervention. It reduces spinal cord injury risk (3%).1021–1024 Left subclavian artery (LSA) coverage during TEVAR for proximal sealing is required in up to 50% of cases.1025 This is associated with an increased risk of cerebrovascular events, spinal cord ischaemia (SCI), and upper-limb ischaemia,1026,1027 justifying previous surgical or concomitant endovascular (with branched or fenestrated grafts) revascularization of the LSA in an elective setting.1026,1028,1029 In cases of inadequate distal zone sealing, safe coverage of the coeliac artery has been proposed when sufficient collateral circulation exists,1030,1031 but results are controversial.1032
9.2.5.4 Surgical treatment of thoracoabdominal aorta aneurysms
9.2.5.4.1. General considerations. Since AAEs increase when TAAA diameter exceeds 60 mm,902,1002,1033 and there are more technical surgical challenges in TAAA repair (compared with DTA aneurysm or AAA), TAAA repair, in low-moderate surgical risk patients, is proposed if the aortic diameter is ≥60 mm. However, surgical repair should be considered at diameters ≥55 mm if patients present with high-risk features (Figure 24) or are at very low risk and under the care of experienced surgeons in a multidisciplinary aorta team.1004,1033,1034 HTAD, distal location, chronic dissection, and BAV903 are associated with rapid growth rate and will require closer follow-up.
9.2.5.4.2 Open repair. Open TAAA repair is a complex aortic pro-
cedure. Post-operative mortality risk increases with left ventricular (LV) dysfunction, renal insufficiency, and advanced age.1035–1037 Since organs and tissues distal to the aortic clamp will suffer from prolonged ischaemia, extracorporeal circulation is mandatory to reduce complications,1011,1038 especially SCI (2.5%–15%).1011,1039–1044 The mortality rate after open TAAA repair varies between 6% and 8% in high-volume centres1006,1011,1039 vs. 30% in less experienced centres,1045,1046 raising the recommendation to perform these complex procedures only in specialized institutions.
9.2.5.4.3 Endovascular repair. Endovascular repair is a promising al-
ternative for treating challenging aortic anatomy like juxta-renal AAA (Figure 22).1047,1048 The use of fenestrated and branched endografts has shown excellent results, allowing perfusion of visceral vessels.1049–1053 While direct comparison studies with open TAAA repair are lacking,1054 the increasing adoption of endovascular procedures is notable, especially for high-risk patients, with low post-operative mortality rates (<10%).1051,1052,1055–1058 A recent meta-analysis confirms these excellent outcomes, endorsing endovascular repair for TAAA.1059 The incidence of post-operative SCI (around 5%) is similar between endovascular and open repair.1052,1057,1060,1061 Thus, at mid-term follow-up, endovascular repair is durable with acceptable secondary re-intervention rates, which remain one of the major limitations.1052,1057,1058,1060,1061 Factors favouring endovascular vs. open repair in TAAA are presented in Table 15.
In patients with an isolated aortic arch aneurysm who are asymptomatic and have low operative risk, open surgical replacement should be considered at an arch diameter of ≥55 mm.70,172,899 IIa B In patients undergoing open surgical repair of an ascending aortic aneurysm, concomitant hemi-arch replacement should be considered if the dilatation extends into the proximal aortic arch (>50 mm).70,172,1000 IIa C In patients undergoing open surgical repair of an aortic arch aneurysm, an elephant trunk or frozen elephant trunk procedure should be considered if the aneurysmal disease extends into the proximal descending thoracic aorta.70,172,997,1001 IIa C In patients undergoing open surgical repair of an ascending aortic aneurysm, concomitant hemi-arch or arch replacement may be considered in experienced centres if the dilatation extends into the aortic arch (>45 mm).70,172,1001 IIb C In patients with an aortic arch aneurysm who meet criteria for intervention but have high surgical risk, a hybrid or endovascular approach may be considered.70,172 IIb C © ESC 2024
For heritable thoracic aortic disease refer to Section 10. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.76
9.2.5.5 Surgical treatment of abdominal aorta aneurysms
9.2.5.5.1. General considerations. Rupture remains the most feared AAA complication, and is associated with the maximum diameter,1063 as well as other risk factors (Figure 23). Different studies1064–1071 (including the United Kingdom Small Aneurysm Trial [UKSAT] and American Aneurysm Detection and Management [ADAM] trial) reported no benefits from open or endovascular interventions (despite lower peri-operative complication rates) in asymptomatic AAA patients with a maximal diameter <55 mm in men and <50 mm in women. Evidence that women are more likely to rupture under surveillance and at a smaller aortic diameter justified a lower (50 mm) threshold. Another interesting method to quantify the risk of rupture based on body size, which seems a better predictor in women, has been proposed.1072 However, in the absence of recent studies, thresholds for intervention have not changed in recent years. Considering the complexity of patient management, it is advisable to centralize complex procedures in centres with a high level of expertise in aortic diseases and a multidisciplinary team.
9.2.5.5.2 Pre-operative cardiovascular evaluation and choice of
treatment. Coronary artery disease is the leading cause of early mortality after AAA repair,937,1073 and is associated with a 5%–10% rate of peri-operative CV complications such as death, MI, or stroke.1074,1075 Since endovascular repair is associated with lower mortality (<1%) and CV complications,1076–1079 the need for pre-operative cardiac
Recommendation Table 40 — Recommendations for the management of patients presenting with descending thoracic aortic and thoracoabdominal aortic aneurysms
Recommendations Classa Levelb
In patients with unruptured DTA aneurysm (without HTAD), elective repair is recommended if diameter ≥55 mm.902,1002 I B In patients without HTAD with unruptured DTA aneurysm, when elective repair is indicated and anatomy is suitable, TEVAR is recommended over open repair.1006,1019,1020 I B In patients with DTA aneurysm who undergo TEVAR with planned LSA coverage, it is recommended to revascularize the LSA before TEVAR to reduce the risk of SCI and stroke.1026,1028,1029 I B In patients with unruptured degenerative TAAA, elective repair is recommended when the diameter is ≥60 mm.902,1002,1033 I B In patients without significant comorbidities and with unruptured DTA aneurysm, when elective repair is indicated and anatomy is unsuitable for TEVAR, open repair should be considered if life expectancy exceeds 2 years.1013 IIa B In TAAA, surgical repair should be considered at diameters ≥55 mm if patients present with high-risk features, are at very low risk, and are under the care of experienced surgeons in a multidisciplinary aorta team.1004,1033,1034 IIa B In patients with unruptured degenerative TAAA and suitable anatomy, when elective repair is indicated, endovascular repair using fenestrated and/or branched endografts should be considered in experienced centres.1051,1052,1055–1059 IIa B
Continued In patients with unruptured DTA aneurysm (without
HTAD) and high-risk features,c elective repair may be considered if the diameter is <55 mm.904,1003,1004,1033,1034 IIb B © ESC 2024
DTA, descending thoracic aorta; HTAD, heritable thoracic aortic disease; LSA, left subclavian artery; SCI, spinal cord ischaemia; TAAA, thoracoabdominal aortic aneurysm; TEVAR, thoracic endovascular aortic aneurysm repair. For heritable thoracic aortic disease refer to Section 10. aClass of recommendation. bLevel of evidence. cSee Figure 23 for high-risk features.
Table 15 Overview of factors favouring open vs. endovascular repair in thoracoabdominal aortic aneurysm
Characteristic Favours open repair Favours endovascular repair
Biological age and life expectancy • Younger age • Considerable life expectancy with acceptable
quality of life • Older age • Limited life expectancy
Anatomical considerations • If aortic and branch anatomy preclude endovascular
approach • Poor vascular access • Suitable proximal and distal landing zones
• Favourable visceral and renal configuration • Vascular access obtainable
Pathological • Chronic dissection • Acute dissection Background/causal factor • Hereditary aortic disease • Degenerative aortic disease Cardiopulmonary condition • Good cardiopulmonary reserve • Poor cardiopulmonary reserve Fitness • No significant comorbidities
• Successful rehabilitation likely • Severe organ impairment (renal, kidney, pulmonary)
• Obesity • Limited mobility, unlikely to rehabilitate successfully
Urgency • Elective repair • Emergency repair without a viable endovascular
solution • Elective repair • Emergency repair with time for custom-made graft or suitable for
standard grafts © ESC 2024
Adapted from Ouzounian et al. with permission.1062
ESC Guidelines 3613
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.77
Patients with abdominal aortic aneurysm
Aortic aneurysm Graft Aortic aneurysm
Stent graft
Surveillance (See aneurysm follow-up algorithm) N
N
Low/medium High Prohibitive
Either of the following:
Life expectancy 2 years
Operative mortality risk
Elective repair Anatomy appropriate for EVAR
Open repair
(Class I)
If suitable anatomy, EVAR (Class IIa) Optimal medical
treatment
Elective repair
(Class III)
EVAR (Class IIa)
Fusiform AAA ≥55 mm (men), ≥50 mm (women) Saccular aneurysm 45 mm N
Y
Y
Y
A B
Figure 26 Algorithm for individual decision-making process in the treatment of patients with abdominal aortic aneurysm. (A) Illustration of open repair (graft). (B) Illustration of endovascular treatment (EVAR). AAA, abdominal aortic aneurysm; EVAR, endovascular aortic aneurysm repair. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.78
work-up will depend on procedure risk, symptoms, and patient-specific CVRFs (see Sections 4 and 12, and the 2022 ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery).1080 Coronary revascularization before elective aortic surgery in patients with stable cardiac symptoms cannot be recommended, since there is evidence that this strategy does not improve outcomes or reduce the 30 day MI rate.1080,1081 A complete vascular evaluation (that includes not only the AA but also the entire aorta: ascending, arch, and descending aorta) is mandatory to determine the best strategy in AAA management, CCT being, by consensus, the optimal pre-operative imaging modality.1082,1083 When CCT is contraindicated, consider CMR, though calcification assessment is challenging. Pre-operative planning should determine EVAR feasibility by sizing the aorto-iliac system, yet adherence to device-specific instructions remains uncertain.1084–1090 DUS assessment of the femoro-popliteal segment is advocated since femoropopliteal aneurysms are commonly associated with AAA.1091,1092 Additionally, the technique of choice should be discussed between the treating physician and the patient based on the patient’s life expectancy and preferences, operator and hospital volumes, and surveillance compliance.910,1093–1097 Elective AAA repair is not recommended in frail patients or those with life expectancy <2 years.1098,1099 The individual decision-making process in AAA patients is displayed in Figure 26. Different studies have demonstrated a significant short-term survival benefit for EVAR, but with similar long-term outcomes compared with open repair (up to 15 years)1100–1103 also reported in females.1104 However, loss of early benefit is associated with an increased rate of late complications occurring after 8 years, especially late ruptures.1079 These trials used earlier-generation EVAR devices, so the durability of the latest-generation devices remains uncertain. Recent data, however, suggest a reduced risk of late complications and fewer reinterventions.1105–1108
9.2.5.5.3 Open abdominal aorta aneurysm repair. Open AAA re-
pair through mid-line laparotomy (with <30 min clamping time) with a Dacron graft has been the preferred choice for years, despite notable CV morbidity1078,1100,1109–1113 and a 2%–5% mortality rate.1110,1111,1113,1114 In ruptured AAA, open repair results are worse than those of elective surgery, with an unchanged complication rate of around 48%.1115 Thus, endovascular repair is recommended to reduce peri-operative morbidity and mortality.1116–1118 Open AAA repair raises incisional hernia risk, particularly in obese patients, suggesting prophylactic mesh use in high-risk cases.1119–1121
9.2.5.5.4. Endovascular abdominal aorta aneurysm repair. Endovascular abdominal aorta aneurysm repair reduces peri-operative mortality to <1%, although it implies higher risk of re-intervention in the long term.1122–1124 Current devices offer features like active fixation, repositioning ability, low-profile design, and polymer-filled rings for improved sealing.1106,1125–1128 New devices demonstrate similar long-term outcomes with reduced re-intervention risk,1090 expanding treatment possibilities to 60%–70% of infrarenal AAA cases.1129,1130 In cases of juxta- or para-renal AAA (Figure 22), both open and endovascular treatment can be proposed in high-volume centres, with similar short- and long-term results. The choice between open surgical repair and endovascular repair depends on various factors, including the patient’s anatomy, overall health, and the extent of the aneurysm (see Table 15). In cases of complex endovascular treatment, a fenestrated or branch stent endograft should be considered.1096,1131 A percutaneous femoral approach is suitable since it provides quicker access, reduced invasiveness, and allows local anaesthesia. Some evidence supports the use of ultrasound-guided percutaneous access for EVAR due to a lower rate of access-related complications and a shorter operation time.1132–1135
As patients treated by EVAR are more prone to late complications (endoleaks, migration, or rupture) and re-interventions, lifelong surveillance is currently mandatory.1096,1136–1140
9.2.6 Endoleaks
Endoleaks are defined as the persistence of blood flow outside the graft but inside the aneurysm sac, preventing complete thrombosis (Figure 27). They are the most common complication, with an incidence up to one-third of either early or late procedures (those appearing after 1 year).1145 Chronic anticoagulation constitutes a risk factor for re-intervention, late conversion surgery, or mortality.1146 Endoleaks exposing the aneurysm sac to systemic pressure and expansion will require re-intervention to prevent rupture. Five types of endoleaks have been described, as detailed in Figure 27. Type I and type III require correction with a new (endovascular) procedure. Type II is present in about 25% of patients but may seal
Recommendation Table 41 — Recommendations for the management of patients presenting with abdominal aortic aneurysm
Recommendations Classa Levelb
Elective repair is recommended if AAA diameter is ≥55 mm in men or ≥50 mm in women.1064–1067 I A In ruptured AAA with suitable anatomy, endovascular repair is recommended over open repair to reduce peri-operative morbidity and mortality.1116–1118 I B Prior to AAA repair, DUS assessment of the femoro-popliteal segment, to detect concomitant aneurysms, should be considered.1091,1092 IIa B In patients with AAA with suitable anatomy and reasonable life expectancy (>2 years), EVAR should be considered as the preferred therapy, based on shared decision-making.910,1096,1141–1143 IIa B In patients with unruptured AAA and aneurysm growth ≥5 mm in 6 months or ≥10 mm per year, repair may be considered.1064,1065 IIb C Elective repair for patients presenting with a saccular aneurysm ≥45 mm may be considered.1144 IIb C In patients with AAA and limited life expectancy (<2 years), elective AAA repair is not recommended.1098,1099 III B Prior to AAA repair, routine evaluation with coronary angiography and systematic revascularization in patients with chronic coronary syndromes is not recommended.1080,1081 III C © ESC 2024
AAA, abdominal aortic aneurysm; DUS, duplex ultrasound; EVAR, endovascular aortic aneurysm repair; TAA, thoracic aortic aneurysm. See also Figure 23. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3615
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.79
Y
N Classification of endoleak types
Type Ia Type Ib Type II Type III Type IV Type V
Surveillance after TEVAR/EVAR and management of endoleaks
CCT and DUS/CEUSa at 1 month and 1 year post-op
No new endoleak Type I or type III endoleak
Consider re-intervention
(Class I)
Type II endoleak
Detected at 1 month post-op
CCT re-evaluation at 6–12 months
Annual surveillance with CCT or DUS/CEUSa for the first 5 years <10 mm or shrinking Consider open surgery, if growing aneurysm sac
CCT or DUS/CEUSa surveillance every 6 months
for 24 months
New endoleak or growing aneurysm sac
CCT, or non-contrast CCT with DUS/CEUS every 5 yearsa Growing aneurysm sac Consider embolization,
if feasible (Class IIa)
CCT
Proceed to endoleak type CCT or DUS/CEUSa
surveillance at 6–12 months
New endoleak ≥10 mm
Y
N
Figure 27 Algorithm for follow-up after thoracic endovascular aortic aneurysm repair, and management of endoleaks and their classification. CEUS, contrast-enhanced ultrasound; CCT, cardiovascular computed tomography; DUS, duplex ultrasound; TEVAR, thoracic endovascular aortic aneurysm repair; EVAR: Endovascular aortic repair. aIn cases of TEVAR, CCT is the preferred imaging technique since DUS/CEUS does not permit the correct evaluation of the thoracic aorta. In cases of renal failure, non-contrast CCT is a good alternative to monitor aneurysm sac growing and is associated to DUS/CEUS for EVAR monitoring. Endoleaks are classified into five types: Type Ia, proximal attachment site endoleak; Type Ib, distal attachment site endoleak; Type II, backfilling of the aneurysm sac through branch vessels of the aorta; Type III, graft defect or component misalignment; Type IV, leakage through the graft wall attributable to endograft porosity; and Type V; caused by ‘endotension’, possibly resulting from aortic pressure transmitted through the graft/thrombus to the aneurysm sac. Adapted from Rokosh et al. with permission.1147 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.80
spontaneously in approximately 50% of cases. Risk factors for type II endoleaks include patent collaterals, presence of accessory arteries, and anticoagulation. In cases of significant sac expansion (≥10 mm), re-intervention should be considered, preferably by vessel or sac embolization. Type IV, attributed to device porosity, is rare with modern devices and no intervention is needed. Type V induces sac expansion without any visible endoleak. Treatment may be considered for significant sac growth (≥10 mm) and consists of stent graft relining or definitive endograft explant and open surgical repair. Cardiovascular computed tomography with(out) contrast, and DUS and/or CEUS, are the main imaging modalities for TEVAR/EVAR followup. Imaging within the first 30 days is recommended to assess treatment success and/or complications. For TEVAR, contrast-enhanced CCT is the preferred imaging technique for follow-up and should be performed regularly (shorter or longer intervals are based on the expansion rate). In renally impaired patients, combined follow-up using DUS and non-contrast enhanced CCT is a suitable alternative (see follow-up algorithm, Figure 27). For EVAR, CCT and DUS/CEUS are recommended at 1 month following repair. Thereafter, surveillance should be based on the risk of late complications and includes DUS and/or CEUS (Figure 27).
9.2.7 Long-term follow-up after aortic repair
Long-term success in the management of aortic aneurysms depends also on strict post-treatment surveillance, for both secondary prevention of the aortic disease and early identification of post-repair complications. In endovascularly treated patients, surveillance aims to detect endoleaks, aneurysmal sac dilatation, and graft structural failure or migration.1150 Surgical treatments, while carrying higher operative risks, often yield more durable results with rarer late complications mostly related to laparotomy.1151 After intervention on the thoracic aorta, TTE, TOE, CCT, and CMR are used for follow-up, CCT being the most used and available method for both endovascular and surgical treatments.1150–1152 After intervention on the AA, CCT, CMR, and DUS/CEUS are used. DUS/CEUS can detect the most common drawbacks of EVAR, except for graft structural issues. For chronic and periodic monitoring, the use of CMR, especially in young women, should be considered (to reduce radiation exposure). However, the choice between these modalities should consider patient factors, potential artefacts, and local imaging expertise and availability. Both for the thoracic and abdominal aorta, due to the lack of studies systematically comparing different surveillance time intervals, recommendations are mostly based on consensus or evidence from single-centre observational studies.70,1153
9.2.7.1 Follow-up after thoracic aortic aneurysm treatment
Complications after ascending aorta graft replacement, though rare, include pseudo-aneurysms and graft infections. Pseudo-aneurysms, occurring in roughly 5% of cases, are most common within the first 2 post-operative years, linked to aortic dissection surgery, HTAD, and synthetic glues.1154 CMR studies systematically following perianastomotic haematomas have reported higher rates (15%).1155 Graft infections can occur in 0.5%–6% of surgical patients with high morbidity and mortality rates, requiring rapid diagnosis. Treatment typically involves surgery and antibiotics, tailored to factors like overall health, infection severity, and underlying conditions.1156 Residual aortic disease progression depends on the underlying condition, such as HTAD, and requires individualized surveillance. After TEVAR for DTA aneurysm, late complications are higher than with surgery (up to 38%), leading to re-operation in 24% of cases.1150 However, over 80% of TEVAR complications arise within the initial post-operative years.1157 Notably, FET results in fewer stent graft-related complications: 2% stent-induced intimal tear, 3% endoleak, and 7% need for additional TEVAR.1158 After surgical treatment of TAAs, the protocol is a first CCT scan at discharge or 1 month, then another in the first post-operative year (at 6, 9, or 12 months), followed by a 2 year scan, and if no issues arise, scans every 5 years thereafter (Figure 25).1062,1159 Stricter lifelong surveillance is recommended after TEVAR: after first imaging at 1 month, yearly controls are recommended for at least the first 5 post-operative years, then less frequently if no complications are detected (Figure 27). Cardiovascular risk profile modification, cardiac rehabilitation, and lifestyle adjustments are an integral part of post-aneurysm repair follow-up (Figure 7).24
9.2.7.2 Follow-up after abdominal aortic aneurysm treatment
Evidence for follow-up after AAA is more robust than after TAA repair.70,1096 Post-surgery, anastomotic or para-anastomotic complications are rare (2%–4%).1160 In contrast, EVAR has higher complication rates (16%–30%), necessitating lifelong surveillance.1079,1150 EVAR’s survival advantage over surgery diminishes after 8 years, with higher aneurysm-related mortality risk for EVAR.1079 However, most failures are detectable early, and complications seldom occur later in patients with normal early controls.1161,1162 CCT effectively detects early EVAR abnormalities,1163 but DUS/CEUS surveillance proves accurate, reducing the need for radiation and nephrotoxic agents, and lowering costs (Figure 27).1164–1167 Interestingly, a meta-analysis found low compliance of patients to post-operative surveillance without differences in all-cause mortality, aneurysm-related mortality, and re-intervention between compliant and non-compliant patients.1168 Altogether, the above-mentioned evidence supports stratified methods of surveillance,1096 with
Recommendation Table 42 — Recommendations for the management of patients presenting with endoleaks
Recommendations Classa Levelb
It is recommended to perform 30 day imaging after TEVAR/EVAR, by CCT and DUS/CEUS, to assess the success of intervention.1096 I B It is recommended to re-intervene to achieve a seal in patients with type I endoleak after TEVAR/ EVAR.1137,1148 I B It is recommended to re-intervene, principally by endovascular means, to achieve a seal in patients with type III endoleak after TEVAR/EVAR.1139 I B Re-intervention, principally with an endovascular approach or embolization, should be considered in patients with type II or V endoleak and significant sac expansion ≥10 mm or significantly decreasing proximal or distal seal.1096,1149 IIa C © ESC 2024
CCT, cardiovascular computed tomography; CEUS, contrast-enhanced ultrasound; DUS, Duplex ultrasound; TEVAR/EVAR, thoracic endovascular aortic aneurysm repair. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3617
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.81
identification of high-risk situations (e.g. older patients, inadequate sealing, type II endoleaks, no early post-procedural shrinkage of the aneurysmal sac) for which more frequent evaluation should be planned.1161,1169,1170
Follow-up of OMT is highly important in AAA patients (Figure 7).24 Statin use after AAA repair (surgical or EVAR) is associated with decreased short- and long-term mortality.1171 In addition, surveillance for aneurysm development in other arterial locations is recommended.
9.3 Acute thoracic aortic syndromes
9.3.1. General concepts Acute aortic syndromes are life-threatening emergencies, including classic AAD, IMH, PAU, aortic pseudo-aneurysm, and traumatic aortic injuries (TAI). They involve aortic wall damage and share a dynamic, overlapping pathophysiology, clinical presentation, and diagnostic and therapeutic approaches.24,172,174,910 AAS may also be iatrogenic following open or endovascular/percutaneous procedures, or cardiac surgery.1172 To guide AAS management, several anatomical classifications have been developed, the Stanford and the DeBakey systems being the most widely used. The Stanford system classifies AAS according to whether the ascending aorta is involved (type A or DeBakey type I and type II) or not (type B or DeBakey type IIIa and type IIIb) regardless of the site of origin of the intimal tear.172,174,910,1173 This classification considers not only anatomical and treatment aspects, but also prognostic implications, since patients with DeBakey type II AAS will probably be left without structural aortic wall lesions after surgery (Figure 28). Furthermore, if time elapsed from symptom onset to diagnosis is considered, AAS can be divided into hyperacute (<24 h), acute (1–14 days), subacute (15–90 days), and chronic (>90 days) (Figure 28).1174–1176 A new classification considers the intimal tear’s entry site and dissection extension (Figure 29).136 Subscript P describes the proximal involved aorta, and subscript D indicates the distal zone. This classification guides treatment decisions for sealing the entry tear. AADs limited to the aortic arch or originating as retrograde dissections from the descending aorta that extend into the arch and stop before the ascending aorta are termed as non-A non-B AD.1177–1179 Recently, a European update of the Stanford classification—Type Entry Malperfusion (TEM) classification—has been proposed.1180 This combines information about the type of dissection, its extent, and the presence of complications (malperfusion), thus providing greater prognostic insights (Figure 29). This classification is recommended by the European Association for Cardio-Thoracic Surgery. The TEM and other classifications are described in the Supplementary data online, Section 1.6.
9.3.1.1 Epidemiology and risk factors
Classic AAD (comprising 80%–90% of AAS; incidence of 2.6–3.5 cases per 100 000 person-years)24,1181 is characterized by the presence of an intimal flap separating the true from the false lumen (FL).24,172,910
Recommendation Table 43 — Recommendations for follow-up after treatment of aortic aneurysms (see also Evidence Table 12)
Recommendations Classa Levelb
Thoracic aortic aneurysm After open repair of TAA, an early CCT is recommended within 1 month, and then yearly CCT follow-up for the first 2 post-operative years and every 5 years thereafter is recommended if findings are stable.c,70,1153,1159 I B After TEVAR, follow-up imaging is recommended at 1 and 12 months post-operatively, then yearly until the fifth post-operative year if no abnormalitiesd are documented.70,1153,1158 I B After 5 post-operative years without complications, continuing long-term follow-up of TEVAR by CCT every 5 years should be considered.70,1153,1158 IIa B If growth of the excluded aneurysm is observed, without evidence of type I or III endoleak, repeating CCT every 6–12 months, depending on the growth rate observed, should be considered.1150 IIa C When frequent controls are required in TAA patients treated either by open or endovascular repair, CMR should be considered instead of CCT after the first year of follow-up. However, the choice between these imaging modalities should be based on individual patient factors, the potential for artefacts, and the local availability and expertise in specific imaging techniques.1155 IIa C Abdominal aortic aneurysm After open repair of AAA, first follow-up imaging is recommended within 1 post-operative year, and every 5 years thereafter if findings are stable.1079,1096 I A After EVAR, follow-up imaging is recommended with CCT (or CMR) and DUS/CEUS at 1 month and 12 months post-operatively, then, if no abnormalitiesd are documented, DUS/CEUS is recommended every year, repeating CCT or CMR (based on potential artefacts) every 5 years.70,1079,1100,1163–1165,1167 I A In higher-risk patients, i.e. with inadequate sealing or type II endoleak at first CCT control, more frequent DUS/CEUS imaging should be considered.e,1096,1161,1164,1165,1167 IIa B In low-riskf patients, from 1 year post-operatively after EVAR, repeating DUS/CEUS every 2 years should be considered.1096 IIa B
Continued If any abnormality during DUS/CEUS is found,
confirmation should be considered using additional CCT or CMR (based on potential artefacts).1163,1166 IIa B In post-treatment surveillance, administration of OMT (see 8.1.2.2 and 8.2.4) and assessment of aneurysm development/growth in other arterial segments should be considered. IIa C © ESC 2024
AAA, abdominal aortic aneurysm; CCT, cardiovascular computed tomography; CEUS, contrast-enhanced ultrasound; CMR, cardiovascular magnetic resonance; DUS, Duplex ultrasound; EVAR, endovascular aortic repair; OMT, optimal medical treatment; TAA, thoracic aortic aneurysm; TEVAR, thoracic endovascular aortic repair. aClass of recommendation. bLevel of evidence. cBoth at the level of the treated segment and in the residual native aorta. dIncluding: endoleak (any type), enlargement of the excluded aneurysm, and stent graft migration/separation/fracture. ee.g. imaging every 6 months during the first year, thereafter every 2–3 years. fLow-risk: early sac shrinkage >10 mm, relatively younger age (<70 years), proximal and distal sealing >10 mm, no endoleak. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.82
Acute aortic dissection occurs mostly in males (∼65%) and in the seventh decade of life (∼63 years).1175,1182 Multiple risk factors often coexist directly linked to factors like wall stress (with systemic hypertension being the most common) and/or aortic media abnormalities, including syndromic and non-syndromic genetic diseases. HTAD, BAV, prior aortic surgery, and larger aortic dimensions are more frequent among young patients (<40 years).24,1182,1183 Systemic hypertension and cocaine abuse are more common among African-American
Classification of timing
Frequency of acute aortic syndrome
Classification of acute aortic syndromes
DeBakey I
Stanford A Stanford B
DeBakey II DeBakey IIIa DeBakey IIIb
60% 10–15% 25–30%
Hyperacute
AAS
Time Acute
AAS Subacute
AAS Chronic
AAS
AAS onset 24 hours
post-AAS 14 days
post-AAS 90 days
post-AAS
Figure 28 Anatomical and temporal classification of acute aortic syndrome. AAS, acute aortic syndrome.
ESC Guidelines 3619
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.83
than among white patients.1184,1185 Of note, the incidence of iatrogenic AD during cardiac catheterization is very low (around 0.01%–0.02%) and during cardiac surgery is 0.06%–0.23%, with favourable in-hospital and long-term prognosis.1186,1187 9.3.1.1.1 Sex differences. A specific female sex phenotype appears to
be evident in acute TAAD. At admission, acute TAAD female patients are usually older but have lower body mass index (BMI), BSA, and creatinine plasma levels. They present less frequently with active smoking,
Proximal
extent
Distal extent Type
AD Entry tear:
Zone 0 0 1 2 3 4 5 6 7 8 9 10 11 12 0 1 2 3 4 5 6 7 8 9 10 11 12
BPD Entry tear: ≥Zone 1
ID Unidentified entry
tear involving
Zone 0
Type
Entry 0 1 2 3 4
5 6 7 8
9 10
11 11
10
A B Non-A non-B
M0 - no malperfusion M1 - coronary M2 - supra-aortic M3 - spinal, visceral, iliac (-) no clinical symptoms (+) clinical symptoms
E0 E1
E E E
E2 E3 E
E0 E3 E E
E0 E3 E2
Malperfusion
T
E
M TEM aortic dissection classification
Figure 29 Aortic dissection classification system based on the 2020 Society for Vascular Surgery/Society of Thoracic Surgeons Reporting Standards and the European update of the Stanford classification—Type Entry Malperfusion classification. A, type A aortic dissection; B, type B aortic dissection; non-A, non-B, aortic dissection limited to the aortic arch or retrograde dissection extending into the arch (but not in the ascending aorta). Upper panel: Classification of AAD considering the intimal tear’s entry site and dissection extension. Subscript P describes the proximal involved aorta, and subscript D indicates the distal zone. Lower panel: The TEM classification is the European update of the Stanford classification combining information about the Type of dissection (T), the Entry site (E), and the presence of Malperfusion (M). Also refer to Supplementary data online, Section 1.6. Society for Vascular Surgery/Society of Thoracic Surgeons (SVS/STS). Reproduced with permission from.136,1180 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.84
BAV, and previous cardiac surgery,1188 but diabetes mellitus is more common in women than in men. In-hospital surgical mortality does not differ between sexes, although 10 year survival appears to be higher in men. Among only medically treated acute TAAD patients, prohibitive high in-hospital mortality has been equally registered for both sexes (men 58.6% vs. women 53.8%).1188 However, further studies are needed to explore AAD sex differences to design appropriate diagnostic and therapeutic interventions and preventive strategies.1189 Pregnancy increases the risk of AAS, more often in the last trimester (50%) or post-partum (33%).1190 9.3.1.1.2 Chronobiology. Acute aortic dissection presents chrono-
biological patterns, with a higher incidence in morning hours (peak between 8 am and 9 am) and winter (peak in January in the Northern Hemisphere).24,1175
9.3.1.1.3 Outcomes. For acute TAAD, in-hospital mortality has de-
creased from 31% to 22% due to better surgical outcomes; for acute type B aortic dissection (acute TBAD), in-hospital mortality has remained stable over the years (14%).1175,1182 Including deaths before admission, 30 day mortality for AAD ranges from 23% to 55.8% in Western Europe.1181
D-dimer and
chest X-Ray D-dimer Chest X-Ray POCUS
High risk: ADD-RS ≥2
AAS confirmed AAS excluded
+ + + –
Low risk: ADD-RS <2
Clinical suspicion of AAS: determine ADD-RSa
ECG: exclude STEMI (2023 ESC ACS Guidelines)
Chest X-Ray and laboratory test and POCUS (if available)
Consider alternative diagnosis
CCT neck-pelvis without delay
and/or focused TTEa + ECG
CCT
Aortic dissection detection-risk score (ADD-RS)a
High-risk examination feature High-risk pain feature High-risk condition
If one present = 1 ADD-RS point If present = 1 ADD-RS point If one present = 1 ADD-RS point
Marfan syndrome Family history of aortic disease Known aortic valve disease Recent aortic manipulation Known aortic aneurysm Haemodynamic instability (hypotension/shock) Perfusion deficit (pulse deficit, differential systolic blood pressure) Focal neurological deficit New AR murmur
Chest, back, or abdominal pain described as abrupt onset, severe intensity, or ripping/tearing
+ –
Figure 30 Multiparametric diagnostic work-up of acute aortic syndrome. AAS, acute aortic syndrome; ADD-RS, aortic dissection detection-risk score; CCT, cardiovascular computed tomography; ECG, electrocardiogram; POCUS, point-of-care ultrasound; STEMI, ST elevation myocardial infarction; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography; +, findings compatible with AAS. aIn haemodynamically unstable patients: consider TTE and/or TOE as first-line imaging technique depending on local expertise and availability.
ESC Guidelines 3621
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.85
Non-A, non-B dissection patients tend to be younger (median age 59 years) and have a lower mortality than acute TAAD patients.1180,1191 The 30 day mortality in patients medically treated is around 14%,1179 and 4.4% for those successfully treated surgically.1177
9.3.1.2 Clinical presentation
Acute TAAD typically presents with sudden, severe chest/back pain, often described as ‘sharp’, alongside a history of arterial hypertension. However, around 6.4% of patients do not experience pain.1182,1192,1193 Hypotension and shock are frequent. Unique clinical features specific to acute TAAD include pericardial effusion, aortic regurgitation, and coronary artery involvement leading to ACS (particularly the right coronary artery).1194 Stroke may occur when supra-aortic branches are involved. Additional complications encompass paraplegia (resulting from spinal ischaemia), acute kidney injury, intestinal ischaemia, or limb ischaemia. Isolated abdominal aortic dissection occurs in about 1.3% of acute TBAD cases when the intimal flap originates below or at the renal arteries.1195 A complete clinical evaluation is mandatory, consisting of a central neurological evaluation, heart and lung auscultation (aortic diastolic murmur, pericardial rubbing, etc.), abdominal palpation (tenderness, etc.), and assessment of peripheral pulsations as well as mobility and sensibility in upper and lower limbs. SBP differences (pulse deficit) should be sought.
9.3.1.3 Diagnostic work-up
Early diagnosis is still a major pitfall in managing AAD patients, therefore, a diagnostic multiparametric algorithm is proposed (Figure 30). It combines the aortic dissection detection-risk score (ADD-RS) with D-dimer (DD) and has been validated with an excellent capacity to rule out AAS.1196–1200 In patients presenting with chest pain, a routine chest radiography and ECG are recommended to exclude other aetiologies; however, the absence of these findings should not delay further investigations.163 Laboratory tests should be obtained, but awaiting results should not delay imaging if there is a high probability of AAD. The most common finding is an increase in DD level, which is the case in several other conditions such as pulmonary embolism or infections. When DD levels are below 500 ng/mL, AAD is unlikely.172,1201 A focused TTE at the emergency department, if available, is recommended1202,1203 to assess pericardial effusion, wall motion abnormalities, aortic regurgitation, and aortic diameters. Sometimes a dissection flap can be visualized, especially when using contrast.165 When AAD is suspected, ECG-gated CCT from neck to pelvis is the preferred imaging technique, with 100% sensitivity and 98% specificity, and should be performed as soon as possible to confirm diagnosis, localize entry tear, extension (type A vs. type B), and malperfusion.170,172,1182,1204 When ACS or pulmonary embolism are still in the differential diagnosis, a triple rule-out ECG-gated CCT scan protocol can be performed be performed to avoid motion artefacts mimicking acute TAAD.170,1205,1206 However, this strategy is associated with higher contrast and radiation doses, might be less accurate for AAS, and does not reduce the need for additional imaging tests.170,1207 If CCT is not available or in haemodynamically unstable patients, TOE can confirm diagnosis. TOE is especially useful pre-, intra, and postoperatively to monitor changes in the anatomical AAD configuration or surgical complications. CMR could be a valuable alternative for CCT, however, it is less available, requires a longer examination time, relies on patient collaboration, and consequently, is less frequently used in the acute setting. CCT, CMR, and TOE all provide good diagnostic accuracy172,1204 (See Supplementary data online, Table S4). 9.3.1.4 Therapeutic intervention in acute aortic dissection
9.3.1.4.1. Initial treatment. Acute aortic syndrome care should be centralized in experienced centres and managed by aorta teams.1211 The cornerstone in AAS is initial reduction of the pulse pressure by lowering SBP below 120 mmHg and heart rhythm ≤60 beats per minute (b.p.m.). The aim is to decrease aortic wall stress to avoid further extension of dissection with possible rupture or malperfusion.174,1212–1216 Intravenous beta blockade (labetalol as a first choice due to its alphaand beta-blocking properties) is generally accepted as the best option. Also, esmolol, an ultra-short-acting beta-blocker, can be titrated quickly and easily, making it particularly useful in the acute setting. If contraindicated, i.v. non-dihydropyridine CCBs could be used for heart rate control. If the BP target is not reached after initiating beta-blockers, i.v. vasodilators such as nitrates or dihydropyridine CCBs (e.g. nicardipine) can be administered concomitantly with rate-controlling agents first to avoid reflex tachycardia. In cases of malperfusion, higher BP could be tolerated to optimize perfusion to the threatened region. Early placement of an arterial line to monitor BP invasively is mandatory and admission to an intensive care unit is advisable (including ECG and urine output monitoring).1205,1217,1218 Antihypertensive treatment can be gradually switched to oral therapy once BP and heart rate targets are reached and the patient has normal gastrointestinal transit. Adequate pain control is necessary to help reach these haemodynamic goals. Intravenous morphine can be cautiously titrated to induce pain relief (Figure 31). In-hospital mortality, reaching 60%, correlates with AAS type, location, patient comorbidities, and treatment. Risk rises with complications like pericardial tamponade, coronary involvement, or malperfusion. Figure 32 describes the main signs and symptoms of complications and the mortality rate associated with them.1219–1223
Recommendation Table 44 — Recommendations for diagnostic work-up of acute aortic syndromes
Recommendations Classa Levelb
In unstable patients who cannot be transferred to CCT, TOE is recommended for diagnosis1204,1208,1209 and evaluation of the coeliac trunk and mesenteric artery.1210 I B In patients presenting with clinical features compatible with possible AAS, a multiparametric algorithm for ruling in or out AAS using the ADD-RS is recommended.1196–1200 I B ECG-gated CCT from neck to pelvis is recommended as the first-line imaging technique in patients with a suspected AAS since it is widely available, accurate, and provides information about the entry tear, extension, and possible complications (malperfusion, dilatation, or rupture).170 I C In patients with suspected AAS, focused TTE (with use of contrast if feasible) is recommended during the initial evaluation.170 I C In patients with suspected AAS, TOE is recommended to guide peri-operative management and detect complications.170 I C In patients with suspected AAS, CMR should be considered as an alternative imaging technique if CCT is not available.170 IIa C © ESC 2024
AAS, acute aortic syndrome; ADD-RS, aortic dissection detection-risk score; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; ECG, electrocardiogram; TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography. See also Figure 30. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.86
Interventional treatment in acute TAAD and acute TBAD is described in the next sections and summarized in Figure 33.
9.3.1.4.2. Type A aortic dissection interventional treatment. Immediate surgical repair is recommended for acute TAAD, however, a high mortality rate (∼50% and 1%–2% per hour) within the first 48 h is described if managed medically only.1232 Despite advances in surgical and anaesthetic techniques, there is still a high risk of perioperative mortality (17%–25%) and neurological complications (18%).1233 In recent reports from the International Registry of Acute Aortic Dissection (IRAD), medically managed patients had a 23.7% mortality rate (0.5% per hour) compared with 4.4% (0.09% per hour) for those undergoing surgery.1234 Analyses of pre- and post-July 2007 IRAD data showed no difference in 48 h mortality for medically treated patients, but surgical mortality decreased (from 5.5% to 3.9%).1234 As surgical techniques have improved, data have shown improved post-operative survival rates.1235 The use of the GERAADA (German Registry of Acute Aortic Dissection Type A) score1236 should be considered in patients undergoing surgery to determine 30 day mortality (https://www.dgthg.de/de/GERAADA_ Score). Surgical intervention surpasses conservative therapy in long-term follow-up,1237 even for challenging cases. Thus, all acute TAAD patients should receive surgical treatment; however, cardiogenic shock secondary to pericardial tamponade, malperfusion of coronary arteries, mesenteric circulation, lower extremities, kidneys, or brain, and/ or coma are major predictors for post-operative mortality (Figure 32).1234,1238 Among octogenarians, in-hospital mortality was lower after surgery than with conservative treatment (37.9% vs. 55.2%), but with a non-significant difference due to small sample size.1239 While some have reported excellent surgical and quality of life (QoL) outcomes in elderly patients,1239 others found
(Class I)
(Class I) (Class I)
+
1
2 3
Intravenous labetalol or esmolol (if contraindication to beta-blockade, substitute with diltiazem or verapamil)
Titrate to heart rate ≤60 b.p.m.
Intravenous opiates Titrate to pain control Intravenous vasodilator (nitroprusside or angiotensin-converting enzyme inhibitor)
(Goal is lowest possible BP that maintains
adequate organ perfusion)
Continue to step 3
if systolic BP ≥ 120mmHg
Titrate to BP <120 mmHg
Rate/pressure control
Pain control Pressure control
Figure 31 Medical management of acute aortic syndrome. BP, blood pressure; b.p.m: beats per minute.
Recommendation Table 45 — Recommendation for medical treatment in acute aortic syndromes
Recommendations Classa Levelb
In patients with AAS, immediate anti-impulse treatment targeting SBP <120 mmHg and heart rate ≤60 b.p.m. is recommended. In cases of spinal ischaemia or concomitant brain injury, maintaining higher MAP is recommended.1214–1216 I B Intravenous BBs (e.g. labetalol or esmolol) are recommended as first-line agents. If necessary, i.v. vasodilators (e.g. dihydropyridine calcium blockers or nitrates) could be added.174,1224 I B Invasive monitoring with an arterial line and continuous three-lead ECG recording, as well as admission to an intensive care unit, is recommended.1205,1217,1218,1225 I B In patients with AAS who can be managed conservatively and who achieved haemodynamic targets with i.v. anti-impulse therapy, switching to oral BBs and, if necessary, up-titration of other BP-lowering agents, is recommended after 24 h if gastrointestinal transit is preserved.174,1216 I B Adequate pain control to achieve haemodynamic targets is recommended.174 I C If the patient has a contraindication for BBs, a non-dihydropyridine calcium blocker should be considered.174,1224 IIa B © ESC 2024
AAS, acute aortic syndrome; BB, beta-blocker; BP, blood pressure; b.p.m., beats per minute; ECG, electrocardiogram; i.v., intravenous; MAP, mean arterial pressure; SBP, systolic blood pressure. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3623
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.87
a higher rate of post-operative neurological complications.1240 Based on the current evidence, age per se should not be considered an exclusion criterion for surgery. For optimal repair of acute TAAD regarding long-term outcomes, including risk of late death and late re-operation, the following points need to be addressed. First, in most cases of aortic regurgitation associated with acute TAAD, the aortic valve is essentially normal and can be preserved.1241–1243 Alternatively, valve replacement can be performed in cases of pre-existent structural valve disease. The decision whether to replace the aortic root is based on the presence of tears in the sinuses, extensive dissection of sinuses/coronary ostia, or significant dilatation of the root. The risk of late dilatation of the aortic sinuses when spared should be considered.1242,1244 Additionally, the distal extent of aortic repair is a topic of debate. Ascending aortic replacement or hemi-arch replacement alone is technically easier and effectively closes the entry site but leaves a large part of the diseased aorta untreated. In acute TAAD with visceral or renal malperfusion, the primary entry tear is often in the descending aorta. Consider extended therapies like FET repair for these patients, offering a complete repair with a low chance of late re-intervention despite increased technical complexity.1245–1247 For potential cardiac arrest from pericardial tamponade, consider an emergency pericardial puncture as a temporary life-saving measure before transferring to the operating room.1248,1249 The frozen elephant trunk technique The FET technique addresses complex aortic and aortic arch issues in a single operation,1260–1263 creating a secure landing zone for future interventions. Recent advances involve ‘proximalization’— placing the FET in the aortic arch’s zone 0 or 1, treating proximal arch aortic issues, and enhancing the landing zone for downstream procedures—which surpasses the standard elephant trunk technique.1264,1265
Malperfusion in type A aortic dissection In acute TAAD with malperfusion, operative mortality correlates with the number of affected organs. Around 30% of patients develop malperfusion syndrome due to elevated pressure in the FL caused by substantial proximal inflow and insufficient distal outflow, leading to visceral organ and limb ischaemia.1175 The intimal flap may extend into peripheral arteries, causing a static ‘stenosis-like’ blockage. Malperfusion typically combines dynamic and static obstructions, necessitating surgical and hybrid interventions for affected patients (Figure 34). Mesenteric malperfusion, a life-threatening complication with a mortality rate of 65%–95%, leads to diverse treatment approaches. Some centres prefer early direct reperfusion before aortic surgery,
Recommendation Table 46 — Recommendations for intervention in type A acute aortic dissection
Recommendations Classa Levelb
In patients with acute TAAD, emergency surgical consultation and evaluation and immediate surgical intervention is recommended.1182,1250 I B In patients with acute TAAD who have extensive destruction of the aortic root, a root aneurysm, or a known genetic aortic disorder, aortic root replacement is recommended with a mechanical or biological valved conduit.1251–1255 I B In patients presenting with acute TAAD, transfer from a low- to a high-volume aortic centre with the presence of a multidisciplinary team should be considered to improve survival if transfer can be accomplished without significant delay in surgery.1256,1257 IIa B In selected patients, a valve-sparing root repair may be considered, when performed by experienced surgeons.1251,1258,1259 IIb B © ESC 2024
TAAD, type A aortic dissection. aClass of recommendation. bLevel of evidence. Recommendation Table 47 — Recommendations for aortic repair strategies in type A acute aortic dissection
Recommendations Classa Levelb
In patients with acute TAAD and a partially dissected aortic root but no significant aortic valve leaflet pathology, aortic valve resuspension is recommended over valve replacement.1251–1255 I B In patients with acute TAAD undergoing aortic repair, an open distal anastomosis is recommended to improve survival and increase FL thrombosis rates. 1266–1269 I B
In patients with acute TAAD without an intimal tear in the arch or a significant arch aneurysm, hemi-arch repair is recommended over more extensive arch replacement.1270–1272 I B In patients with acute TAAD and a secondary intimal tear in the arch or proximal DTA, an extended aortic repair with stenting of the proximal DTA (e.g. by using the frozen elephant trunk technique) may be considered to reduce late distal aortic complications (e.g. aneurysm evolution of the remaining dissected descending aorta).1273,1274 IIb C © ESC 2024
DTA, descending thoracic aorta; FL, false lumen; TAAD, type A aortic dissection. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.88
while others favour conventional central aortic repair.1275 The IRAD registry highlights the superiority of a surgical and hybrid approach over medical or endovascular therapy alone. Central aortic repair effectively restores perfusion, showing promising results for renal malperfusion, extremity malperfusion, uncomplicated mesenteric malperfusion, or combinations.
Cerebral malperfusion, equally grave, triggers treatment debates necessitating a multidisciplinary strategy. Evidence supports surgical
Hypotension/shock
Cardiogenic shock related to: Tamponade (pulsus paradoxus) Aortic regurgitation (diastolic murmur) Major coronary occlusion by compression or dissection flap
Hypovolaemic shock (aortic rupture)
Branch vessel involvement
Bowel ischaemia Lactic acidosis Elevation liver function test Hemiplegia, hemiparesis or paraplegia Stroke, coma or altered mental status Acute kidney injury or oliguria
Peri-aortic haematoma
Mortality 56% 28.6% 10.5% 4.4%
N
N
N
Y
Y
Y
Figure 32 Complications in acute aortic syndromes, clinical evidence associated with malperfusion syndrome, and in-hospital mortality associated with these complications.
ESC Guidelines 3625
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.89
Initial diagnosis based on CCT
Type A AAD Type B AAD
Favourable TEVAR anatomyc
Favourable TEVAR anatomyc + life expectancy >5 years OMT + surveillance
Complicated type B AAD Uncomplicated type B AAD
Open cardiac surgery
(Class I)
Endovascular repair
(Class I) Open surgical repair
(Class I)
Endovascular repair in the subacute phased
(Class IIa) OMT + more frequent
surveillance
One of the following: Contained or free aortic rupture Organ malperfusion Extension of the dissectiona Progressive aortic enlargementa
One of the following: High-risk features at CCT or CMR
Ao diameter >40 mm FL diameter >20–22 mm Entry tear >10 mm Entry tear at lesser curvature
Haemorrhagic pleural effusion Evidence of malperfusion High-risk clinical features
Refractory hypertensionb Refractory pain >12 h
Need for readmission
Total Ao diameter >5 mma
Y N
Y N
Y N
Y N
Reappearance of pain/symptoms
Figure 33 Interventional treatment algorithm in acute aortic dissection. AAD, acute aortic dissection; Ao, aorta; CCT, cardiovascular computed tomography; OMT, optimal medical treatment; TEVAR, thoracic endovascular aortic repair. aOn serial imaging in the acute phase during the hospital stay. bOngoing hypertension despite more than three classes of antihypertensive drugs. cDefined as the presence of adequate proximal and distal landing zones for the prosthesis and adequate iliac/femoral vessels for vascular access. dBetween 14 and 90 days after dissection onset.172,1226–1231 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.90
(Class I)
(Class IIa) (Class IIa)
(Class I)
Acute type A aortic dissection
Acute type B aortic dissection
Check for presence of acute type A aortic dissection complications
Aortic rupture
or CPR Tamponade
Consider pericardial drainage
Cerebral malperfusion
or stroke Mesenteric malperfusion Lower extremity
malperfusion
Invasive diagnostics and/or percutaneous
malperfusion repair or TEVAR/EVAR
If not performed before aortic surgery and malperfusion persists, optional angiographic control and/or percutaneous malperfusion repair/TEVAR/EVAR
Direct admission to hybrid-OR with onsite aortic team Anaesthesiological monitoring and intraoperative TOE (if feasible) and preparation for surgery Immediate aortic surgery (ascending and consider aortic arch or FET based on extension)
Angiographic control and/or percutaneous malperfusion repair or TEVAR or EVAR
Check for presence of acute type B aortic dissection complications
If malperfusion persists
Aortic rupture/
tamponadea Cerebral malperfusion/strokea Mesenteric malperfusion Lower extremity
malperfusion
TEVAR or EVAR and/or percutaneous malperfusion repair
Static
thrombus
thrombus Dynamic Static + dynamic
F T
thrombus
Consider pericardial
drainage
In case of retrograde aortic dissection, immediate aortic surgery (ascending aorta, aortic arch or FET, based on extension)
Consider extra-anatomic bypass if lower extremity malperfusion persists
Figure 34 Mechanisms and clinical management of aortic branch obstruction in acute aortic dissection. CPR, cardiopulmonary resuscitation; F, false lumen; FET, frozen elephant trunk; OR, operating room; T, true lumen; TOE, transoesophageal echocardiography; TEVAR/EVAR, thoracic endovascular aortic aneurysm repair. aDevelops only in retrograde type A dissection.
ESC Guidelines 3627
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.91
intervention, reducing mortality rates to 25%–27%, compared with 76% with medical management alone.1255,1276 Close monitoring and rapid intervention are essential to achieve optimal outcomes and minimize the risk of permanent neurological damage. A recommended algorithm for malperfusion management is displayed in Figure 34.
Endovascular treatment in type A aortic dissection Endovascular therapy alone has been attempted in highly selected cases and the concept of a single endovascular valve-carrying conduit was suggested recently but has not yet been validated.1281,1282 Treatment in non-A non-B aortic dissection Conservative management leads to high mortality (malperfusion, aortic rupture); thus, surgery or endovascular therapy is favoured within 14 days of symptom onset. For complicated non-A non-B aortic dissection with an arch tear, consider FET repair, though if feasible, stent-graft implantation for primary tear coverage is an alternative.1179,1283
9.3.1.4.3. Acute type B aortic dissection interventional treatment. Acute TBAD presents without complications (uncomplicated) in around 50% of cases.1250 Complicated acute TBAD includes aortic rupture, malperfusion-related issues, rapid aortic expansion, paraplegia/ paraparesis, aortic haematoma, refractory pain, and hypertension despite optimal therapy, which associates with an approximately 50% mortality risk with conservative treatment.1193,1250,1284,1285 Open surgery used to be the sole option for complicated acute TBAD but carried a mortality rate of 25%–50%. Consequently, medical management, now considered the standard for uncomplicated cases, significantly reduces mortality. Goals include lowering SBP and heart rate with BBs (see Section 9.3.1.4.1). However, adherence is the main limitation of chronic medical treatment, with a rate below 50%.1286,1287 Compliance increases with previous aortic surgery, severity of hypertension, and understanding of the disease process. Thus, surveillance and disease awareness are imperative for these patients.
Endovascular therapy for complicated acute TBAD is now the firstline treatment, provided there is favourable anatomy, due to positive short- and long-term outcomes.1288–1294 Open surgery is reserved for unsuitable cases, and fenestration could be considered as an ultima ratio. In selected instances, correcting side branch compression before proximal sealing may be considered.136 In recent years, the ADSORB (Acute Dissection Stentgraft OR Best Medical Treatment) and INSTEAD-XL (Investigation of Stent Grafts in Aortic Dissection with extended length of follow-up) trials1219,1226,1295 have reported that early intervention for uncomplicated acute and subacute TBAD is beneficial compared with medical management, and there is important debate on whether to treat patients with uncomplicated acute TBAD to improve their life expectancy.1296–1298 Intervention is considered early within 90 days after onset of symptoms and may be safer when performed in the subacute phase (>14 days after onset of symptoms), but data are scarce.1298–1300 The Society of Thoracic Surgeons/ American Association for Thoracic Surgery (STS/AATS) 2022 guidelines1294 state that prophylactic TEVAR may be considered also in patients with suitable anatomy and high-risk features (Figure 33) to reduce late aortic-related adverse events. However, this matter is not entirely settled, and the Improving outcomes in vascular disease—aortic dissection (IMPROVE-AD trial) is currently underway. This trial aims to evaluate clinical outcomes in patients with subacute (from 48 h to 6 weeks) uncomplicated type B aortic dissection (uTBAD), comparing upfront TEVAR plus medical therapy against medical therapy with surveillance for deterioration. Aortic characteristics change over time, and endovascular treatment in the chronic phase offers limited potential for aortic remodelling. Identifying specific characteristics at the time of acute TBAD diagnosis that predict a complicated course has been attempted. Independent predictors of TBAD outcomes include a primary entry tear >10 mm located at the inner aortic curvature,1301 initial aortic diameter >40 mm,1301,1302 initial FL diameter >20 mm,1301 number/size of fenestrations between the true lumen and FL,1303 stent graft-induced new entry tear,1304,1305 and partial FL thrombosis.1306,1307 These parameters are summarized in a new system for the categorization of AD, DISSECT (Duration from onset of symptoms, Intimal tear location, Size of the aorta based on maximum trans-aortic diameter, Segmental Extent, Clinical complications related to the dissection, Thrombosis of the FL),1308 which serves as a guide to support a therapeutic decision (Figure 33).1308 A recent meta-analysis found TEVAR to be superior to best medical therapy in uncomplicated acute TBAD. Early outcomes were similar, but TEVAR was associated with fewer long-term events and better aortic remodelling.1297,1298,1309 Thus, in stable TBAD with suitable anatomy and high-risk features, pre-emptive TEVAR to improve the late outcome should be considered. Accurate endograft sizing is vital for TEVAR success, as errors may lead to complications. Disease-specific factors, such as acute thoracic aortic syndromes, pose challenges due to fluctuations in aorta diameter from haemorrhagic shock and resuscitation. Sizing decisions must account for these changes. Measuring the thoracic aorta based on admission CCT may be imprecise, even with proper centreline measurements. Real-time imaging, especially IVUS, enhances accuracy, particularly in hypovolaemic cases. However, further research is required to clarify the role of intraoperative imaging methods (e.g. IVUS, TOE, 3D CCT) in endograft sizing and long-term outcomes for optimal patient care.194
Recommendation Table 48 — Recommendations for the management of malperfusion in the setting of acute aortic dissection
Recommendations Classa Levelb
In patients with acute TAAD presenting with malperfusion (cerebral, mesenteric, lower limb, or renal), immediate aortic surgery is recommended.1275,1277 I B In patients with acute TAAD presenting with cerebral malperfusion or non-haemorrhagic stroke, immediate aortic surgery should be considered to improve neurological outcome and reduce mortality.1255,1276,1278 IIa B In patients with acute TAAD presenting with clinically significant mesenteric malperfusion syndrome, immediate invasive angiographic diagnostics to evaluate percutaneous malperfusion repair before or directly after aortic surgery, in aortic centres with expertise, should be considered.1278–1280 IIa C © ESC 2024
TAAD, type A aortic dissection. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.92
9.3.1.4.4. Chronic type B aortic dissection interventional treatment. Type B aortic dissection is considered as chronic 3 months after the onset of symptoms, but it also includes residual type B dissection after repair of TAAD. Aortic complications, especially aneurysmal degeneration, will occur in up to 50% of these patients.1302,1313 Therefore, in chronic TBAD, indications for treatment include the onset of new aortic symptoms such as rapid expansion, malperfusion, or rupture.1314 In asymptomatic patients, aneurysmal dilatation is the most important risk factor for rupture, reaching 20% when the diameter exceeds 55 mm.1302,1315 Risk of rupture increases with diameter; it has been reported a risk of 15.3% and 18.8% between 50–55 mm and 54–56 mm, respectively, thus suggesting 50–55 mm as a threshold for elective surgery.1316 However, smaller diameters should be considered in patients with HTAD. According to several studies, mortality in the chronic phase is high (40%–70%) and it is mainly related to patients’ comorbidities, such as heart disease and stroke. Open repair Despite the lack of data comparing open repair vs. TEVAR in chronic TBAD, open surgery remains the first-line treatment in low-risk patients or those with HTAD. The STS/AATS guidelines1294 state that open repair should be considered in chronic TBAD patients with indication for intervention, unless comorbidities are prohibitive or anatomy is not suitable for TEVAR. The surgical technique for chronic TBAD is like those for degenerative aneurysms, but repair is more complex due to the dissection flap.1317 Surgical mortality rates between 6% and 11% and SCI rates between 3% and 11% have been reported.1317–1321 Patients treated in low-volume centres present higher mortality rates (up to 20%), which reinforces the recommendation for centralization in experienced centres. Endovascular repair Thoracic endovascular aortic aneurysm repair (TEVAR) is the preferred treatment for eligible chronic TBAD patients, offering low early mortality (<5%), with stroke and SCI rates below 3%. It is also suitable for high-risk patients who are not candidates for open repair. The primary goal is to close the entry tear, induce FL thrombosis, and promote aortic remodelling to mitigate growth and rupture risk.1322,1323 A systematic review showed 90% immediate technical success and 86% complete FL thrombosis. However, FL thrombosis usually occurs above the coeliac trunk, necessitating lifelong distal FL surveillance.1324
Coverage of the LSA is often necessary and should be associated with revascularization. In a recent meta-analysis1325 comparing TEVAR to open repair in chronic TBAD, TEVAR showed lower early mortality, stroke rates, SCI, and respiratory complications but a higher reintervention rate. Long-term survival rates were similar, but open repair offered greater durability.1326 Adequate distal sealing poses a challenge due to the dissection extending to the iliac artery, with additional re-entries, allowing retrograde flow into the thoracic aneurysm. In chronic TBAD patients with AA enlargement, insufficient distal landing, or large re-entry tears, TEVAR alone is discouraged. Instead, a comprehensive repair involving the visceral aorta, infra-renal aorta, and iliac artery is needed. Recent studies have shown favourable results using custom or improvized fenestrated/branched endografts with careful patient selection.1062,1327–1329 A multidisciplinary team-based approach in experienced centres is necessary for good outcomes.1330
9.3.1.4.5 Management during pregnancy. Management of AD dur-
ing pregnancy requires a multidisciplinary team and specialized centres. Initial care should consider general medical recommendations (as previously described), using drugs with the lowest teratogenic impact. In cases of type A dissection, if the foetus is viable, caesarean delivery will be performed before aortic repair. If the foetus is not viable, surgery will be done with the foetus in place.1335,1336 In uncomplicated type B
Recommendation Table 49 — Recommendations for the management of patients presenting with acute type B aortic dissection
Recommendations Classa Levelb
Medical therapy including pain relief and blood pressure control is recommended in all patients with acute TBAD.1215,1219,1310,1311 I B In patients with complicated acute TBAD, emergency intervention is recommended.1193,1250,1284,1285,1288,1289,1291–1293 I B In patients with complicated acute TBAD, TEVAR is recommended as the first-line therapy.c,910,1288–1293 I B In patients with acute TBAD, BBs should be considered as the first-line medical therapy.1216,1312 IIa B In patients with uncomplicated acute TBAD, TEVAR in the subacute phase (between 14 and 90 days) should be considered in selected patients with high-risk featuresd to prevent aortic complications.1219,1226,1295,1297,1298,1308,1309 IIa B © ESC 2024
BBs, beta-blockers; HTAD, heritable thoracic aortic disease; TBAD, type B aortic dissection; TEVAR, thoracic endovascular aortic repair. See also Figure 33. aClass of recommendation. bLevel of evidence. cExcept in patients with known or suspected HTAD. dFor high-risk features see Figure 33. Recommendation Table 50 — Recommendations for the management of patients presenting with chronic type B aortic dissection
Recommendations Classa Levelb
Antihypertensive therapy is recommended in all patients with chronic TBAD.1331–1333 I B In chronic TBAD with acute symptoms of malperfusion, rupture, or progression of disease, emergency intervention is recommended.1302,1313,1314 I C In patients with chronic TBAD and a descending thoracic aortic diameter ≥60 mm, treatment is recommended in patients at reasonable surgical risk.1302,1315,1334 I B In patients with chronic TBAD and a descending thoracic aortic diameter ≥55 mm, an indication for intervention should be considered in patients with low procedural risk.1302,1316 IIa C In patients with chronic post-dissection thoracoabdominal aortic aneurysms, the use of fenestrated/branched stent grafts may be considered, when treatment is indicated.1062,1327–1329 IIb C © ESC 2024
TBAD, type B aortic dissection. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3629
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.93
dissections, strict control of the pregnant patient and foetus with conservative medical management is recommended.1224,1335 Although limited to selected cases, successful TEVAR has been described in complicated TBAD.1227 More information is detailed in the 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy.1337
9.3.2 Intramural haematoma
Intramural haematoma, constituting 5%–25% of AAS cases, involves vasa vasorum haemorrhage within the aortic media, with or without intimal disruption (ID).70,172,1338 Most cases (60%–70%) involve the DTA (ascending aorta ∼30%, aortic arch ∼10%).70,172,1192 Although it usually occurs at an older age than AAD, risk factors and symptoms are similar;70,172,1192,1338 however, aortic regurgitation, malperfusion syndrome, and pulse deficits are less frequent in type A IMH than in TAAD.70,172
9.3.2.1 Diagnostic work-up
Diagnostic IMH work-up should be similar to that proposed for AAS (Figure 30), but with different morphological features in the imaging techniques. CCT and CMR (followed by TOE) are the leading techniques for diagnosis.70,159,171–173 Unenhanced followed by contrast-enhanced CCT represents the most used tool in the acute setting (hyperintense signal of aortic wall before contrast administration).70,171,172 The IMH diagnostic hallmark consists of crescentic or circular aortic wall thickening in the absence of an intimal flap or aortic wall enhancement following contrast administration.70,171,172 CMR is an excellent imaging technique to detect small IMHs and for the differentiation of IMH (hyperenhanced images in T1-weighted images) from atherosclerotic thickening of the aorta, thrombus, or thrombosed dissection.172 TTE yields low sensitivity (<40% for IMH cut-off limit of 5 mm).171
9.3.2.2 Clinical outcomes
Intramural haematoma may evolve into AAD (12% of patients), saccular (8%) or fusiform aneurysm (22%), and/or ID (54%).1192,1339–1342 Partial or total regression is reported in 34% of patients.70,1192,1343 Outcomes are comparable to those in AAD. In-hospital mortality for type A IMH is 26.6% (surgical 24.1% and medical 40.0%). In this regard, higher mortality for IMH involving the aortic valvular complex has been observed.1175 In-hospital mortality for type B IMH is 4.4% but worsens once surgery is indicated (surgical 20.0% vs. medical 3.8%).1175,1344
9.3.2.3 Geographical variations
Reports from South Korea and Japan reveal notable disparities with Western nations in IMH incidence (28.9% vs. 5.7% of overall AAD as reported by IRAD), treatment strategies, and outcomes. In Eastern regions, the majority (80.8%) of type A IMH patients received medical treatment, resulting in significantly improved clinical outcomes (in-hospital mortality 6.6% [5.9% for medical and 9.4% for surgical]).1345 These results may be partially explained by the detection of early-stage IMH (mild, uncomplicated cases) at primary centres.1345–1347 9.3.2.4 Management
Current IMH therapeutic interventions are similar to AAD, with the first step consisting mainly of pain and BP control regardless of the anatomopathological features (Figure 31).
9.3.2.4.1 Type A intramural haematoma. As in AAD, type A IMH
involves the ascending aorta. Surgery (emergency or urgent depending on clinical status) is recommended. In selected patients with increased operative risk (i.e. multiple comorbidities) and uncomplicated type A IMH without high-risk imaging features (Table 16) a ‘wait-and-see strategy’ in a reference/experienced centre may be reasonable.70,172,1348,1349
9.3.2.4.2 Type B intramural haematoma. In type B IMH, the disease
is in the descending aorta, distal to the left subclavian artery. For uncomplicated type B IMH, initial management involves medical treatment and thorough clinical and imaging monitoring.70,172 If uncomplicated type B IMH presents high-risk imaging characteristics (see Table 16), the multidisciplinary team should consider endovascular repair as an option. In contrast, complicated type B IMH warrants consideration of TEVAR.1350,1351 However, in unfavourable anatomy, open surgery remains an alternative.
ID has been described in 54% of type B IMH cases.1192,1339–1342 Approximately 28% of them are tiny intimal disruptions (≤3 mm) that are not related to AAEs. However, 14% of them evolve into focal intimal disruptions (FID) (>3 mm), with prognostic implications; thus, all patients with ID require close follow-up with imaging techniques. In the acute phase, FID has a poor prognosis owing to the high risk of aortic rupture and should be treated early and invasively, especially large FID (≥10 mm length and ≥5 mm depth).1342,1352 However, in the chronic phase, most FIDs evolve with slow aortic dilatation and without complications, and they can be managed with medical treatment and close imaging surveillance.1352
Table 16 High-risk features of intramural haematoma type A and B
Ascending aorta involvement Difficult BP control Persistent/recurrent pain despite aggressive BP control Maximum aortic diameter: • Type A: >45–50 mm • Type B: >47–50 mm Progression to aortic dissection Focal intimal disruption with ulcer-like projection Haematoma thickness >10 mm (type A) or >13 mm (type B) Enlarging haematoma thickness Enlarging aortic diameter Pericardial effusion at admission (type A) Recurrent pleural effusion Detection of organ malperfusion © ESC 2024
BP, blood pressure. Adapted with permission from.172 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.94
9.3.3 Penetrating atherosclerotic ulcer
Penetrating atherosclerotic ulcer (2%–7% of all AAS cases) is characterized by localized ulceration of an aortic atherosclerotic plaque penetrating through the internal elastic lamina into the media, frequently associated with IMH and diffuse atherosclerosis.70,172,174,910,1338,1343 Often, multiple PAUs are present, ranging from 5 to 25 mm in diameter and 4 to 30 mm in depth.70,172,174,1338 They occur mostly in the middle and lower DTA, with the aortic arch and AA less involved. The ascending aorta is rarely affected,70,172,910,1192 but when this occurs, especially complicated with IMH, the risk of rupture is 33%–75% and progression to dissection is associated with a high mortality rate. Most patients are older males, smokers, aged >65, with multiple comorbidities like systemic hypertension, CAD, COPD, renal insufficiency, and concurrent abdominal aneurysm.24,172,910,1357 Symptoms are like those in AAD and may manifest in older age after a long asymptomatic phase (often PAU is diagnosed as an incidental finding during an imaging examination).24,172,910,1357 It should be highlighted that symptom onset may indicate PAU expansion (tunica adventitia involvement); thus, urgent imaging (CCT or CMR) and appropriate therapeutic intervention are needed to prevent aortic rupture.70,171,172,174
9.3.3.1 Diagnosis
Diagnostic work-up is described in Figure 30. CCT represents the technique of choice for diagnosis. TOE and CMR represent possible valid alternatives considering availability and local expertise.70,159,171–173 Of note, 18FDG-PET-CT is a promising technique since it can detect increased glucose uptake in PAUs as a marker of increased metabolic activity and inflammation, which has been associated with major adverse events.1358,1359 This information may be used to guide treatment decisions, such as the selection of patients who may benefit from endovascular or surgical intervention.1360
9.3.3.2 Treatment
Medical treatment as described for AD is recommended (Figure 31). Management of incidental cases is not clearly defined.174 Small series suggest that isolated, asymptomatic, small PAUs may be safely managed conservatively with regular surveillance.1361,1362 Surgery is recommended in type A PAU with the option of a ‘wait-and-see strategy’ in highly selected high-risk patients with no highrisk features (Figure 35). However, in uncomplicated type B PAU, medical treatment along with careful clinical and imaging surveillance is recommended.174,1350 When intervention is needed, endovascular treatment (early and 3 year aortic mortality 7.2% and 10.4%, respectively)1350 should be preferred to open surgery (early and 3 year aortic mortality of 15.9% and 25.0%, respectively).174,1350 In cases of uncomplicated PAU with high-risk imaging features1363–1365 (Figure 35), endovascular treatment should also be considered. The natural history of PAU of the abdominal aorta (AA) with associated IMH is less known. In a review of PAU of the AA, endovascular stenting was the preferred treatment of choice (62%), followed by open surgical repair (35%) and conservative therapy (3%).1366
Recommendation Table 51 — Recommendations for the management of intramural haematoma
Recommendations Classa Levelb
In patients with IMH, medical therapy including pain relief and blood pressure control is recommended.24,172 I C In type A IMH, urgent surgery is recommended.172,1175,1192 I C In type B IMH, initial medical therapy under careful surveillance is recommended.1175,1192,1347,1350,1353 I C In uncomplicatedc type B IMH, repetitive imaging (CCT or CMR) is indicated.1175,1192,1347,1350,1353 I C In complicatedc type B IMH, TEVAR is recommended.1175,1192,1347,1350,1353 I C In uncomplicatedc type B IMH but with high-risk imaging featuresd, TEVAR should be considered.1347,1350 IIa C In complicatedc type B IMH, surgery may be considered in patients with anatomy unfavourable for TEVAR.1175,1192,1347,1350,1353 IIb C In selected patients with increased operative risk and uncomplicatedc type A IMH without high-risk imaging featuresd, a ‘wait and see’ strategy may be considered.1348,1354–1356 IIb C © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; IMH, intramural haematoma; TEVAR, thoracic endovascular aortic repair. aClass of recommendation. bLevel of evidence. cUncomplicated/complicated IMH refers to the absence or presence of recurrent pain, expansion of the IMH, periaortic haematoma, and intimal disruption. dHigh-risk features of intramural hematoma type A and B are described in Table 16. Recommendation Table 52 — Recommendations for the management of penetrating atherosclerotic ulcer
Recommendations Classa Levelb
In all patients with PAU, medical therapy including pain relief and blood pressure control is recommended.24,172 I C In cases of type A PAU, surgery is recommended.172 I C In cases of type B PAU, initial medical therapy under careful surveillance is recommended.1347,1350 I C In uncomplicated type B PAU, repetitive imaging (CMR, CCT, or TOE) is recommended.1347,1350 I C In complicated type B PAU, endovascular treatment (TEVAR) is recommended.1347,1350,1357 I C In uncomplicated type B PAU with high-risk imaging features,c endovascular treatment should be considered.1347,1350 IIa C In selected patients with increased operative risk and uncomplicated type A PAU without high-risk imaging features,c a ‘wait-and-see’ strategy may be considered.1367 IIb C In complicated type B PAU, surgery may be considered based on anatomy and medical comorbidities.1347,1350 IIb C In isolated, asymptomatic, small PAUs with no high-risk features,c conservative management with regular surveillance and medical treatment may be considered.24,1361 IIb C © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; PAU, penetrating atherosclerotic ulcer; TOE, transoesophageal echocardiography; TEVAR, thoracic endovascular aortic repair. aClass of recommendation. bLevel of evidence. cSee Figure 35 for high-risk imaging features of PAU.
ESC Guidelines 3631
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.95
9.3.4 Aortic pseudo-aneurysm
Aortic pseudo-aneurysms, or false aneurysms, result from aortic wall disruption, typically caused by factors like trauma,1368 surgery, or infections. They are often symptomless, detected incidentally during post-aortic procedure imaging. Symptoms may include chest pain, compression, and if untreated, they can lead to fatal rupture or other severe complications.1369,1370
Type B PAU
Acute or symptomatic PAU Chronic or asymptomatic PAU
Follow-up
Appearance of symptoms or signs of impending rupture
Endovascular
treatment (Class IIa) Optimal medical
treatment (Class I)
Endovascular treatment
(Class I)
Haemodynamic instability Rupture, contained rupture or signs of impending rupture Refractory pain Aortic diameter 55 mm (C) Large pseudoaneurysm Presence of IMH or high-risk imaging features (see box below)
High-risk imaging features of PAUs
Maximum PAU width (A) 13–20 mm Maximum PAU depth (B) 10 mm Significant growth of PAU width (A) or depth (B) >5 mm/year PAU associated with a saccular aneurysm PAU with an increasing pleural effusion Significant growth of PAU width (A) or depth (B) >5 mm/yr Aortic diameter 55 mm (C) High-risk imaging features (see box below)
N
Y
Y
Y N
N
A B C
Presence of any of the following
Presence of any of the following
Figure 35 High-risk features in penetrating atherosclerotic ulcer and management of patients with type B penetrating atherosclerotic ulcer. IMH, intramural haematoma; PAU, penetrating atherosclerotic ulcer; TEVAR, thoracic endovascular aortic repair. (A) Maximum PAU width. (B) Maximum PAU depth; (C) Maximal aortic diameter at the site of the PAU.910 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.96
Pseudo-aneurysm repair seems always indicated regardless of size or position to prevent progression and rupture. Nevertheless, in some circumstances and under close follow-up, patients could be monitored by CCT, CMR, or TOE and intervention could be postponed unless size expansion, symptoms, or compression of surrounding structures occur.1371 Pseudo-aneurysms could be treated by open surgery or endovascular treatment (occluders, stent grafts, or coils). There is no randomized study comparing open surgery vs. TEVAR; however, treatment of choice is commonly based on anatomical features, clinical presentation, and the patient’s comorbidities and decided by a multidisciplinary team in specialized centres.1045,1371
9.3.5 Traumatic aortic injury
Traumatic aortic injury (TAI), commonly from high-speed motor accidents or falls, involves partial or complete aorta transection. It results from rapid deceleration causing torsion and shearing forces, often affecting relatively immobile aorta segments like the aortic isthmus (90%), aortic root (5%), or diaphragmatic hiatus (5%).24,70,172 Traumatic aortic injury is classified based on the degree of lesion in the aortic wall (Figure 36): grade I (intimal tear), grade II (IMH), grade III (pseudo-aneurysm), and grade IV (aortic rupture). In the Crash Injury Study, 130/613 deaths (21%) were associated with TAI (mortality associated with aortic rupture 91%; at-scene survival 9%).1372
9.3.5.1 Diagnosis and therapeutic interventions
Due to non-specific symptoms and signs (often obscured by concomitant multiple organ injury) a timely diagnosis relies on a high level of clinical suspicion.70,172 CCT (accuracy close to 100%) represents the technique of choice, acting as a ‘one-stop shop’ to rapidly assess the entire skeletal system and internal organs.70,171,172 TOE may be an alternative, although limited by availability, local expertise, and potentially a patient’s multiple traumas.24,70,172 Therapeutic interventions are dependent on the extent of aorta lesion and patient clinical status as assessed by a multidisciplinary team. Generally, aggressive fluid administration should be avoided because it may exacerbate bleeding, coagulopathy, and hypertension. To reduce risk of rupture, mean BP should not exceed 80 mmHg.172 Minimal aortic injury (grades 1 and 2) may be managed medically along with strict clinical and imaging surveillance; moderate aortic injury (grade 3) with semi-elective repair (within 24–72 h) to allow patient stabilization (though in some patients urgent repair is needed);24,1373 and severe aortic injury (grade 4) with immediate repair.1374 If there is progression of the IMH (grade 2), semi-elective repair (within 24–72 h) may be considered. TEVAR is preferred (if feasible) to open surgery (in-hospital mortality 7.9% vs. 20% and 1 year mortality 8.7% vs. 17%). In semi-elective repair, if the LSA needs to be covered, prior LSA revascularization before TEVAR is suggested to reduce the risk of paraplegia 172,1373,1374
9.3.5.2 Long-term surveillance in traumatic aortic injury
In addition to clinical assessment, CCT is the imaging choice for followup.70,171,172 Cumulative exposure to radiation and iodinated contrast medium remains the major limitation in young patients, especially in women. A combination of a chest X-ray and CMR (if no graft artefacts) would be a valid alternative.24,171,172 9.3.6 Iatrogenic aortic injuries
Iatrogenic aortic lesions are those associated with invasive procedures (cardiac surgery, most commonly dissection type A, or coronary angiography, with a similar proportion of type A and B dissections) (see Section 9.3.2.1). Incidence is low and ADs are the most common lesions. Main risk factors are advanced age, presence of CVRFs, atherosclerosis, aortic aneurysms, or PAD (Figure 37). Patients with iatrogenic AAS are often painless with correspondingly less chest or back pain.1375 While historically associated with high mortality,1375 recent registries like the German GERAADA indicate a mortality rate similar to that for spontaneous dissections.1186 Clinical management is based on the underlying lesion (AAD, IMH) and location; however, conservative management has been described with good results in type A iatrogenic dissection if the coronary flow is preserved and the dissection is small.1376 Iatrogenic lesion classification is depicted in Figure 37.1377 Although scarce, data support a conservative approach based on evolution in type 1 and 2 lesions (Dunning classification), and surgery in type 3.1377 In cases of coronary involvement, stent implantation sealing the flap may be proposed.1376,1377
9.3.7 Long-term follow-up of acute aortic syndrome
Imaging modalities and time intervals for surveillance vary according to lesion location (ascending/descending aorta), type of treatment (medical, endovascular, surgical), and underlying disease (HTAD).70,1062,1153 Compared with the chronic disease setting, follow-up of AAS patients is characterized by a higher risk of complications and need for re-operation.1378 Patients receiving TEVAR for AAS involving the descending aorta are more prone
Recommendation Table 53 — Recommendations for traumatic aortic injury
Recommendations Classa Levelb
In cases of severe aortic injury (grade 4), immediate repair is recommended.24,1373,1374 I A In cases of TAI with suitable anatomy requiring intervention, TEVAR is recommended over open surgery.24,1373,1374 I A In all TAI patients, medical therapy including pain relief, and blood pressure and heart rate control, is recommended.24,172 I C In cases of TAI suspicion, CCT is recommended.159,172 I C In cases of moderate aortic injury (grade 3), repair is recommended.24,1373 I C If CCT is not available, TOE should be considered.159,172 IIa C In minimal aortic injury (grades 1 or 2), initial medical therapy under careful clinical and imaging surveillance should be considered.24,1374 IIa C In cases of progression of the IMH (grade 2), semi-elective repair (within 24–72 h) should be considered.24,1374 IIa C © ESC 2024
CCT, cardiovascular computed tomography; IMH, intramural haematoma; TAI, traumatic aortic injury; TOE, transoesophageal echocardiography; TEVAR, thoracic endovascular aortic repair. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3633
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.97
(27%–49%) to requiring a second intervention than patients undergoing surgical repair.1379,1380 However, need for re-intervention at follow-up (after initial treatment of AAD) seems to have a significant impact on survival for TAAD1381 but not for TBAD.1380
9.3.7.1 Follow-up after invasive treatment
Following surgery for AAS, imaging surveillance will focus on persistence/obliteration of the FL, anastomotic dehiscence, progressive dilatation of residual native aorta (with or without residual dissection), or graft infection. CCT is the most used modality, but in patients requiring frequent examinations CMR can be considered to reduce radiation.
Compared with outcomes of open surgery for aortic aneurysms, time to re-intervention in patients developing complications is significantly shorter,1159 also due to the faster average growth of the dissected aorta (about 1 mm per year).70 Considering the reported incidence rates (around 10%) of complications requiring re-operation, it is reasonable to follow patients every 6 months in the first year (including an early—within 1 month—echocardiography to follow native or prosthetic aortic valve function), then yearly up to the third post-operative
GRADE
I
GRADE
II
GRADE
III
GRADE
IV MedTX (Class IIa)
Med TX/TEVAR
(Class IIa)
TEVAR/OR
(Class I)
TEVAR/OR (Emergent)
(Class I)
Intimal tear
Intramural haematoma
Pseudoaneurysm
Rupture
Figure 36 Classification and treatment of traumatic aortic injuries. Med, medical; OR, open surgery repair; TEVAR, thoracic endovascular aortic repair; Tx, treatment. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.98
Grade 1 Grade 2 Grade 3
Dunning classification
Older age Cardiovascular
risk factors Atherosclerosis Aortic aneurysm PAD
Risk factors
Aortic canulation Coronary angiography
4 cm Aetiology
4 cm
4 cm
Figure 37 Aetiology, risk factors, and classification of iatrogenic aortic injuries. PAD, peripheral arterial disease. Dunning classification of iatrogenic aortic dissection:1377: type 1, dissection limited to the sinuses of Valsalva; type 2, dissection of the ascending aorta outside the sinuses but < 40 mm from the aortic annulus. type 3, dissection > 40 mm from the annulus.
ESC Guidelines 3635
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.99
year and then every 2–3 years if there are no complications (Figure 38).1153,1159 TEVAR implies a higher risk for late re-interventions,1159,1378 and a sequence of imaging intervals at 1, 6, 12, 24, 36, 48, and 60 months is recommended if no abnormality is detected (shorter intervals should be considered in high-risk patients). Thereafter, controls can be performed every 2–3 years. Compared with the time points after surgery, an adjunctive early control at 1 month is necessary to exclude asymptomatic retrograde type A dissection induced by TEVAR (70% of cases occurring within 30 post-operative days).1382 Besides imaging surveillance, clinical follow-up is aimed at achieving strict BP control, limiting the burden of CVRFs, and providing patients with counselling for lifestyle modifications and prescriptions for sport activity.24 There is evidence that statin treatment may improve survival in AAS patients under medical treatment, whereas BBs may improve survival in surgically treated patients.1333 9.3.7.2 Follow-up under medical treatment (chronic type B aortic
dissection, intramural haematoma, penetrating atherosclerotic ulcer) Around 70% of TBAD patients survive the hyperacute phase. If there is no malperfusion, uncontrolled hypertension, or impending rupture, initiate anti-impulse therapy alongside surveillance. Chronic aortic dilatation, reaching 55 mm, is the leading cause (about 40%) of intervention, while acute complications necessitating immediate treatment are rare.1301,1383 Imaging controls should be performed at least at 1, 6, and 12 months after discharge and yearly thereafter; however, one additional earlier scan, e.g. within 3 months, may reveal important changes occurring in the subacute phase, when the dissected aorta remains successfully amenable to early TEVAR.1383 During surveillance, late complications may be predicted by imaging features, including the number and location of the entry tear(s), and dimensions of the FL, total (true + false) lumen, or entry tear.1383 This might help in risk stratification to modulate the stringency of surveillance in the individual patient (Figure 33).1213
Concerning
findings
Stable
1 6 months
3 1 year 2 years 3 years 4 years 5 years 6 years
Pre-discharge
(1 month)
Pre-discharge
Recommendation for CCT or CMR From this point on, extend the time intervals for monitoring according to the clinical context
Residual false lumen
No false lumen
Stable (AD or IMH)
PAU or concerning
findings
Treated AAS (open or endovascular
repair)
Medically treated AAS
Figure 38 Algorithm for follow-up after acute aortic syndrome. AAS, acute aortic syndrome; AD, aortic dissection; CMR, cardiovascular magnetic resonance; CCT, cardiovascular computed tomography IMH, intramural haematoma; PAU, penetrating atherosclerotic ulcer. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.100
Type B IMH and PAU are usually conservatively treated with antihypertensive therapy and watchful monitoring. Most of the medically treated IMHs have a favourable course, whereas PAUs are less predictable in terms of risk of acute TBAD or rupture.1350 Therefore, for IMH the same surveillance criteria as for medically treated uncomplicated TBAD can be employed; for PAU more frequent controls are advisable, i.e. one every 6 months instead of every year. Selectively, in asymptomatic patients with 2 year growth-rate stabilization and no high-risk features, intervals between controls can be longer (every 1–2 years) (Figures 35 and 38).70,1384 10 Genetic and congenital diseases
of the aorta
10.1 Genetic and chromosomal diseases
This section discusses genetic and congenital aortic diseases. Aortic root and ascending aortic disease is commonly linked to congenital or hereditary factors, while descending aortic problems, especially in the AA, often result from atherosclerosis.1385 Unless noted otherwise, recommendations provided herein are intended for adults. Genetic diseases affecting the thoracic aorta are grouped under the broader term of HTAD. HTAD comprises a clinically and genetically heterogeneous group of disorders sharing the common denominator of aneurysm or dissection of the thoracic aorta. Familial forms (thoracic aortic disease [TAD] affecting ≥2 individuals in one family) or confirmed genetic entities (familial or sporadic) as well as syndromes conferring a risk for TAD fall under the definition of HTAD.70 Due to the rarity of these conditions, robust evidence for many scenarios, such as intervention thresholds, surgical methods, open surgery vs. endovascular approaches, and pregnancy planning, is lacking. Thus, a multidisciplinary and individualized approach is advisable.70,1386,1387
Clinically, HTADs can manifest as either syndromic or nonsyndromic entities. The genes identified to date may underly both entities and predominantly show autosomal dominant inheritance patterns. While TAD is the primary feature in HTAD, extra-aortic features (skeletal/ocular) may be key to diagnosing certain syndromic cases. In some cases, the presence of extra-aortic manifestations may aid in risk stratification and hence in defining optimal management.1388–1390 The main clinical and genetic data on syndromic and non-syndromic HTADs are summarized in the Supplementary data online, Table S5. Numerous underlying gene defects have been discovered in both syndromic and non-syndromic cases, leading to the constitution of three major molecular groups: genes encoding components of: (i) the extracellular matrix; (ii) the transforming growth factor-beta (TGF-ß) signalling pathway; and (iii) the smooth muscle cell contractile apparatus. Clinical and CV outcomes vary between these groups and will
Recommendation Table 54 — Recommendations for follow-up after treatment of acute aortic syndrome
Recommendations Classa Levelb
After TEVAR for AAS, follow-up imaging is recommended at 1, 6, and 12 months post-operatively, then yearly until the fifth post-operative year if no abnormalitiesc are documented.1159,1378,1382 I B In medically treated type B AAS or IMH, follow-up imaging is recommended at 1, 3, 6, and 12 months after onset, then yearly if imaging findings are stable.1301,1383 I C In medically treated PAU, follow-up imaging is recommended at 1 month after diagnosis, then every
6 months if imaging findings are stable.70,1350,1384 I C After open surgery for AAS, follow-up imaging by CCT and TTE within 6 months, then CCT at 12 months and then yearly if findings are stable,d should be considered.1153,1159,1383 IIa B If no complicationsc occur within the first 5 years, CCT every 2 years thereafter should be considered.1159,1378 IIa B If no residual patent FL is documented for 3 post-operative years, subsequent surveillance by CCT every 2–3 years should be considered.1153,1159,1383 IIa C If abnormalitiesc are documented at any time of follow-up after TEVAR for AAS, then CCT should be considered every 3–6 months.1159,1378,1382 IIa C When frequent controls are required in AAS patients treated either by open or endovascular repair, CMR should be considered instead of CCT after the first-year follow-up.70,1153 IIa C In the follow-up of medically treated PAU, after 2 years of imaging stability, larger intervals should be considered in low-risk patientse.70,1350,1384 IIa C © ESC 2024
AAS, acute aortic syndrome; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; FL, false lumen; IMH, intramural haematoma; PAU, penetrating atherosclerotic ulcer; TEVAR, thoracic endovascular aortic repair; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. cIncluding: pseudo-aneurysm, graft infection, endoleak (any type), enlargement of the excluded aneurysm, and stent graft migration/separation/fracture. dBoth in terms of extent of residual FL and of aortic diameters at any level. eLow-risk: based on width and depth of PAU (See Figure 35 for high-risk features). Recommendation Table 55 — Recommendations for the management of patients with heritable thoracic aortic disease
Recommendations Classa Levelb
It is recommended that medical management of patients with HTAD is individualized and based on shared decision-making.1386 I C It is recommended that patients with known or suspected syndromic or non-syndromic HTAD are evaluated in a centre with experience in the care of this patient group.888 I C © ESC 2024
HTAD, heritable thoracic aortic disease. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3637
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.101
help pave the way to precision medicine in HTAD.1391 Extensive clinical and imaging studies in HTAD revealed arterial vasculature involvement beyond the thoracic aorta. Patients may develop aneurysms and/or dissections beyond the aorta in diseases such as MFS, Loeys–Dietz or vascular Ehlers–Danlos syndrome (vEDS),1390,1392,1393 or can be prone to occlusive vascular disease in the setting of alpha-actin gene (ACTA2) variants.1394 Large clinical variability is observed within families carrying an identical variant and instances of incomplete penetrance (a ‘skipped generation’) are observed. All HTAD entities display cystic medial degeneration, hindering precise diagnosis using pathology. Both genetic testing and imaging (mainly by TTE, but also consider CMR or CCT if the aortic root/ascending aorta are not properly visualized) in patients and family members are important in the diagnosis of HTAD. In those patients in whom no genetic cause is identified, but in whom there is a high suspicion of an underlying genetic defect, genetic re-evaluation needs to be considered after 3–5 years. Genetic testing should always be accompanied with appropriate counselling. Furthermore, appropriate assessment of HRQoL and psychological support should be offered to patients and families.1395 Indications for genetic testing and aortic screening in HTAD are illustrated in the algorithm in Figure 39. Although isolated AAA is less frequently associated with a genetic basis, patients with high-risk features (syndromic features, early onset of disease, absence of CVRFs, and/or family history of TAD or AAA) should be evaluated in centres with experience in HTAD to evaluate the need for genetic testing and specific surveillance, including active clinical screening in family members. 10.1.1 Turner syndrome
10.1.1.1. Diagnosis, clinical presentation, and natural history Turner syndrome (TS), resulting from partial or complete monosomy of the X-chromosome, affects 1 in 2500 live-born females. About 50% of patients experience CV issues like ascending aortic dilatation, BAV, aortic coarctation, elongated aortic arch, and partial abnormal pulmonary venous return.1417–1419 All women present with generalized arteriopathy and TS itself is an independent risk factor for thoracic aortic dilatation. AD risk (type A in 85% and type B in 15%) is elevated in this population,1420–1422 although recent studies indicate that this risk may be lower with proper treatment guidelines.1423–1426 Risk factors include aortic dilatation, BAV, coarctation, and arterial hypertension. Defining aortic dilatation in TS requires adjustment for anthropometric parameters and aortic growth data for dissection risk estimation.1427 Z-scores used in the general population are equivalent to Turner-specific z-scores.1428 Imaging surveillance In newly diagnosed TS, TTE and CMR are recommended at baseline for the evaluation of congenital heart defects and aortic anatomy/diameters. For women aged 15 years and older with TS, adjusting for their smaller body size is essential when assessing aortic dimensions. Utilize metrics like the ascending aortic size index (ASI), aortic height index (AHI), or aortic z-scores to gauge aortic dilation and dissection risk. Further follow-up is dictated by baseline aortic diameters, age, and risk factors (Figure 40).
Recommendation Table 57 — Recommendations for imaging in women with Turner syndrome
Recommendations Classa Levelb
To take the smaller body size of women (≥15 years) with TS into account, the use of the ascending ASI (ratio of aortic diameter [mm] to BSA [m2]), AHI (ratio of aortic diameter [mm] to height [m]), or aortic z-score is recommended to define the degree of aortic dilatation and assess the risk of aortic dissection.153,1417,1421,1423,1428,1429 I C It is recommended to define imaging and clinical surveillance intervals according to the estimated risk for dissection, based on the ascending ASI and concomitant lesions.c,1420,1421 I C © ESC 2024
AHI, aortic height index; ASI, aortic size index; BSA, body surface area; TS, Turner syndrome. aClass of recommendation. bLevel of evidence. cConcomitant lesions: hypertension, aortic coarctation, bicuspid aortic valve (Figure 40).
Recommendation Table 56 — Recommendations for genetic testing and aortic screening in aortic disease
Recommendations Classa Levelb
Genetic testing In patients with aortic root/ascending aneurysms or thoracic aortic dissection, gathering family history information for at least three generations about TAD, unexplained sudden deaths, and peripheral and intracranial aneurysms is recommended.880,1396–1402 I B In patients with aortic root/ascending aortic aneurysms or thoracic aortic dissection and risk factors for HTAD,c genetic counselling at an expert centre and subsequent testing, if indicated, is recommended.1399,1403–1408 I B In patients with HTAD who have a pathogenic/likely pathogenic variant, genetic testing of at-risk biological relatives (i.e. cascade testing) is recommended, irrespective of age.70,1407,1409 I C In patients with HTAD, guidance of clinical management by the underlying gene/variant, when known, should be considered.70,1391,1410–1416 IIa B Aortic imaging screening In patients with TAD with risk factors for HTAD,c with a negative family history of TAD and in whom no (likely) pathogenic variant is identified, TTEd screening aortic imaging of FDRse is recommended.1396,1402 I B
Imaging screening of family members of patients with TAD with risk factors for HTADc in whom no (likely) pathogenic variant is identified should be considered starting at age 25, or 10 years below the youngest case, whichever is younger. If the initial screening is normal, continued screening every 5 years until the age of 60 should be considered.25 IIa C © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; FDR, first-degree relative; HTAD, heritable thoracic aortic disease; TAD, thoracic aortic disease; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. cSee Figure 39. dCMR/CCT may be indicated if the aortic root/ascending aorta cannot be visualized adequately. eParents, siblings, children. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.102
≤ 60 years
HTN HTN
Patient with TAD
Aortic dilatation Aortic dissection
Aortic root/ascending
z-score ≥3 or any additional risk feature (see box below)
Aortic root/ascending z-score ≥3
or aortic dissection
Genetic testing
(Class I)
Re-evaluate genetic testing in the proband (after 3–5 years) Cascade screening
(Class I)
Gene-based management
(Class IIa) Reimaging of FDRs (after 5 years)
(Class IIa) Aortic imaginga screening of FDRs
(Class I)
No further investigation
for HTAD No further investigation
for HTAD
Referral to a centre with experience in the care of this patient group
(Class I)
Any additional risk feature (see box below)
Syndromic features of:
Y N
Y N
Y
N
Y
N Y
N
Marfan syndrome Loeys-Dietz syndrome Vascular Ehlers-Danlos syndrome Family history of (either one):
TAD Peripheral/intracranial artery aneurysm Unexplained Sudden death <60 years
Positive Negative
or VUS
Any additional risk feature
Figure 39 Algorithm for genetic and imaging screening in patients with thoracic aortic disease. CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; FDR, first-degree relative; HTAD, heritable thoracic aortic disease; HTN, arterial hypertension; TAD, thoracic aortic disease; TTE, transthoracic echocardiography; VUS, variant of uncertain significance. amainly by TTE, but also consider CMR or CCT if the aortic root/ascending aorta are not properly visualized.
ESC Guidelines 3639
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.103
10.1.1.2 Medical treatment
In the absence of clinical trials, a pragmatic approach in a shared-decision model is adopted regarding TS medical treatment. Adoption of the strategy for inhibition of aortic growth with BBs and/or ARBs as in MFS may be considered. Hypertension should be treated according to general guidelines.300 Hormonal treatment with growth hormone (in childhood), sex (oestrogen and/or progesterone), and thyroid hormones needs to be discussed in a multidisciplinary team with the paediatrician and endocrinologist.1430–1434
10.1.1.3 Surgery of aortic aneurysms
Aortic aneurysm surgery in TS should be informed, individualized, and consider factors beyond aortic diameter (indexed). These include BAV, coarctation, uncontrolled hypertension (despite more than three classes of antihypertensive drugs), rapid aortic growth (≥3 mm per year) and planned pregnancy. 10.1.1.4. Pregnancy and physical exercise Turner syndrome often involves fertility challenges, but assisted reproductive therapy has increased pregnancy rates. However, pregnancy in TS can elevate the risk of AD, particularly with additional risk factors (Figure 40). Recent studies suggest improved pregnancy outcomes due to better guideline adherence.1435,1436 Prophylactic aortic root surgery in women with TS contemplating pregnancy is recommended when the ASI reaches 25 mm/m2.1337 These decisions should be made by an expert team in a shared-decision process.
Physical exercise has a beneficial impact on CVD risk and HRQoL in TS.1437 Structural congenital heart defects and aortic diameters (ASI, AHI and z-score) (Figure 40) need to be considered in the recommendations on the level of sports practice.1418
ASI AHI Z-score
Risk group Low Moderate Moderate Moderate High High
<20 mm/m2 ≥20–<23 mm/m2 ≥23–25 mm/m2 >25 mm/m2
>25 mm/m
>4
≥23–25 mm/m ≥20–<23 mm/m <20 mm/m
3.5–4 23 mm/m2 >23 mm/m2
>23 mm/m 23 mm/m
- - >3.5 -
Every 5–10 years: Cardiology evaluation and
TTEb Every 3–5
years: Cardiology evaluation and
TTEb Every 2–3
years: Cardiology evaluation and
TTEb
Every year: Cardiology evaluation and
TTEb Consider
surgery (Class IIb) Consider
surgery (Class IIa)
None of CoA, BAV, HTNa CoA, BAV, HTNa or aortic growth ≥3 mm/year
Figure 40 Algorithm for surveillance in women (≥15 years) with Turner syndrome. AHI, aortic height index (ratio of aortic diameter [mm] to height [m]); ASI, aortic size index (ratio of aortic diameter [mm] to BSA [m2]); BAV, bicuspid aortic valve; BSA, body surface area; CCT, Cardiovascular Computed Tomography; CMR, cardiovascular magnetic resonance; CoA, coarctation of the aorta; HTN, arterial hypertension; TTE, transthoracic echocardiography. aHTN: arterial hypertension, not under control despite more than three classes of antihypertensive drugs. bCMR (preferably) or CCT if inadequate visualization of the ascending aorta.
Recommendation Table 58 — Recommendations for aortic surgery in women with Turner syndrome
Recommendations Classa Levelb
Elective surgery for aneurysms of the aortic root and/ or ascending aorta should be considered in women with TS who are ≥15 years of age, have an ascending ASI >23 mm/m2, an AHI >23 mm/m, a z-score >3.5, and have associated risk factors for aortic dissectionc or are planning pregnancy.70,1417,1421 IIa C
Continued Elective surgery for aneurysms of the aortic root and/
or ascending aorta may be considered for women with TS who are ≥15 years of age, have an ascending ASI >25 mm/m2, an AHI >25 mm/m, a z-score >4, and who do not have associated risk factors for aortic dissectionc.70,1417,1421 IIb C © ESC 2024
AHI, aortic height index (ratio of aortic diameter [mm] to height [m]); ASI, aortic size index (ratio of aortic diameter [mm] to BSA [m2]); TS, Turner syndrome. aClass of recommendation. bLevel of evidence. cBicuspid aortic valve, elongation of the transverse aorta, coarctation of the aorta, and/or uncontrolled hypertension (despite more than three classes of antihypertensive drugs). See Figure 40. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.104
10.1.2 Vascular Ehlers–Danlos syndrome
10.1.2.1. Diagnosis, clinical presentation, and natural history Vascular Ehlers–Danlos syndrome is a rare (prevalence of 1/50 000 to 1/200 000) autosomal dominant disease caused by pathogenic variants in the COL3A1 gene, which encodes the pro-alpha1 chains of type III procollagen. The most common COL3A1 variants provoke a disruption in the assembly of type III collagen fibrils, causing an important loss of mechanical strength of arteries and other hollow organs, especially the bowel and uterus.1438 Identification of a causal COL3A1 variant is a requirement for the diagnosis of vEDS.1439 vEDS is the most severe form of Ehlers–Danlos syndrome because of its clinical life-threatening vascular complications, making early identification and a thorough family inquiry particularly crucial. Clinical complications may start during adolescence and repeat at unpredictable time intervals. The most common complications involve medium-sized arteries: dissections, aneurysms, arterial ruptures, and arteriovenous fistulas. AD (both type A and B) occurs in up to 10% of patients.1440 Prognosis depends on the type of COL3A1 variant, with null variants (no gene product or absence of function) showing a better outcome.1441 The rate of recurrence of organic complications in patients with vEDS is 1.6 events per 5 year period. Life expectancy is reduced to an average of 51 years.1442
10.1.2.2 Surveillance and imaging
Management of vEDS is complex and requires a multidisciplinary approach. Recommendations include: lifestyle modification to minimize injury and risk of vessel/organ rupture, identification of a care team, individualized emergency care plans, maintaining BP in the normal range, aggressive hypertension treatment, and annual surveillance of the vascular tree by DUS, CCT (low radiation alternatives), or CMR (if feasible).1439 A recent survey among European expert centres indicated that arterial monitoring is standard clinical practice and that frequency of follow-up should be adapted individually.1443 The prognosis improves when patients are properly managed.1441
10.1.2.3 Medical treatment
Medical management is based on optimal BP control. Celiprolol, a BB with vasodilatory properties, has been shown to reduce vascular morbidity in two retrospective studies1441,1444 and one randomized, openlabel trial.1445 There is no consensus about the age at which to start treatment, but starting after 10 years of age is considered reasonable by many experts. 10.1.2.4 Surgical treatment
Acute, unexplained pain requires urgent imaging to exclude arterial rupture. Acute arterial complications usually require hospitalization and a conservative approach in most cases. Interventional vascular or intestinal procedures are limited to vital risk. Procedures requiring organ inflation should be avoided or performed with extreme caution. There are no clear recommendations regarding aortic/arterial diameters at which to intervene in patients with vEDS. Thus, decisions need to be made on a case-by-case basis.
10.1.2.5 Pregnancy
Pregnancy in vEDS incurs a risk of (fatal) arterial and uterine complications. Pregnancy does not appear to affect overall mortality compared with nulliparous vEDS women.1446 However, patients need to be engaged in a shared-decision process, informed by vascular status and underlying variant type.
10.1.3 Marfan syndrome
10.1.3.1. Diagnosis, clinical presentation, and natural history Marfan syndrome, the most common syndromic HTAD condition (prevalence of 1/5000–1/10 000), arises from pathogenic fibrillin-1 gene (FBN1) variants. Beyond the CV system, multiple organ systems are often affected, including the eyes and skeleton. Diagnosis relies on recognizing clinical features in line with the revised Ghent nosology, which includes genetic testing.1447 Aortic aneurysm and dissection involving the aortic root are a hallmark of the disease. Less commonly, the descending thoracic and abdominal aorta may be involved. With increasing survival and age in MFS, the prevalence of TBAD seems to be increasing, exceeding type A dissection rates in recent reports.1448,1449 TBAD will often occur at diameters below surgical thresholds. Previous aortic root replacement, mitral valve surgery, and a longer life span are associated with TBAD. Additional CV features include mitral valve prolapse, extra-aortic arterial involvement, myocardial dysfunction, and arrhythmias.1393,1450–1452 Thanks to improved diagnosis in earlier stages, proper management including surveillance, medical treatment, and timely prophylactic aortic surgery, life expectancy in MFS patients is now approaching that of the general population.1416,1453 The major determinant of TAAD is the aortic root diameter, with increased risk of rupture when it exceeds 50 mm.1454 Other risk factors include family history of AAS at low diameter, aortic root growth rate (annualized growth rate ≥3 mm or more in adults), pregnancy, and hypertension (hypertension persisting notwithstanding three or more antihypertensive medications prescribed by a physician with experience in hypertension treatment). Increasing evidence for variant-based differences in aortic risk is emerging and may be considered.1413,1416
10.1.3.2 Imaging surveillance
Transthoracic echocardiography is the appropriate imaging modality for initial evaluation and follow-up of the aortic root in most patients and allows evaluation of the distal segments of the aorta in many. Also, TTE is useful for assessing mitral and aortic valve regurgitation, mitral valve prolapse with/out annular disjunction, and LV dysfunction. In some cases (especially when pectus abnormalities are present) TTE windows may be suboptimal, and CMR (preferably)/CCT may be preferred. Periodical evaluation of the global aorta and peripheral arteries with CMR/CCT and DUS (every 3–5 years based on the patient’s evolution) is indicated since they also present a higher incidence of
Recommendation Table 59 — Recommendations for medical treatment in patients with vascular Ehlers– Danlos syndrome (see also Evidence Table 13)
Recommendations Classa Levelb
In patients with vEDS, regular vascular surveillance of the aorta and peripheral arteries by DUS, CCT, or CMR is recommended.1439,1443 I C Treatment with celiprolol should be considered in patients with vEDS.1441,1444,1445 IIa B © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; DUS, duplex ultrasound; vEDS, vascular Ehlers–Danlos syndrome. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3641
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.105
peripheral aneurysms,1455 which are associated with more aggressive forms of the disease.1393 CMR is preferred over CCT to avoid radiation exposure; however, its use should be adapted to local availability/expertise. Additionally, CMR allows evaluation of biomechanical and haemodynamic parameters that can be useful in risk stratification.181,1456,1457 Given its superior spatial resolution, CCT may be recommended for pre-operative planning and in cases of measurement inconsistency. Imaging of intracerebral vessels is indicated in cases of symptoms and/or clinical manifestations of aneurysms/rupture. Recommendations for imaging surveillance are illustrated in Figure 41 and should be adjusted to the individual patient, taking the history and presence of abnormalities during preceding studies into account.
10.1.3.3 Medical treatment
Medical treatment is described in Recommendation Table 61. Some caution may be warranted with the use of CCBs: these have shown an increased aortic risk in a mouse model and in retrospective case control studies,1460 and alternatives are preferred for hypertension treatment. 10.1.3.4 Aortic surgery
Open surgery is preferred over endovascular procedures in patients with MFS. Endovascular procedures may be considered in selected cases in emergency settings and/or in centres with a high level of expertise.1465 The thresholds for aortic root surgery need to take additional risk factors, as well as the expertise of the team, into account.1466
Recommendation Table 60 — Recommendations for vascular imaging in Marfan syndrome
Recommendations Classa Levelb
In patients with MFS, TTE is recommended:70,171,1458,1459 • At least annually in patients with an aortic root
diameter <45 mm in the absence of additional risk factorsc • At least every 6 months in patients with an aortic
root diameter <45 mm in the presence of additional risk factorsc • At least every 6–12 months in patients with an
aortic root diameter ≥45 mm in the absence of additional risk factorsc I C In patients without previous aortic surgery, complete peripheral vascular and thoracoabdominal aorta imaging by CMR or CCT and DUS is recommended at the first evaluation, and subsequently every 3–5 years if stable.70,1455,1459 I C In patients with MFS who have undergone aortic root replacement, surveillance imaging of the thoracic aorta by CMR (or CCT) is recommended at least every 3 years.70,1458 I C © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; DUS, duplex ultrasound; MFS, Marfan syndrome; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. cRisk factors: aortic root diameter >40 to ≤45 mm and family history of aortic dissection at small aortic dimensions (i.e. <50 mm); resistant hypertension (hypertension persisting notwithstanding three or more antihypertensive medications prescribed by a physician with experience in hypertension treatment); and rapid growth of the aorta (annualized growth rate ≥3 mm or more in adults). Recommendation Table 62 — Recommendations for aortic surgery in Marfan syndrome
Recommendations Classa Levelb
Surgery is indicated in patients with MFS who have aortic root disease with a maximal aortic sinus diameter ≥50 mm.70,172,1466–1468 I B Surgery to replace the aortic root and ascending aorta, using the valve-sparing surgery technique, is recommended in patients with MFS or related HTAD with aortic root dilatation when anatomical features of the valve allow its preservation and the surgeon has specific expertise.70,1466,1469 I B Surgery should be considered in patients with MFS who have an aortic root aneurysm with a maximal aortic sinus diameter ≥45 mm and additional risk factors.c,1467,1469 IIa C In patients with MFS and an aneurysm of the ascending aorta, aortic arch, descending thoracic aorta, or abdominal aorta of ≥50 mm, surgical replacement of the aneurysmal segment by a surgeon with specific expertise should be considered.1467,1469 IIa C © ESC 2024
HTAD, heritable thoracic aortic disease; MFS, Marfan syndrome. aClass of recommendation. bLevel of evidence. cFamily history of aortic dissection at small aortic dimensions (i.e. <50 mm); resistant hypertension (hypertension persisting notwithstanding three or more antihypertensive medications prescribed by a physician with experience in hypertension treatment); and rapid growth of the aorta (annualized growth rate ≥3 mm or more in adults).
Recommendation Table 61 — Recommendations for medical treatment in Marfan syndrome (see also Evidence Table 14)
Recommendations Classa Levelb
In patients with MFS, treatment with either a BB or an ARB, in maximally tolerated doses (unless contraindicated), is recommended to reduce the rate of aortic dilatation.1461,1462 I A In patients with MFS, the use of both a BB and an ARB, in maximally tolerated doses (unless contraindicated), should be considered to reduce the rate of aortic dilatation.1463,1464 IIa A © ESC 2024
ARB, angiotensin receptor blocker; BB, beta-blocker; MFS, Marfan syndrome. aClass of recommendation. bLevel of evidence. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.106
10.1.3.5 Pregnancy and physical exercise
In pregnant MFS women, the risk of AD increases up to eight times relative to the general population.1470 The risk for TAAD is determined by the aortic diameter, but type B dissections tend to occur even more commonly and may occur without prior dilatation.1470,1471 Patients should be aware of the persisting risk of TBAD after aortic root replacement.1471 Women unaware of the diagnosis are at the highest risk of dissection.1470–1472 The Registry Of Pregnancy And Cardiac disease (ROPAC) indicates that women managed according to guidelines are at low risk of pregnancy-related complications and major effects of BBs on foetal growth were not shown, although this needs to be carefully monitored.70,1337,1435,1471,1472
Exercise is potentially associated with an increased risk of aortic dilatation and AAD. It is recommended to individualize physical activity in MFS based on aortic diameter, family history of dissection or sudden death, and pre-existing fitness status.71 Although competitive sports are contraindicated, moderate aerobic exercise is recommended with a level of intensity based on aortic diameters.71 Two studies1481,1482 showed that mild-moderate dynamic exercise improved aortic wall structure and function and reduced aortic growth rate in MFS mouse models. Recent data in MFS children and young adults indicate that adhering to daily physical exercise (10 000 steps a day) had a beneficial effect on aortic root growth.1483 Although a limited number of clinical studies have evaluated physical activity rehabilitation programmes, two studies1484,1485 evidenced that physical activity, up to a moderate specific intensity, may be recommended. Thus, although physical activity poses a dilemma, individualized adapted programmes are most likely successful in encouraging exercise in MFS.
10.1.4 Other syndromic and non-syndromic
heritable thoracic aortic diseases and/or arterial disorders Main clinical and genetic data of known syndromic and non-syndromic HTAD entities are summarized in the Supplementary data online, Table S5. The two most prevalent diseases for each entity include Loeys–Dietz syndrome and ACTA2-related HTAD, respectively. Given the rarity of these entities, specific recommendations regarding surveillance and treatment are lacking and largely adopted from the recommendations for MFS. Some disease-specific recommendations are mentioned below.
10.1.4.1 Loeys–Dietz syndrome
10.1.4.1.1. Diagnosis, clinical presentation, and natural evolution. The spectrum of clinical presentations in Loeys–Dietz syndrome is very wide. Some patients fulfil criteria for MFS,1447 while some features such as bifid uvula and hypertelorism are very specific to the disease. Clinical manifestations are listed in the Supplementary data online, Table S5. There is a tendency for AD and rupture at lower vessel dimensions than is typically seen in other similar conditions.1390,1487 Pathogenic variants in six genes (TGFBR1 and TGFBR2, TGFB2 and TGFB3, SMAD2 and SMAD3), all encoding components of the TGF-ß signalling pathway, cause Loeys–Dietz syndrome. Differences in clinical manifestations and aortic outcome according to the underlying gene and the extent of extra-aortic features have been reported and need to be considered in surveillance and defining thresholds for surgery.1388,1390,1391 Surveillance in Loeys–Dietz syndrome is described in Recommendation Table 65 and Figure 41. Although the indication for surgery must be considered according to the underlying genetic defect and the presence of risk factors (Recommendation Table 66 and Figure 42), a 45 mm aortic diameter threshold should be considered (≥40 mm in cases of associated high-risk features).
Recommendation Table 63 — Recommendations for pregnancy in women with Marfan syndrome
Recommendations Classa Levelb
It is recommended that all women with MFS: • Have a pre-conception evaluation to address the risks of maternal CV and other complications • Have follow-up in a centre with access to a pregnancy heart and vessel team.1473 I C It is recommended that couples in which a partner has or is at risk for HTAD be offered pre-conception genetic counselling. I C Imaging of the whole aorta (by CMR/CCT) is recommended prior to pregnancy. I C Follow-up during pregnancy is recommended with a frequency determined by aortic diameter and growth.1337,1474,1475 I C Intake of BBs during pregnancy is recommended.1476 I C Prophylactic aortic root surgery is recommended in women desiring pregnancy with aortic diameters >45 mm.1435,1472 I C Prophylactic aortic root surgery may be considered in women desiring pregnancy with aortic diameters of 40–45 mm.1472,1475,1477 IIb C ARBs are not recommended during pregnancy.1478–1480 III B © ESC 2024
ARBs, angiotensin receptor blockers; BBs, beta-blockers; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; CV, cardiovascular; HTAD, heritable thoracic aortic disease; MFS, Marfan syndrome. aClass of recommendation. bLevel of evidence. Recommendation Table 64 — Recommendations for physical exercise in patients with Marfan syndrome
Recommendations Classa Levelb
It is recommended to individualize physical activity in patients with MFS based on aortic diameter, family history of aortic dissection, and pre-existing fitness. I C Regular moderate aerobic exercise with a level of intensity informed by aortic diameter is recommended in most patients with MFS. I C For patients who present with aortic dissection and/ or have undergone aortic surgery, post-operative cardiac rehabilitation aiming at improving both physical and mental health should be considered.73,1483,1484,1486 IIa B © ESC 2024
MFS, Marfan syndrome. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3643
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.107
CCTa Surgery if risk factorsb
(Class IIa)
Aortic root/ ascending diameter (mm)
Marfan/FBN1
Loeys-Dietz/ TGF-ß genes
ACTA2/ SMC genes
TTE Follow-up Every 6–12 months Surgery (Class I)
CMR/CCT head-to-pelvis every 1–3 years
Baseline CMR/CCT
Baseline CMR/CCT
Baseline CMR/CCT
TTE yearly
TTE yearly CMR/CCT every 3–5 years
CMR/CCT every 3–5 years CCTa
CCTa
CCTa
35 mm 40 mm
42 mm 45 mm 50 mm
CCTa Surgery if risk factorsb
(Class IIb)
Every 6–12 months
TTE yearly
Surgery (Class IIa)
Surgery (Class IIa)
Figure 41 Algorithm for imaging surveillance in patients with syndromic and non-syndromic heritable thoracic aortic disease. CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; DUS, duplex ultrasound; HTAD, heritable thoracic aortic disease; SMC, smoth muscle cell; TTE, transthoracic echocardiography. aPre-surgical CCT. bSee respective tables of recommendations for aortic surgery in Marfan (Table 62) and Loeys-Dietz syndrome (Table 66).
Recommendation Table 66 — Recommendations for aortic root surgery in Loeys–Dietz syndrome
Recommendations Classa Levelb
Aortic root replacement should be considered for patients with Loeys–Dietz syndrome if the aortic root diameter exceeds 45 mm.1388,1390,1489–1492 IIa C It may be considered to adjust the threshold for surgery according to the underlying gene, taking associated risk featuresc into account.1391 IIb C © ESC 2024 aClass of recommendation. bLevel of evidence. cHigh-risk features include certain specific pathogenic variants; women with TGFBR2 variants and small body size; severe extra-aortic features; family history of aortic dissection (especially at young age or relatively small aortic diameter); and aortic growth rate ≥3 mm per year.
Recommendation Table 65 — Recommendations for imaging follow-up in Loeys–Dietz syndrome
Recommendations Classa Levelb
In patients with Loeys–Dietz syndrome, TTE at baseline and subsequently every 6–12 months, depending on aortic diameter and growth,c is recommended.70,1390,1488 I C In patients with Loeys–Dietz syndrome, a baseline arterial imaging study from head to pelvis with CMR or CCT and subsequent surveillance with CMR or CCT or DUS every 1–3 years is recommended.70,1488 I C © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; DUS, duplex ultrasound; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. cMore frequent imaging if aortic root/ascending diameter >42 mm and aortic growth rate ≥3 mm per year. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.108
10.1.4.2 ACTA2-related heritable thoracic aortic disease
Pathogenic variants in the ACTA2 gene, encoding for smooth musclespecific alpha-actin (a critical component of the vascular smooth muscle cell contractile apparatus), lead to aortic aneurysms and dissections in non-syndromic patients.1496 Patients primarily present with type A or B aortic dissection, and with aneurysms that involve the root and/or ascending aorta. A subset of pathogenic variants predisposes to occlusive vascular diseases.1497 Surveillance is summarized in Recommendation Table 67 and Figure 41. TAAD may occur at aortic diameters <45 mm, and consideration of surgery at diameters <45 mm should be informed by the presence of additional clinical and genetic risk factors.1410 Genetic and imaging cascade screening of first-degree family members is an essential element of care, as treatable disease may otherwise be missed in family members—with fatal consequences.
High risk features include:
Known high risk genetic variants (R528H/C in TGFBR2) Women with TGFBR2 variants and small body size Severe extra-aortic features
Aortic root surgery if risk factors
(see box below) Aortic root
surgery
Family history of aortic dissection (especially at young age or relatively small aortic diameter) Aortic growth rate ≥3mm per year
TGFBR2a,b
35 mm 40 mm 45 mm 50 mm 55 mm
TGFBR1a TGFBR2a
TGFBR1a
Consider aortic root
surgery Consider aortic root
surgery
SMAD3c,d
TGFB2e,f,g TGFB3h,i
Figure 42 Suggested thresholds for prophylactic aortic root/ascending replacement in Loeys–Dietz syndrome. From a1388, b1391, c1492, d1491, e1490, f1489, g1493, h1494, i1495.
Recommendation Table 67 — Recommendations for imaging and surgery in ACTA2-related heritable thoracic aortic disease (see also Evidence Table 11)
Recommendations Classa Levelb
Annual monitoring of the aortic root/ascending aorta with TTE to evaluate aortic root/ascending aorta enlargement is recommended.1498 I C Imaging of the aorta with CMR/CCT every 3–5 years is recommended.1498 I C Prophylactic aortic root surgery should be considered with an aortic diameter ≥45 mm, or lower in cases with other risk factors.c,1499 IIa C © ESC 2024
CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. cRisk factors for aortic dissection: family history of dissection with no or minimal dilatation or young age; rapid growth ≥3 mm per year.
ESC Guidelines 3645
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.109
10.2 Aortic disease associated with
bicuspid aortic valves Bicuspid aortic valves, the most common congenital heart defect (0.5%–2% of live births), besides being a risk factor for aortic valve disease, is associated with a peculiar form of aortopathy, characterized by morphological and clinical heterogeneity (bicuspid valvulo-aortopathy). Its inheritance is high, with autosomal dominant transmission of BAV in a minority of cases, but no single-gene model clearly explaining BAV inheritance.1500–1502 Several genes, generally implicated in embryogenesis and cell differentiation, have been associated with BAV/BAV-related aortopathy, but each of them explained <5% of cases.1503–1507 Therefore,
1 2a 2b Ascending phenotype
(70–75%)
Fused BAV (90–95% of BAV) 3 phenotypes
2-sinus BAV (5–7% of BAV) 2 phenotypes
Partial-fusion BAV - short fusion of 1 commisure
Right - left cusp fusion
(70–80%) Right - non cusp fusion
(20–30%) Left - non cusp fusion
(3–6%)
Root phenotype
(15–20%)
Extended phenotype
(5–10%)
BAV morphologies Aortic phenotypes
L A A
P P L
Laterolateral Anteroposterior
Figure 43 Bicuspid aortic valve, valvulo-aortopathy nomenclature. Modified from Michelena et al.1510 A, anterior; BAV, bicuspid aortic valve; L, lateral; P, posterior. Although preferential associations exist, each of the three valve types—‘fused BAV’, ‘2-sinus BAV’, and ‘partial-fusion BAV’—can be variably associated with dilatation predominantly located at the sinuses of Valsalva (‘root phenotype’, 15%–20%) or at the tubular (supra-coronary) tract (‘ascending phenotype’, 70%–75%). A minor proportion of patients present with equal dilatation of the sinusal and tubular segments or ascending dilatation extending into the proximal arch (‘extended phenotype’, 5%–10%). Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.110
genetic testing is not indicated for isolated BAV disease, but reserved for patients with syndromic features, family history of aortic disease, or aneurysms/dissections of medium-sized arteries other than the thoracic aorta, and may be considered in patients with the root phenotype.1389,1508,1509 We recommend adopting a new international consensus nomenclature and classification, established by a panel of experts, to replace the previous various concurrent nomenclatures used1510 (Figure 43). Aneurysm prevalence reaches 40% in clinical series and 0.85 per 100 patient-years in population studies. AAEs are rare, but 8- to 10-fold more frequent than in the general population.1001,1511 The longest available follow-up of BAV subjects was recently reported,1512 showing a total lifetime morbidity burden as high as 86%, a predominant part of which was driven by valve-related complications (aortic stenosis, endocarditis, HF). When a BAV is first detected, a complete study of the thoracic aorta is necessary; vice versa, in every patient with ascending aortic dilatation, valve morphology should be ascertained.70,969 When TTE detects BAV-associated aortic dilatation, CCT or CMR is recommended to confirm measurements, exclude coarctation, and record baseline diameters at different levels for subsequent periodic assessments.137,1001 Surveillance by TTE becomes necessary when the maximum diameter exceeds 40 mm. In mixed tricuspid aortic valve (TAV) and BAV series, AAEs occurred in 2/10 000 patient-years with a diameter >40 mm (vs. 0.1–0.3/10 000 patient-years in the general population)894 (Figure 43). Considering average aortic diameter growth of 0.2–0.6 mm per year,893,1513 once fast progression is excluded, follow-up can be scheduled every 2–3 years (according to risk profile). In 5%–15% of cases, BAV patients have at least one FDR with either BAV or ascending aortic dilatation; root phenotype and aortic regurgitation in the proband predict ascending dilatation in FDRs.1514 FDR screening is considered costeffective, but the age at which relatives should undergo TTE remains to be determined.1515,1516 A diameter exceeding 55 mm at any level mandates surgery.70,969,1001 However, the historically known relation between diameter and acute complications has been recently reappraised. Both in large mixed153 and purely BAV series,981 an ascending diameter of about 52 mm already marked an AAE risk increase from ∼1% to 4%–5%. Additionally, early post-operative mortality for elective surgery of the proximal aorta ranges today between 0.25% and 2%.980,981 Therefore, aortic surgery in low surgical risk (<3%) patients with an ascending diameter >52 mm implies a lower risk than observed in the natural history of the disease. For aortic root dilatation in BAV patients, the ‘hinge point’ was at 50 mm;981 this phenotype is associated with faster growth rate,893 higher risk of events following isolated aortic valve replacement,1517 worse survival if not operated,1518 and higher risk of acute TAAD.976,1519 Surgery should be considered when the diameter is ≥50 mm in selected ascending phenotype patients (Figures 23, 24 and 43).70,1001 Among those factors, family history of AAEs, poorly controlled hypertension, aortic coarctation, and rapid (≥3 mm per year) diameter growth should be noted. Surgery at >50 mm may also be considered in a shared decision with the patient, taking lifestyle and psychological factors into consideration,70,1001 since 50 mm should correspond to an approximately 10-fold increase in the risk of AAEs.894 In a study of patients with aortic diameter ≥40 mm, those with diameters of 50 mm faced a 1% risk of AAEs within 5 years, compared with 0.1% for those with 40 mm diameters, explaining the 10-fold difference; however, this study did not exclusively involve BAV patients.894
Another recent study1520 specifically focused on BAV patients found a 0.4% incidence of AAEs per patient-year for diameters above 50 mm, in contrast to the general BAV population’s 0.03% incidence.1521 Previous guidelines also suggested aortic repair for a cross-sectional area-to-height ratio (CSA/h) >10 cm2/m;70 nevertheless, more recently, it has been suggested that the CSA/h threshold for the ascending tract in BAV should be 13 cm2/m.981 For the average height of male and female Europeans (1.8 m and 1.67 m, respectively), a CSA/h of 10 cm2/m would correspond to a diameter of 48 mm or 46 mm, respectively, whereas 13 cm2/m means 54 mm or 53 mm. It is reasonable to refer to the 13 cm2/m CSA/h cut-off for ascending aortic repair, especially in individuals ≤1.69 m in height (since 13 cm2/m corresponds to ≤52 mm diameter). Recently, besides dilatation, aortic elongation is also considered a risk factor,974 and a curvilinear length >11.5 cm at the vessel’s centreline increases the yearly risk of AAEs.155 Age is another factor to consider: at 50 years, a 40 mm ascending aorta corresponds to the upper normal limit for patients with large body size,149 and therefore the same diameter at a higher age could imply a lower risk of AAEs.
Recommendation Table 68 — Recommendations for bicuspid aortic valve-associated aortopathy management
Recommendations Classa Levelb
When a BAV is first diagnosed, initial TTE to assess diameters of the aorta at several levels is recommended.1001,1510,1522 I B Surgery for bicuspid aortopathy is recommended when the maximum aortic diameter is ≥55 mm.70,172,899,969,1001 I B Surgery for bicuspid aortopathy of the root phenotypec is recommended when the maximum aortic diameter is ≥50 mm.70,893,981,986,1001,1519,1523 I B CCT or CMR of the entire thoracic aorta is recommended at first diagnosis and when important discrepancies in measurements are found between subsequent TTE controls during surveillance, or when the diameter of the aorta exceeds 45 mm.1001,1510 I C Screening by TTE in FDRs of BAV patients with root phenotypec aortopathy and/or isolated aortic regurgitation is recommended.1001,1510,1514 I C Surveillance serial imaging by TTE is recommended in BAV patients with a maximum aortic diameter >40 mm, either with no indication for surgery or after isolated aortic valve surgery, after 1 year, then if stability is observed, every 2–3 years.70,1001 I C Screening by TTE in FDRs of all BAV patients should be considered.70,1001,1500,1510,1515 IIa B In patients with low surgical risk, surgery for bicuspid aortopathy of ascending phenotyped should be considered when the maximum aortic diameter is >52 mm.153,172,981 IIa B
Continued
ESC Guidelines 3647
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.111
10.3 Coarctation of the aorta and aortic
arch variants 10.3.1. Coarctation of the aorta This topic is extensively discussed in the ESC 2020 Guidelines for the management of adult congenital heart disease.1468 Coarctation of the aorta (CoA) manifests as a discrete stenosis or a hypoplastic segment typically located at the insertion of the ductus arteriosus. More distal locations are known as mid-aortic syndrome and require dedicated management.1524 Associated lesions include BAV (up to 50%–85%), intracerebral aneurysms (10%), and ascending aortic aneurysms.1525,1526 CoA may be associated with syndromes such as TS. Research indicates that up to 12.6% of females diagnosed with CoA also have TS, and coarctation is observed in 7%–18% of patients with TS.1417,1468,1527
10.3.1.1 Diagnostic work-up
Mild cases of CoA may only become evident in adulthood. Symptoms reflect pre-stenotic hypertension (e.g. headache, nosebleeds) and poststenotic hypoperfusion (e.g. abdominal angina and claudication). The natural course is largely driven by hypertension-related complications, including HF, intracranial haemorrhage, premature coronary/cerebral artery disease, and aortic rupture/dissection.1528 Presently, there is no evidence supporting screening for intracerebral aneurysms in asymptomatic patients. A systolic non-invasive gradient between upper and lower extremities, an abnormal ABI, or an invasive peak-to-peak gradient ≥20 mmHg indicates significant CoA. In the presence of collaterals or decreased LV function, gradients or ABI may underestimate severity. A diastolic tail in the DTA or abdominal diastolic antegrade flow by TTE is suggestive of significant narrowing. Criteria to consider significant CoA are listed in Figure 44. TTE is also useful to detect LV hypertrophy, which is a marker of disease. CMR and CCT are the preferred imaging techniques, depicting the narrowing as well as the surrounding anatomy, necessary for interventional decision-making.
10.3.1.2 Treatment and follow-up
In native CoA and re-coarctation (Figure 44) covered stenting is the firstchoice treatment. Interposition of a tube graft is the preferred surgical therapy if stenting is less suitable.1529 Hypertension remains an important complication, even after successful treatment, and is more common when the initial repair is performed in adulthood.1528 Right arm 24 h ambulatory BP measurement or exercise tests better detect hypertension.1530,1531 All CoA patients require lifelong follow-up.1532 Imaging of the aorta with CMR/CCT every 3–5 years, adjusted to previous imaging findings and type of intervention, is required to document post-repair or post-interventional complications (such as re-coarctation). Patch repairs are at particular risk of repair-site para-anastomotic aneurysms or pseudo-aneurysms, the latter possibly occurring following interposition grafts as well.1533
Recommendation Table 69 — Recommendations for evaluation and medical treatment of patients with coarctation of the aorta
Recommendations Classa Levelb
In patients with native or repaired coarctation, lifelong follow-up is recommended, including regular imaging of the aorta with CCT/CMR every 3–5 years (adapted to clinical status and previous imaging findings).1534,1535 I B Coarctation or re-coarctation repair (either surgical or endovascular) is indicated in patients with hypertension with an increased non-invasive gradient between the upper and lower limbs (decreased ABI) confirmed with invasive measurement (peak-to-peak >20 mmHg), with a preference for stenting when technically feasible.1536 I C In patients with coarctation, BP measurements at both arms and one lower extremity are recommended. I C It is recommended to treat hypertension in patients with coarctation according to ESC hypertension guidelines.300 I C Endovascular treatment should be considered in patients with hypertension with >50% narrowing relative to the aortic diameter at the diaphragm, even if the invasive peak-to-peak gradient is <20 mmHg, when technically feasible.1537 IIa C Endovascular treatment should be considered in normotensive patients with an increased non-invasive gradient confirmed with invasive peak-to-peak gradient >20 mmHg, when technically feasible.1468 IIa C © ESC 2024
ABI, ankle–brachial index; BP, blood pressure; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; ESC, European Society of Cardiology. aClass of recommendation. bLevel of evidence.
In patients with low surgical risk and ascending phenotype bicuspid aortopathy, surgery should be considered at a maximum diameter ≥50 mm if any of the following is the case:70,153,155,981,1001 • Age <50 years • Shorter staturee • Ascending aortic length ≥11 cmf • Aortic diameter growth rate ≥3 mm per yearg • Family history of acute aortic syndrome • Aortic coarctation • Resistant hypertensionh • Concomitant non-aortic-valve cardiac surgery • Desire for pregnancy IIa C Surgery for bicuspid aortopathy in patients undergoing aortic valve surgery should be considered at a root or ascending diameter ≥45 mm.70,172,969 IIa C © ESC 2024
BAV, bicuspid aortic valve; BP, blood pressure; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; CSA/h, cross-sectional area-to-height ratio; FDRs, first-degree relatives; TTE, transthoracic echocardiography. aClass of recommendation. bLevel of evidence. cRoot phenotype = aortic dilatation with sinus diameter > tubular diameter. dAscending phenotype = aortic dilatation with tubular diameter > sinus diameter. ePatient height between 1.50 and 1.69 m (yielding a CSA/h ratio >13 cm2/m). fCurvilinear distance at aortic centreline between the ventriculo-aortic junction and the origin of the innominate artery. gIn order to ascertain real rapid growth, side-by-side re-evaluation of images obtained with the same modality and technique should be performed. hHypertension persisting notwithstanding three or more antihypertensive medications prescribed by a physician with experience in hypertension treatment, including diuretics. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.112
Y N
≥20 mmHg <20 mmHg
Perform catheterization (Re)coarctation
not likely
Surveillance: TTE every year and CMR or CCT 3–5 years
BP measurement and investigationa
Intervention
(Class IIa)
Intervention
(Class IIa)
Intervention
(Class I) BP measurement and investigationa
≥50% narrowing on any imaging modality
HTN HTN
N Y N
Y
N
Y
Suspicion of significant (re)coarctation: any of the following:
Non invasive (right arm-to-leg) BP gradient >20 mmHg >50% narrowing on any imaging modality Abdominal antegrade diastolic flow on DUS Diastolic run off in the descending thoracic aorta on DUS Mean gradient >20 mmHg across the CoA region on DUS Collateral flow >30% on phase contrast CMR
A A
B
B
C C
E E
D D
F F
D >35 mmHg peak gradient >20 mmHg mean gradient
Post CoAo
Pre CoAo
mL/s
>30% increase
Figure 44 Criteria for significant coarctation/re-coarctation of the aorta and management algorithm. BP, blood pressure; CCT, cardiovascular computed tomography; CMR, cardiovascular magnetic resonance; CoA, coarctation of the aorta; DUS, duplex ultrasound; HTN, hypertension; TTE, transthoracic echocardiography. aDiagnosis of hypertension may require confirmation with ambulatory BP measurement and should also be considered in cases of exercise-induced hypertension and/or left ventricular hypertrophy on TTE.
ESC Guidelines 3649
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.113
10.3.2 Aortic arch anatomic variants
A type I arch, where the three great vessels directly arise from the aorta, is the most common form, occurring in about 70% of the population. The type II (bovine) arch is the most frequent variant: type II-A (9% of the population) has the left common carotid artery arising from the innominate artery, and type II-B (13% of the population) has both the innominate and left common carotid arteries originating from a common point on the aortic arch.1538,1539 Limited data suggest that a bovine arch is associated with a higher risk of aortic dilation and aortic events/complications.1540,1541 These variations are important to report as they can impact specific medical procedures and diagnostic interpretations.
10.3.3 Aberrant subclavian artery and Kommerell’s
diverticulum The most common variant is the aberrant right subclavian artery, where the right subclavian artery arises as the last branch of the aortic arch, usually after the left subclavian artery, and often passes behind the oesophagus through the mediastinum, potentially causing dysphagia lusoria, respiratory symptoms, or recurrent laryngeal nerve palsy. The less common variant, the aberrant left subclavian artery, is typically associated with congenital heart defects, such as a right aortic arch. However, in adulthood, both variations are often incidental findings.1542 Kommerell’s diverticulum is a remnant of the fourth dorsal aortic arch due to incomplete regression, found in 20%–60% of those with an aberrant subclavian artery.1543 Surgical intervention is advised for a diverticulum orifice >30 mm or combined diverticulum and adjacent descending aorta diameter >50 mm, or both.1544 Successful repair has been described using open, endovascular, or hybrid approaches depending on anatomy, comorbidities, and expertise.1543 11 Polyvascular peripheral arterial
disease and peripheral arterial disease in patients with cardiac diseases
11.1 Polyvascular disease
Polyvascular disease is defined as the simultaneous presence of clinically relevant obstructive atherosclerotic lesions in at least two major arterial territories.
11.1.1 Epidemiology and prognosis
Approximately 1 in 4–6 patients with atherosclerosis have PVD (Figure 45).620,1545 According to the REACH registry, patients with PAD were most likely both to have PVD at baseline and to develop PVD over the observational period.1546,1547 PVD independently increases major CV event risk, roughly doubling it compared with single arterial bed symptoms.1547–1549 Event rates rise with the number of affected arterial beds.1546,1550
11.1.2 Screening for atherosclerosis in other arterial
territories Screening for PVD in atherosclerotic patients relies on medical history, clinical exam, and ABI measurement. If suspected, start with non-invasive DUS, followed by CTA/MRA if needed.1557 Assessing concurrent atherosclerosis in other vascular regions is detailed in Table 17.
CAD Carotid stenosis >70% PAD (ABI ≤0.90) RAS >70%
9% 5% 16% 4% 61%
39%
22%
18%
7% 15% 25%
70%
60%
40%
20%
0% 19%
14% 23%
10%
CAD Carotid stenosis >70% PAD (ABI ≤0.90)
Figure 45 Reported rate ranges of other localizations of atherosclerosis in patients with a specific arterial disease. The graph reports the rates of concomitant arterial diseases in patients presenting an arterial disease in one territory (e.g. in patients with CAD, 5%–9% of cases have concomitant carotid stenosis >70%). Adapted from 2017 ESC Guidelines on PAD.77,493,784,1549,1551–1556 ABI, ankle–brachial index; CAD, coronary artery disease; PAD, peripheral arterial disease; RAS, renal artery stenosis. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.114
11.1.2.1 Screening for coronary artery disease in patients with
symptomatic peripheral arterial disease The morbidity and mortality of patients with PAD is high due to CV complications. Given high CAD event rates in patients with PAD, CAD screening may be helpful to optimize medical treatment and is not intended to increase the rate of coronary interventions.431 Evaluation can be performed by stress testing or CCT; however, there is no evidence that systematic screening for CAD in stable PAD improves outcomes. Coronary angiography is less suitable due to invasiveness. In patients requiring lower-limb revascularization, CAD management should be based on the 2022 ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery.1080
11.1.2.2 Screening for peripheral arterial disease in patients with
coronary artery disease In high-risk CAD patients with three-vessel disease or recent ACS, systematic screening for multisite atherosclerotic disease through ABI and DUS of carotids, lower-extremity, and renal arteries did not improve outcomes.1563 However, a subgroup analysis of the COMPASS trial suggests potential benefits when adding vascular-dose rivaroxaban to aspirin in stable patients with CAD and PAD, raising the question of whether identifying PAD in stable CAD patients could be advantageous.429,1559 In patients undergoing CABG, the presence of concomitant PAD is associated with a three-fold risk of subsequent CV events after CABG.1560,1561 The GSV should be spared whenever possible, since the success of peripheral arterial revascularization in complex lesions is strongly associated with the availability of sufficient autologous venous segments.567,1564
11.1.2.3 Screening for coronary artery disease in patients with
carotid stenosis Due to the high prevalence of CAD among patients scheduled for elective CEA,1565,1566 pre-operative CAD screening, including coronary angiography, may be considered in suspected patients.1558 CAD requires prioritization of revascularization according to the patient’s clinical status and the severity of carotid disease and CAD. Coronary revascularization should generally be performed first; the exception is recently symptomatic patients with unstable neurological symptoms in whom carotid revascularization should be prioritized.680
11.1.2.4 Screening for carotid stenosis in patients with coronary
artery disease Carotid artery stenosis screening may be useful in patients undergoing elective CABG. Ischaemic stroke after CABG is multifactorial,1567 but also depends on the degree of carotid disease.1556 Two studies suggest that limiting DUS to patients with at least one risk factor (age >65 years, history of cerebrovascular disease, presence of a carotid bruit, multivessel CAD or PAD) identifies most patients with significant (≥70%) CS.1555,1562 Nevertheless, addition of CEA to CABG is unlikely to provide significant stroke reduction. In a study in patients with CAD with >80% CS undergoing staged or synchronous carotid procedures (two-thirds were neurologically asymptomatic and 73% had unilateral asymptomatic carotid stenosis), in-hospital stroke rates and 30 day mortality were similar in patients treated with CABG + CEA and in those treated with isolated CABG.1568 Another study suggests that selective use of DUS should be considered before CABG in patients with a history of neurological events or PAD.1569
11.1.3 Management of patients with polyvascular
disease Polyvascular disease requires proactive management of all modifiable risk factors through lifestyle changes and drug therapy. Scientific evidence suggests the benefit of intensified antithrombotic therapy, with no increase in risk of bleeding.1570 ILT offers comparable benefits for PVD patients and those with single arterial territory disease. However, the benefits of ILT in patients with PVD are not dependent on baseline LDL-C.1571 Revascularization should be reserved for symptomatic arterial territories, using the least invasive strategy in a multidisciplinary vascular team approach.
11.2 Peripheral arterial disease and heart
failure Left ventricular (LV) dysfunction is observed in 20%–30% of PAD patients,1572,1573 mostly associated with CAD.1574 High aortic stiffness
Table 17 Need for assessment of associated atherosclerotic disease in additional vascular territories in symptomatic patients with coronary artery disease, peripheral arterial disease, or carotid stenosis
Leading disease
Assessment in other vascular territories CAD PAD Carotid stenosis CAD May be helpful to optimize medical treatment431 and
to be considered in patients scheduled for open vascular surgery with poor functional capacity or significant risk factors or symptoms. 1080 Consider in patients scheduled for
carotid endarterectomy and suspected CAD.1558
PAD Potential benefits in identifying
high-risk patients and guiding treatment decisions.429,1559–1561
Carotid stenosis Useful in patients undergoing elective
CABG.1555,1562 © ESC 2024
CABG, coronary artery bypass grafting; CAD, coronary artery disease; PAD, peripheral arterial disease.
ESC Guidelines 3651
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.115
can increase LV afterload and impair coronary blood flow, resulting in hypertension, LV hypertrophy, LV diastolic dysfunction, and HF.1575,1576 Skeletal muscle involvement and deconditioning due to PAD may aggravate HF severity.1577,1578 Peripheral arterial disease and HF are independently associated with poor outcomes and those with concomitant HF have a 30% higher risk of MACE and 40% higher risk of all-cause mortality.1574 Evaluation of LV function in patients with PAD may be useful for better CV risk stratification and comprehensive management of their CV disease.1579 This is of particular importance when an intermediate- or high-risk vascular intervention is planned. Expectedly, the presence of PAD in patients with HF is also associated with poor outcomes.1580–1584 These patients represent a high-risk group in which intense risk-factor modification strategies and optimization of HF therapy are warranted.
11.3 Peripheral arterial disease and AF
The prevalence of AF among patients with PAD is around 12%.1585–1590 A meta-analysis revealed that in patients with AF and PAD, risk of allcause mortality, CV mortality, and MACE is 40%, over 60%, and over 70% higher, respectively compared with patients with AF without PAD.1591 PAD is included in the CHA2DS2-VASc (congestive heart failure, hypertension, age ≥75 [doubled], diabetes, stroke [doubled], vascular disease, age 65 to 74 and sex category [female]) risk score, which underlies the prognostic importance of PAD in patients with AF.1592
11.4 Peripheral arterial disease and aortic
stenosis Peripheral arterial disease frequently accompanies symptomatic aortic stenosis, especially among patients not eligible for surgical aortic valve replacement (20%–30%).198,1593–1595 In these patients, pre-procedural CCT/CTA or CMR1596 of the aorta and major peripheral arteries is mandatory to evaluate the access site for transcatheter aortic valve implantation (TAVI) and plan a closure strategy for the access site. Patients with PAD have increased risk of all-cause mortality and vascular complications after TAVI,198 thus, screening for PAD in these patients may be helpful. 12 Key messages
Peripheral arterial and aortic diseases are highly prevalent, often asymptomatic, and linked to increased morbidity and mortality. Early diagnosis is crucial for better outcomes and management requires a multidisciplinary team. CVRF control is crucial to prevent progression and complications. Despite the benefit of medical therapy, lifestyle changes, healthy diet, abstinence from smoking, exercise/rehabilitation, and education are essential for effective management. Patient empowerment is essential to improve adherence and close/regular monitoring is essential to improve prognosis. Use of web- or app-based calculators for estimation of CV risk in the secondary prevention of ASCVD may aid patient motivation for lifestyle changes and adherence to medication. Peripheral arteries Atherosclerotic lower-extremity PAD is a chronic disease needing lifelong follow-up. Assessment of walking impairment, functional status, and amputation risk is crucial in PAD management. Ankle–brachial index should be the initial diagnostic test for screening and diagnosing PAD, and serves as a surrogate marker for CV and all-cause mortality. DUS is the first-line imaging method to confirm PAD lesions. Supervised exercise training or, if not available, HBET, improves walking and functional performances, and reduces CV risk. Exercise training remains underused and increased awareness is warranted. In asymptomatic PAD patient revascularization is not recommended. In symptomatic PAD patient need for interventional treatment, following a period of optimal medical treatment and exercise, should be discussed in a multidisciplinary setting. Chronic limb-threatening ischaemia increases the risk of CV events, needs early diagnosis, rapid referral to a multidisciplinary vascular team, and revascularization for limb salvage. Acute limb ischaemia warrants rapid clinical assessment by a vascular team and urgent revascularization. Duplex ultrasound is the first-line diagnostic modality for carotid stenosis. Routine revascularization is not recommended if asymptomatic. In symptomatic patients multidisciplinary assessment is recommended.
Recommendation Table 70 — Recommendations for screening and management of polyvascular disease and peripheral arterial disease with cardiac diseases (see also Evidence Table 15)
Recommendations Classa Levelb
In patients with PVD, an LDL-C reduction by ≥50% from baseline and an LDL-C goal of <1.4 mmol/L (<55 mg/dL) are recommended.242,1571 I A In patients with PAD and newly diagnosed AF with a CHA2DS2-VASc score ≥2, full oral anticoagulation is recommended.1597 I C Screening for ilio-femoral PAD is recommended in patients undergoing TAVI.198,1598 I B Carotid DUS should be considered for stable patients scheduled for CABG with TIA/stroke within the past 6 months without carotid revascularization.1556,1569 IIa B
Continued In patients with stable PVD who are symptomatic in
at least one territory and without high bleeding risk,c treatment with a combination of rivaroxaban (2.5 mg b.i.d.) and aspirin (100 mg o.d.) should be considered.429,1559 IIa A Carotid DUS may be considered for stable patients scheduled for CABG without TIA/stroke within the past 6 months.1555,1562 IIb C © ESC 2024
AF, atrial fibrillation; b.i.d., twice daily; CABG, coronary artery bypass grafting; CHA2DS2-VASc, congestive heart failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65 to 74 and sex category (female); DUS, duplex ultrasound; eGFR, estimated glomerular filtration rate; LDL-C, low-density lipoprotein cholesterol; o.d., once daily; PAD, peripheral arterial disease; PVD, polyvascular disease; TAVI, transcatheter aortic valve implantation; TIA, transient ischaemic attack. aClass of recommendation. bLevel of evidence. cPrior history of intracerebral haemorrhage or ischaemic stroke, history of other intracranial pathology, recent gastrointestinal bleeding or anaemia due to possible gastrointestinal blood loss, other gastrointestinal pathology associated with increased bleeding risk, liver failure, bleeding diathesis or coagulopathy, extreme old age or frailty, or renal failure requiring dialysis or with eGFR <15 mL/min/1.73 m2. Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.116
Atherosclerotic UEAD is most frequently located in the subclavian artery and may be suspected because of an absolute inter-arm SBP difference >10–15 mmHg. DUS is first-line imaging and routine revascularization is not recommended. The key to early diagnosis of acute and chronic mesenteric ischaemia is a high level of clinical suspicion—laboratory tests are unreliable for the diagnosis. Acute SMA occlusion requires immediate revascularization. Aorta Aortic aneurysms are managed based on size, location, and growth rate. Small aneurysms are monitored regularly (Guidelines provide disease-specific follow-up algorithms), while larger ones may require surgical/endovascular repair to prevent rupture. In aortic root aneurysms, aortic replacement may be considered at >52 mm in low-risk patients and at experienced centres. Aortic diameter is the primary risk factor for aortic events. However, evidence supports diameter indexation (especially in extreme BSA populations) and the use of aortic length (>11 cm), the AHI (>32.1 mm/m), growth rate (≥3 mm per year for ascending aorta and arch or >5 mm per 6 months in the thoracoabdominall aorta), and age/sex for risk assessment. Multidisciplinary collaboration, hybrid operating rooms, and advanced stent technology have increased the adoption of hybrid approaches and endovascular therapies for different thoracoabdominal aortic diseases. Acute aortic syndrome management involves medical treatment in critical care units and selective surgical intervention based on location and complications. The main problem in these conditions continues to be a delay in diagnosing patients or transferring them to an aortic centre. Improved diagnostic algorithms and reduced surgical complications have lowered mortality rates. Surgical/endovascular treatment in the subacute phase is advised for high-risk patients with type B aortic syndrome. Suspected genetic aortic conditions require evaluation at experienced centres to assess both the patient and their FDRs for genetic studies. Genetic aortic conditions should be considered based on family history, syndromic features, age <60 years, and no CVRFs (Guidelines offer a screening algorithm for thoracic aorta disease). A comprehensive evaluation of the entire aorta and other vascular territories is recommended in HTAD. Recent advances in genetics are enabling personalized and patient-centred assessment. This includes using different aortic diameter thresholds to indicate surgery and implementing diverse surveillance algorithms.
13 Gaps in evidence
There are several areas where robust evidence is still lacking and which deserve to be addressed in future clinical research. (1) Epidemiology and risk factors in PAAD:
(a) Improve PAAD risk definition. (b) Provide contemporary data on PAAD prevalence in Europe. (c) Inflammation biomarkers, metabolomics, and proteomics may
have prognostic value in PAAD. (2) Evaluation of peripheral arteries and aorta:
(a) Follow-up algorithms can assist PAAD patient management but have limitations and evidence on cost-effectiveness is needed. (b) The best methodology for aortic measurements remains to be elucidated. (3) Screening for carotid, peripheral arterial, and aortic diseases:
(a) Screening in specific populations: research is needed to understand the nuances of screening in particular populations and whether modifications to current guidelines are necessary. (b) Patient outcomes and benefits of screening: impact of screening on patient outcome should be assessed. (4) OMT and PAAD:
(a) Research needed on QoL and workability. (b) Research needed for optimal preventive strategies. (c) Exercise therapy and rehabilitation for PAAD should be more accessible and employed. (d) Anti-inflammatory therapy should be investigated. (e) Antithrombotic therapies in specific risk groups of PAAD and patients undergoing revascularization should be addressed. (5) Aortic aneurysms:
(a) Discovering novel individualized risk stratification parameters beyond well-established markers. (b) Assessing the safety of fluoroquinolone use in patients with aortic aneurysm. (6) Acute aortic syndromes:
(a) Assess the management of pregnancy-related AAS. (b) Identify diagnostic biomarkers other than D-dimer. (c) Management in uncomplicated TBAD and IMH should be assessed. (7) Genetic aortic diseases:
(a) Need to refine risk estimation in AD, particularly in HTAD, especially the risk of type B aortic dissection. (b) There is insufficient evidence to support the efficacy of any medication in reducing the risk of AD. (8) Sex differences in PAAD:
(a) Investigate sex and age differences. (b) Assess the optimal parameter or indexed parameter to guide
intervention decisions in women with aortic and PAD diseases.
14 Sex differences
Sex differences have been evaluated and discussed in the specific sections.
15 ‘What to do’ and ‘What not to do’ messages from the guidelines
Table 18 ‘What to do’ and ’What not to do’. ‘What to do and What not to do’ lists all Class I and Class III recommendations from the text.
ESC Guidelines 3653
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.117
Table 18 ‘What to do’ and ‘What not to do’
Recommendations Classa Levelb
Recommendations for clinical and laboratory, and for functional and quality of life, assessment in patients with peripheral arterial and aortic disease When managing PAAD, it is recommended to adopt a comprehensive approach that addresses the entirety of arterial circulation. I B To assess PAAD, it is recommended to perform thorough clinical, vascular, and CVRF laboratory evaluation. I C Recommendations for diagnostic tests in patients with peripheral arterial disease Measurement of the ABI is recommended as the first-line non-invasive test for screening and diagnosis of PAD, using an ABI ≤0.90 as a diagnostic criterion. I B In the case of non-compressible ankle arteries or ABI >1.40, additional methods such as TP, TBI or Doppler waveform analysis are recommended. I B Recommendations for imaging of the aorta It is recommended that aortic diameters are measured at prespecified anatomical landmarks, and the largest diameter of the section be perpendicular to the longitudinal axis. I C It is recommended in cases of serial imaging of the aorta over time to use the same imaging modality with the same measurement method. I C It is recommended to consider renal function, pregnancy, age, and history of allergy to contrast media to select the optimal imaging modality with minimal radiation exposure and lowest iatrogenic risk, except for emergency cases. I C Recommendations for thoracic aortic measurements TTE is recommended as the first-line imaging technique in evaluating thoracic aortic diseases. I B It is recommended to report aortic diameters using the leading-to-leading edge convention in end-diastole by echocardiography. I C It is recommended to report aortic diameters using the inner-to-inner edge convention in end-diastole by CCT or CMR. I C It is recommended to report aortic diameters from images obtained with the double-oblique technique (not axial images) by CCT or CMR. I C ECG-triggered CCT is recommended for comprehensive diagnosis, follow-up, and pre-invasive treatment assessment of the entire aorta, particularly the root and ascending aorta. I C CMR is recommended for diagnosis and follow-up of thoracic aortic diseases, especially when chronic follow-up is required. I C Recommendations for abdominal aortic aneurysm screening Screening is recommended in men aged ≥65 years and with a history of smoking to reduce the risk of death from ruptured AAA. I A Screening is recommended in FDRs of patients with AAA aged ≥50, unless an acquired cause can be clearly identified. I C Recommendations for lifestyle, physical activity, and patient education In patients with PAAD, cessation and abstinence from smoking of any kind is recommended to reduce the risk of AD, MI, death, and limb ischaemia. I A A healthy diet rich in legumes, dietary fibre, nuts, fruits, and vegetables, with a high flavonoid intake (Mediterranean diet), is recommended for CV disease prevention in patients with PAAD. I A Low- to moderate-intensity (or high if tolerated) aerobic activities are recommended in patients with PAD to increase overall and pain-free walking distance. I A In patients with PAAD, behavioural counselling to promote healthy diet, smoking cessation, and physical activity is recommended to improve the CV risk profile. I B It is recommended to promote patient and caregivers’ education and empowerment through tailored guidance on lifestyle adjustments and the importance of regular physical activity. I C Recommendations for antihypertensive therapy in patients with peripheral and aortic disease In patients with PAAD and hypertension an SBP target towards 120–129 mmHg, if tolerated, is recommended. I A In unilateral RAS patients, it is recommended that antihypertensive medication include ACEIs/ARBs. I B Recommendations for lipid-lowering therapy for patients with peripheral arterial and aortic diseases In patients with atherosclerotic PAAD, lipid-lowering therapy is recommended. I A An ultimate LDL-C goal of <1.4 mmol/L (55 mg/dL) and a >50% reduction in LDL-C vs. baseline are recommended in patients with atherosclerotic PAAD. I A Statins are recommended in all patients with PAD. I A If the target LDL-C level is not achieved, a combination of statins and ezetimibe is indicated in patients with atherosclerotic PAAD, to achieve the given target values. I B
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.118
If the target LDL-C level is not achieved on maximally tolerated statins and ezetimibe, treatment with a PCSK9 inhibitor is recommended in patients with atherosclerotic PAAD, to achieve target values. I A For statin-intolerant patients with atherosclerotic PAAD, at high CV risk, who do not achieve their LDL-C goal on ezetimibe, it is recommended to add bempedoic acid either alone or in combination with a PCSK9 inhibitor. I B Fibrates are not recommended for cholesterol lowering. III B Recommendations for the medical management of patients with peripheral arterial and aortic diseases and diabetes It is recommended to apply tight glycaemic control (HbA1c <53 mmol/mol [7%]) to reduce microvascular complications in patients with PAAD. I A SGLT2i with proven CV benefit are recommended in patients with T2DM and PAAD to reduce CV events, independent of baseline or target HbA1c and concomitant glucose-lowering medication. I A GLP-1RAs with proven CV benefit are recommended in patients with T2DM and PAAD to reduce CV events, independent of baseline or target HbA1c and concomitant glucose-lowering medication. I A It is recommended to avoid hypoglycaemia in patients with PAAD. I B It is recommended to individualize HbA1c targets according to comorbidities, diabetes duration, and life expectancy. I C It is recommended to prioritize the use of glucose-lowering agents with proven CV benefits, followed by agents with proven CV safety, over agents without proven CV benefit or safety. I C Recommendations for diagnostic tests in patients with peripheral arterial disease and diabetes, renal failure and wounds Measuring TP or TBI is recommended in patients with diabetes or renal failure if resting ABI is normal. I C Recommendations for imaging in patients with peripheral arterial disease DUS is recommended as first-line imaging method to confirm PAD lesions. I C In symptomatic patients with aorto-iliac or multisegmental/complex disease, CTA and/or MRA are recommended as adjuvant imaging techniques for preparation of revascularization procedures. I C Analysis of anatomical imaging tests in conjunction with symptoms and haemodynamic tests prior to an invasive procedure is recommended. I C Recommendations for exercise therapy in patients with peripheral arterial disease In patients with symptomatic PAD, SET is recommended. I A In those patients undergoing endovascular revascularization, SET is recommended as an adjuvant therapy. I A Recommendations for antithrombotic therapy in patients with peripheral arterial disease Use of antiplatelet therapy with aspirin alone (range 75–160 mg o.d.) or clopidogrel alone (75 mg o.d.) is recommended for the reduction of MACE in patients with symptomatic PAD. I A Long-term DAPT in patients with PAD is not recommended. III A Oral anticoagulant monotherapy for PAD (unless for another indication) is not recommended. III A The routine use of ticagrelor in patients with PAD is not recommended. III A It is not recommended to systematically treat patients with asymptomatic PAD without any sign of clinically relevant ASCVD with antiplatelet drugs. III B Recommendations on interventional treatment of asymptomatic and symptomatic peripheral arterial disease (general) In patients with symptomatic PAD, after a 3 month period of OMT and exercise therapy, PAD-related QoL assessment is recommended. I B It is recommended to adapt the mode and type of revascularization options to anatomical lesion location, lesion morphology, and general patient condition. I C In patients with PAD, revascularization is not recommended if the reason is to solely prevent progression to CLTI. III B In patients with asymptomatic PAD, revascularization is not recommended. III C Recommendations in patients with peripheral arterial disease: follow-up of patients with peripheral arterial disease It is recommended to regularly, at least once a year, follow-up patients with PAD, assessing clinical and functional status, medication adherence, limb symptoms, and CVRFs, with DUS assessment as needed. I C Recommendations for the management of chronic limb-threatening ischaemia For limb salvage in patients with CLTI, revascularization is recommended. I B Early recognition of CLTI and referral to the vascular team are recommended for limb salvage. I C Recommendations for medical treatment in patients with chronic limb-threatening ischaemia It is recommended that patients with CLTI are managed by a vascular team. I C In patients with CLTI and ulcers, offloading mechanical tissue stress is recommended to allow wound healing. I C
Continued
ESC Guidelines 3655
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.119
It is recommended to treat infection with antibiotics. I C Lower-limb exercise training is not recommended in patients with CLTI and wounds. III C Recommendations for interventional treatment of chronic limb-threatening ischaemia In CLTI patients, it is recommended to perform revascularization as soon as possible. I B In CLTI, it is recommended to use autologous veins as the preferred conduit for infra-inguinal bypass surgery. I B In multilevel vascular disease, it is recommended to eliminate inflow obstructions when treating downstream lesions. I C An individual risk assessment (weighing the patient’s individual procedural risk of endovascular vs. surgical revascularization) by a multidisciplinary vascular team is recommended. I C Recommendations for follow-up in patients with chronic limb-threatening ischaemia In patients with CLTI, following revascularization it is recommended to follow-up patients on a regular basis. I C At follow-up, it is recommended to assess clinical, haemodynamic and functional status, limb symptoms, treatment adherence, and CVRFs. I C Recommendations for the management of patients presenting with acute limb ischaemia In patients with ALI, it is recommended that an urgent evaluation is performed by a vascular clinician with sufficient experience to assess limb viability and implement appropriate therapy. I C In cases of neurological deficit, urgent revascularization is recommended; diagnostic imaging is recommended to guide treatment, provided it does not delay treatment, or if the need for primary amputation is obvious. I C In the absence of severe neurological deficit, revascularization is recommended within hours of initial imaging in a case-by-case decision. I C Treatment with analgesics is recommended as soon as possible for pain control. I C It is recommended to monitor for compartment syndrome after revascularization and treat (fasciotomy). I C It is recommended to assess clinical and haemodynamic success following revascularization. I C In patients with ALI, it is recommended to obtain a comprehensive medical history and determine the cause of thrombosis and/or embolization. I C Recommendations for carotid artery stenosis assessment It is recommended to use the NASCET method or its non-invasive equivalent to assess ICA stenosis. I B It is recommended to use DUS as first-line imaging to diagnose ICA stenosis. I C It is not recommended to use the ECST method for ICA stenosis assessment. III C Recommendations for antithrombotic treatment in patients with carotid stenosis In patients with symptomatic CS, not undergoing carotid endarterectomy or stenting, DAPT with low-dose aspirin and clopidogrel (75 mg) is recommended for the first 21 days or longer, followed by clopidogrel 75 mg or long-term aspirin to reduce the risk of stroke. I A Recommendations for interventional treatment in patients with asymptomatic carotid artery stenosis In asymptomatic patients with ICA stenosis, in the absence of high-risk features and with a life expectancy <5 years, routine revascularization is not recommended. III A Recommendations for evaluation and medical treatment in patients with symptomatic carotid artery stenosis DAPT is recommended in the early phase of minor strokes in patients with ICA stenosis, if not revascularized, for at least 21 days, considering the bleeding risk. I A It is recommended that symptomatic ICA stenosis patients are assessed by a vascular team including a neurologist. I C Recommendations for interventions in patients with symptomatic carotid artery stenosis It is recommended to perform CEA of symptomatic 70%–99% ICA stenosis provided a documented 30 day risk of procedural death/stroke is <6%. I A If indicated, it is recommended to perform CEA within 14 days in symptomatic ICA stenosis patients. I B OMT is recommended for all symptomatic ICA stenosis patients. I A Revascularization is not recommended in patients with ICA lesions <50%. III A Recommendations for follow-up in patients with carotid artery stenosis Once-yearly follow-up is recommended to check for CVRFs and treatment compliance. I A After ICA stent implantation, DAPT with aspirin and clopidogrel is recommended for at least 1 month. I A After ICA revascularization, long-term aspirin or clopidogrel is recommended. I B During follow-up, it is recommended to assess neurological symptoms, CVRFs, and treatment adherence at least yearly in patients with CS. I C After ICA revascularization, surveillance with DUS is recommended within the first month. I C
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.120
Recommendations for the management of subclavian artery stenosis Bilateral arm BP measurement is recommended for all patients with PAAD. I B Routine revascularization in patients with atherosclerotic subclavian artery disease is not recommended. III C Recommendations for diagnostic strategies for renal artery disease DUS is recommended as the first-line imaging modality in patients with suspicion of RAS. I B In cases of DUS-based suspicion of RAS or in inconclusive DUS, MRA or CTA are recommended. I B In patients with atherosclerotic RAS, it is recommended to assess clinical high-risk features and kidney viability when evaluating renal artery revascularization. I B Recommendations for treatment strategies for renal artery disease In patients with atherosclerotic unilateral RAS, routine revascularization is not recommended. III A Recommendations in patients with visceral artery stenosis In patients with acute mesenteric ischaemia due to acute occlusion of the SMA, endovascular revascularization is recommended. I B In patients with suspected acute or chronic mesenteric ischaemia, CTA is recommended. I C In patients with acute or chronic mesenteric ischaemia, assessment by a vascular team is recommended. I C Revascularization of asymptomatic atherosclerotic visceral artery stenosis is not recommended. III C Recommendations for primary and secondary prevention in aortic atheromatous plaques Anticoagulation or DAPT are not recommended in aortic plaques since they present no benefit and increase bleeding risk. III C In patients with an embolic event and evidence of an aortic arch atheroma, intensive lipid management to an LDL-C target <1.4 mmol/L (<55 mg/dL) is recommended to prevent recurrences. I A In patients with an embolic event and evidence of an aortic arch atheroma, SAPT is recommended to prevent recurrences. I C Recommendations for initial evaluation of thoracic aorta aneurysm and abdominal aortic aneurysm When an aortic aneurysm is identified at any location, assessment of the entire aorta is recommended at baseline and during follow-up. I C When a TAA is identified, assessment of the aortic valve (especially for BAV) is recommended. I C Recommendation for the surveillance of patients with thoracic aortic aneurysms (non-heritable thoracic aortic disease) In thoracic aortic dilatation, TTE is recommended at diagnosis to assess aortic valve anatomy and function, aortic root, and ascending aorta diameters. Additionally, a global aortic evaluation using all echocardiographic views is recommended. I C CMR or CCT is recommended for surveillance of patients with aneurysm at the distal ascending aorta, aortic arch, DTA, or TAAA. I C In thoracic aortic dilatation, CCT or CMR is recommended to confirm TTE measurements, rule out aortic asymmetry, and determine baseline diameters for follow-up. I C TTE is not recommended for the surveillance of aneurysms in the distal ascending aorta, aortic arch, or DTA. III C Recommendations for surveillance of patients with abdominal aortic aneurysm DUS surveillance is recommended every 6 months in men with AAA of 50–55 mm and in women with AAA of 45–50 mm. I B DUS is recommended for AAA surveillance. I C CCT or CMR is recommended if DUS does not allow adequate measurement of AAA diameter. I B Recommendations for medical treatment in patients with thoracic aorta or abdominal aortic aneurysms In patients with aortic aneurysm (TAA and/or AAA), optimal implementation of CV risk management and medical treatment (see detailed recommendations in dedicated Tables of Recommendations) are recommended to reduce MACE. I C Recommendations for surgery in aortic root and ascending aorta dilatation associated with tricuspid aortic valve Surgery is recommended in patients with dilatation of the aortic root or ascending aorta with a tricuspid aortic valve and a maximum diameter of ≥55 mm. I B Valve-sparing aortic root replacement is recommended in patients with aortic root dilatation if performed in experienced centres and durable results are expected. I B VKAs are recommended lifelong for all patients with a Bentall procedure with an MHV prosthesis. I B Recommendations for surgery in aortic arch aneurysms In patients with low or intermediate operative risk with an aortic arch aneurysm and recurrent episodes of chest pain not attributable to non-aortic causes, open surgical replacement of the arch is recommended. I C
Continued
ESC Guidelines 3657
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.121
Recommendations for the management of patients presenting with descending thoracic aortic and thoracoabdominal aortic aneurysms In patients with unruptured DTA aneurysm (without HTAD), elective repair is recommended if diameter ≥55 mm. I B In patients without HTAD with unruptured DTA aneurysm, when elective repair is indicated and anatomy is suitable, TEVAR is recommended over open repair. I B In patients with DTA aneurysm who undergo TEVAR with planned LSA coverage, it is recommended to revascularize the LSA before TEVAR to reduce the risk of SCI and stroke. I B In patients with unruptured degenerative TAAA, elective repair is recommended when the diameter is ≥60 mm. I B Recommendations for the management of patients presenting with abdominal aortic aneurysm Elective repair is recommended if AAA diameter is ≥55 mm in men or ≥50 mm in women. I A In ruptured AAA with suitable anatomy, endovascular repair is recommended over open repair to reduce peri-operative morbidity and mortality. I B In patients with AAA and limited life expectancy (<2 years), elective AAA repair is not recommended. III B Prior to AAA repair, routine evaluation with coronary angiography and systematic revascularization in patients with chronic coronary syndromes is not recommended. III C Recommendations for the management of patients presenting with endoleaks It is recommended to perform 30 day imaging after TEVAR/EVAR, by CCT + DUS/CEUS, to assess the success of intervention. I B It is recommended to re-intervene to achieve a seal in patients with type I endoleak after TEVAR/EVAR. I B It is recommended to re-intervene, principally by endovascular means, to achieve a seal in patients with type III endoleak after TEVAR/EVAR. I B Recommendations for follow-up after treatment of aortic aneurysms After open repair of TAA, early CCT is recommended within 1 month, and then yearly CCT follow-up for the first 2 post-operative years and every 5 years thereafter is recommended if findings are stable. I B After TEVAR, follow-up imaging is recommended at 1 and 12 months post-operatively, then yearly until the fifth post-operative year if no abnormalities are documented. I B After open repair of AAA, first follow-up imaging is recommended within 1 post-operative year, and then every 5 years thereafter if findings are stable. I A After EVAR, follow-up imaging is recommended with CCT (or CMR) and DUS/CEUS at 1 month and 12 months post-operatively, then, if no abnormalities are documented, DUS/CEUS is recommended every year, repeating CCT or CMR (based on potential artefacts) every 5 years. I A Recommendations for diagnostic work-up of acute aortic syndrome In unstable patients who cannot be transferred to CCT, TOE is recommended for diagnosis and evaluation of the coeliac trunk and mesenteric artery. I B In patients presenting with clinical features compatible with possible AAS, a multiparametric algorithm for ruling in or out AAS using the ADD-RS is recommended. I B ECG-gated CCT from neck to pelvis is recommended as the first-line imaging technique in patients with a suspected AAS since it is widely available, accurate, and provides information about the entry tear, extension, and possible complications (malperfusion, dilatation, or rupture). I C In patients with suspected AAS, focused TTE (with use of contrast if feasible) is recommended during the initial evaluation. I C In patients with suspected AAS, TOE is recommended to guide peri-operative management and detect complications. I C Recommendation for medical treatment in acute aortic syndromes In patients with AAS, immediate anti-impulse treatment targeting SBP <120 mmHg and heart rate ≤60 b.p.m. is recommended. In cases of spinal ischaemia or concomitant brain injury, maintaining higher MAP is recommended. I B Intravenous BBs (e.g. labetalol) are recommended as first-line agents. If necessary, i.v. vasodilators (e.g. dihydropyridine calcium blockers or nitrates) could be added. I B Invasive monitoring with an arterial line and continuous three-lead ECG recording, as well as admission to an intensive care unit, is recommended. I B In patients with AAS who can be managed conservatively and who achieved haemodynamic targets with i.v. anti-impulse therapy, switching to oral BBs and, if necessary, up-titration of other BP-lowering agents, is recommended after 24 h if gastrointestinal transit is preserved. I B Adequate pain control to achieve haemodynamic targets is recommended. I C
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.122
Recommendations for intervention in type A acute aortic dissection In patients with acute TAAD, emergency surgical consultation and evaluation and immediate surgical intervention is recommended. I B In patients with acute TAAD who have extensive destruction of the aortic root, a root aneurysm, or a known genetic aortic disorder, aortic root replacement is recommended with a mechanical or biological valved conduit. I B Recommendations for aortic repair strategies in type A acute aortic dissection In patients with acute TAAD and a partially dissected aortic root but no significant aortic valve leaflet pathology, aortic valve resuspension is recommended over valve replacement. I B In patients with acute TAAD undergoing aortic repair, an open distal anastomosis is recommended to improve survival and increase FL thrombosis rates. I B In patients with acute TAAD without an intimal tear in the arch or a significant arch aneurysm, hemi-arch repair is recommended over more extensive arch replacement. I B Recommendations for the management of malperfusion in the setting of acute aortic dissection In patients with acute TAAD presenting with malperfusion (cerebral, mesenteric, lower limb, or renal), immediate aortic surgery is recommended. I B Recommendations for the management of patients presenting with acute type B aortic dissection Medical therapy including pain relief and blood pressure control is recommended in all patients with acute TBAD. I B In patients with complicated acute TBAD, emergency intervention is recommended. I B In patients with complicated acute TBAD, TEVAR is recommended as the first-line therapy. I B Recommendations for the management of patients presenting with chronic type B aortic dissection Antihypertensive therapy is recommended in all patients with chronic TBAD. I B In chronic TBAD with acute symptoms of malperfusion, rupture, or progression of disease, emergency intervention is recommended. I C In patients with chronic TBAD and a descending thoracic aortic diameter ≥60 mm, treatment is recommended in patients at reasonable surgical risk. I B Recommendations for the management of intramural haematoma In patients with IMH, medical therapy including pain relief and blood pressure control is recommended. I C In type A IMH, urgent surgery is recommended. I C In type B IMH, initial medical therapy under careful surveillance is recommended. I C In uncomplicated type B IMH, repetitive imaging (CCT or CMR) is indicated. I C In complicated type B IMH, TEVAR is recommended. I C Recommendations for the management of penetrating atherosclerotic ulcer In all patients with PAU, medical therapy including pain relief and blood pressure control is recommended. I C In cases of type A PAU, surgery is recommended. I C In cases of type B PAU, initial medical therapy under careful surveillance is recommended. I C In uncomplicated type B PAU, repetitive imaging (CMR, CCT, or TOE) is recommended. I C In complicated type B PAU, endovascular treatment (TEVAR) is recommended. I C Recommendations for traumatic aortic injury In cases of severe aortic injury (grade 4), immediate repair is recommended. I A In cases of TAI with suitable anatomy requiring intervention, TEVAR is recommended over open surgery. I A In all TAI patients, medical therapy including pain relief, and blood pressure and heart rate control, is recommended. I C In cases of TAI suspicion, CCT is recommended. I C In cases of moderate aortic injury (grade 3), repair is recommended. I C Recommendations for follow-up after treatment of acute aortic syndrome After TEVAR for AAS, follow-up imaging is recommended at 1, 6, and 12 months post-operatively, then yearly until the fifth post-operative year if no abnormalities are documented. I B In medically treated type B AAD or IMH, follow-up imaging is recommended at 1, 3, 6, and 12 months after onset, then yearly if imaging findings are stable. I C In medically treated PAU, follow-up imaging is recommended at 1 month after diagnosis, then every 6 months if imaging findings are stable. I C
Continued
ESC Guidelines 3659
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.123
Recommendations for the management of patients with heritable thoracic aortic disease It is recommended that medical management of patients with HTAD is individualized and based on shared decision-making. I C It is recommended that patients with known or suspected syndromic or non-syndromic HTAD are evaluated in a centre with experience in the care of this patient group. I C Recommendations for genetic testing and aortic screening in aortic disease In patients with aortic root/ascending aneurysms or thoracic aortic dissection, gathering family history information for at least three generations about TAD, unexplained sudden deaths, and peripheral and intracranial aneurysms is recommended. I B In patients with aortic root/ascending aortic aneurysms or thoracic aortic dissection and risk factors for HTAD, genetic counselling at an expert centre and subsequent testing, if indicated, is recommended. I B In patients with HTAD who have a pathogenic/likely pathogenic variant, genetic testing of at-risk biological relatives (i.e. cascade testing) is recommended, irrespective of age. I C In patients with TAD with risk factors for HTAD, with a negative family history of TAD and in whom no (likely) pathogenic variant is identified, TTE screening aortic imaging of FDRs is recommended. I B Recommendations for imaging in women with Turner syndrome To take the smaller body size of women (≥15 years) with TS into account, the use of the ascending ASI (ratio of aortic diameter [mm] to BSA [m2]), AHI (ratio of aortic diameter [mm] to height [m]), or aortic z-score is recommended to define the degree of aortic dilatation and assess the risk of aortic dissection. I C It is recommended to define imaging and clinical surveillance intervals according to the estimated risk for dissection, based on the ascending ASI and concomitant lesions. I C Recommendations for medical treatment in patients with vascular Ehlers–Danlos syndrome In patients with vEDS, regular vascular surveillance of the aorta and peripheral arteries by DUS, CCT, or CMR is recommended. I C Recommendations for vascular imaging in Marfan syndrome In patients with MFS, TTE is recommended: • At least annually in patients with an aortic root diameter <45 mm in the absence of additional risk factors • At least every 6 months in patients with an aortic root diameter <45 mm in the presence of additional risk factors • At least every 6–12 months in patients with an aortic root diameter ≥45 mm in the absence of additional risk factors I C In patients without previous aortic surgery, complete peripheral vascular and thoracoabdominal aorta imaging by CMR or CCT and DUS is recommended at the first evaluation, and subsequently every 3–5 years if stable. I C In patients with MFS who have undergone aortic root replacement, surveillance imaging of the thoracic aorta by CMR (or CCT) is recommended at least every 3 years. I C Recommendations for medical treatment in Marfan syndrome In patients with MFS, treatment with either a BB or an ARB, in maximally tolerated doses (unless contraindicated), is recommended to reduce the rate of aortic dilatation. I A Recommendations for aortic surgery in Marfan syndrome Surgery is indicated in patients with MFS who have aortic root disease with a maximal aortic sinus diameter ≥50 mm. I B Surgery to replace the aortic root and ascending aorta, using the valve-sparing surgery technique, is recommended in patients with MFS or related HTAD with aortic root dilatation when anatomical features of the valve allow its preservation and the surgeon has specific expertise. I B Recommendations for pregnancy in women with Marfan syndrome It is recommended that all women with MFS: • Have a pre-conception evaluation to address the risks of maternal CV and other complications • Have follow-up in a centre with access to a pregnancy heart and vessel team I C It is recommended that couples in which a partner has or is at risk of HTAD be offered pre-conception genetic counselling. I C Imaging of the whole aorta (by CMR/CCT) is recommended prior to pregnancy. I C Follow-up during pregnancy is recommended with a frequency determined by aortic diameter and growth. I C Intake of BBs during pregnancy is recommended. I C Prophylactic aortic root surgery is recommended in women desiring pregnancy with aortic diameters >45 mm. I C ARBs are not recommended during pregnancy. III B Recommendations for physical exercise in patients with Marfan syndrome It is recommended to individualize physical activity in patients with MFS based on aortic diameter, family history of aortic dissection, and pre-existing fitness. I C Regular moderate aerobic exercise with a level of intensity informed by aortic diameter is recommended in most patients with MFS. I C
Continued Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.124
16 Evidence tables
Evidence tables are available on the European Heart Journal website.
17 Data availability statement
No new data were generated or analysed in support of this research.
18 Author information
Author/task force Member Affiliations: Gisela Teixido-Tura, Cardiovascular Imaging section and Aortic diseases Unit (VASCERN), Department of Cardiology, Vall d’Hebron Hospital Universitari, Vall d’Hebron Barcelona Hospital Campus, Vall d′ Hebron Institut de Recerca (VHIR), Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares, Instituto de Salud Carlos III, Madrid, Spain; Stefano Lanzi, Department of Angiology, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland; Vinko Boc, Department of Vascular Diseases, University Medical Centre Ljubljana, Ljubljana, Slovenia; Eduardo Bossone, Department of Public Health, University of Naples “Federico II”, Naples, Italy, Department of Translational Medical Sciences, University of Naples “Federico II”, Naples, Italy; Marianne Brodmann, Division of Angiology, Medical
Recommendations for imaging follow-up in Loeys–Dietz syndrome In patients with Loeys–Dietz syndrome, TTE at baseline and subsequently every 6–12 months, depending on aortic diameter and growth, is recommended. I C In patients with Loeys–Dietz syndrome, a baseline arterial imaging study from head to pelvis with CMR or CCT and subsequent surveillance with CMR or CCT or DUS every 1–3 years is recommended. I C Recommendations for imaging and surgery in ACTA2-related heritable thoracic aortic disease Annual monitoring of the aortic root/ascending aorta with TTE to evaluate aortic root/ascending aorta enlargement is recommended. I C Imaging of the aorta with CMR/CCT every 3–5 years is recommended. I C Recommendations for bicuspid aortic valve-associated aortopathy management When a BAV is first diagnosed, initial TTE to assess diameters of the aorta at several levels is recommended. I B Surgery for bicuspid aortopathy is recommended when the maximum aortic diameter is ≥55 mm. I B Surgery for bicuspid aortopathy of the root phenotype is recommended when the maximum aortic diameter is ≥50 mm. I B CCT or CMR of the entire thoracic aorta is recommended at first diagnosis and when important discrepancies in measurements are found between subsequent TTE controls during surveillance, or when the diameter of the aorta exceeds 45 mm. I C Screening by TTE in FDRs of BAV patients with root phenotype aortopathy and/or isolated aortic regurgitation is recommended. I C Surveillance serial imaging by TTE is recommended in BAV patients with a maximum aortic diameter >40 mm, either with no indication for surgery or after isolated aortic valve surgery, after 1 year, then if stability is observed, every 2–3 years. I C Recommendations for evaluation and medical treatment of patients with coarctation of the aorta In patients with native or repaired coarctation, lifelong follow-up is recommended, including regular imaging of the aorta with CCT/CMR every 3–5 years (adapted to clinical status and previous imaging findings). I B Coarctation or re-coarctation repair (either surgical or endovascular) is indicated in patients with hypertension with an increased non-invasive gradient between the upper and lower limbs (decreased ABI) confirmed with invasive measurement (peak-to-peak >20 mmHg), with a preference for stenting when technically feasible. I C In patients with coarctation, BP measurements at both arms and one lower extremity are recommended. I C It is recommended to treat hypertension in patients with coarctation according to ESC hypertension guidelines. I C Recommendations for screening and management of polyvascular disease and peripheral arterial disease with cardiac diseases In patients with PVD, an LDL-C reduction by ≥50% from baseline and an LDL-C goal of <1.4 mmol/L (<55 mg/dL) are recommended. I A In patients with PAD and newly diagnosed AF with a CHA2DS2-VASc score ≥2, full oral anticoagulation is recommended. I C Screening for ilio-femoral PAD is recommended in patients undergoing TAVI. I B © ESC 2024
AAA, abdominal aortic aneurysm; AAS, acute aortic syndrome; ABI, ankle–brachial index; ACEI, angiotensin-converting enzyme inhibitor; AD, aortic dissection; ADD-RS, aortic dissection detection-risk score; AF, atrial fibrillation; AHI, aortic height index; ALI, acute limb ischaemia; ARB, angiotensin receptor blocker; ASCVD, atherosclerotic cardiovascular disease; ASI, aortic size index; BAV, bicuspid aortic valve; BB, beta-blocker; BP, blood pressure; b.p.m., beats per minute; CCT, cardiovascular computed tomography; CEA, carotid endarterectomy; CEUS, contrast-enhanced ultrasound; CHA2DS2-VASc, congestive heart failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled), vascular disease, age 65 to 74 and sex category (female); CLTI, chronic limb-threatening ischaemia; CMR, cardiovascular magnetic resonance; CS, carotid artery stenosis; CTA, computed tomography angiography; CV, cardiovascular; CVRF, cardiovascular risk factor; DAPT, dual antiplatelet therapy; DTA, descending thoracic aorta; DUS, duplex ultrasound; ECG, electrocardiogram; ECST, European Carotid Surgery Trial; ESC, European Society of Cardiology; FDR, first-degree relative; FL, false lumen; GLP-1RA, glucagon-like peptide-1 receptor agonist; HbA1c, glycated haemoglobin; HTAD, heritable thoracic aortic disease; ICA, internal carotid artery; IMH, intramural haematoma; i.v., intravenous; LDL-C, low-density lipoprotein cholesterol; LSA, left subclavian artery; MACE, major adverse cardiac event; MAP, mean arterial pressure; MFS, Marfan syndrome; MHV, mechanical heart valve; MI, myocardial infarction; MRA, magnetic resonance angiography; NASCET, North American Symptomatic Carotid Endarterectomy Trial; o.d., once daily; OMT, optimal medical treatment; PAAD, peripheral arterial and aortic diseases; PAD, peripheral arterial disease; PAU, penetrating atherosclerotic ulcer; PCSK9, proprotein convertase subtilisin/kexin type 9; PVD, polyvascular disease; RAS, renal artery stenosis; QoL, quality of life; SAPT, single antiplatelet therapy; SBP, systolic blood pressure; SCI, spinal cord ischaemia; SET, supervised exercise training; SGLT2i, sodium-glucose co-transporter-2 inhibitor; SMA, superior mesenteric artery; T2DM, type 2 diabetes mellitus; TAA, thoracic aortic aneurysm; TAAA, thoracoabdominal aortic aneurysm; TAAD, type A aortic dissection; TAD, thoracic aortic disease; TAI, traumatic aortic injury; TAVI, transcatheter aortic valve implantation; TBAD, type B aortic dissection; TBI, toe–brachial index; TOE, transoesophageal echocardiography; TEVAR/EVAR, thoracic endovascular aortic aneurysm repair; TP, toe pressure; TS, Turner syndrome; TTE, transthoracic echocardiography; vEDS, vascular Ehlers– Danlos syndrome; VKA, vitamin K antagonist. aClass of recommendation. bLevel of evidence.
ESC Guidelines 3661
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.125
University Graz, Graz, Austria; Alessandra Bura-Rivière, Vascular Medicine Department, Toulouse University Hospital, Toulouse, France, Faculty of Medicine, University Toulouse 3, Toulouse, France; Julie De Backer, Cardiology and Center for Medical Genetics, Ghent University Hospital, Ghent, Belgium; Sebastien Deglise, Department of Vascular Surgery, University Hospital Lausanne (CHUV), Lausanne, Switzerland; Alessandro Della Corte, Department of Translational Medical Sciences, University of Campania “Luigi Vanvitelli”, Naples, Italy, Unit of Cardiac Surgery, Monaldi Hospital, Naples, Italy; Christian Heiss, Department of Clinical and Experimental Medicine, University of Surrey, Guildford, United Kingdom, Vascular Medicine Department, Surrey and Sussex Healthcare NHS Trust, Redhill, United Kingdom; Marta Kałużna-Oleksy, 1st Department of Cardiology, Poznan University of Medical Sciences, Poznan, Poland; Donata Kurpas, Division of Research Methodology, Department of Nursing, Faculty of Nursing and Midwifery, Wroclaw Medical University, Poland; Carmel M. McEniery, Medicine, University of Cambridge, Cambridge, United Kingdom; Tristan Mirault, Vascular Medicine Department, Université Paris Cité, Paris, France, Vascular Medicine Department, Assistance Publique Hôpitaux de Paris-APHP, Hôpital Européen Georges-Pompidou, Paris, PARCC U970 team 5 Innate and Adaptative Immunity in Vascular Diseases, INSERM, Paris, France; Agnes A. Pasquet, Department of Cardiovascular Diseases, Cliniques Universitaires Saint Luc, Brussels, Belgium, IREC/CARD, UCLouvain, Brussels, Belgium; Alex Pitcher, The Heart Centre, Oxford University NHS Foundation Trust, Oxford, United Kingdom; Hannah A.I. Schaubroeck, Department of Intensive Care Medicine, Ghent University Hospital, Ghent, Belgium; Oliver Schlager, Division of Angiology, Department of Medicine II, Medical University of Vienna, Vienna, Austria; Per Anton Sirnes, Cardiology Practice, Kardiokonsult, Son, Norway, Cardiology section, Volvat Medical Centre, Moss, Norway; Muriel G. Sprynger, Cardiology, University Hospital of Liège, Liège, Belgium; Eugenio Stabile, Division of Cardiology, Health Science Department, Università della Basilicata, Potenza, Italy; Françoise Steinbach (France), ESC Patient Forum, Sophia Antipolis, France; Matthias Thielmann, Department of Thoracic and Cardiovascular Surgery, West-German Heart and Vascular Center, University Hospital Essen, University Duisburg-Essen, Essen, Germany; Roland R.J. van Kimmenade, Department of Cardiology, Radboud University Medical Center, Nijmegen, Netherlands; and Maarit Venermo, Department of Vascular Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
19 Appendix
ESC Scientific Document Group Includes Document Reviewers and ESC National Cardiac Societies. Document Reviewers: Alessia Gimelli (CPG Review Co-ordinator) (Italy), Jean-Baptiste Ricco (CPG Review Co-ordinator) (France), Elena Arbelo (Spain), Christian-Alexander Behrendt (Germany), Michael Böhm (Germany), Michael A. Borger (Germany), Margarita Brida (Croatia), Sergio Buccheri (Sweden), Gill Louise Buchanan (United Kingdom), Christina Christersson (Sweden), Gert J. de Borst (Netherlands), Marco De Carlo (Italy), Roman Gottardi (Austria), Lydia Hanna (United Kingdom), Lynne Hinterbuchner (Austria), Borja Ibanez (Spain), Ignatios Ikonomidis (Greece), Stefan James (Sweden), Thomas Kahan (Sweden), Klaus Kallenbach2 (Luxemburg), Lars Køber (Denmark), Konstantinos C. Koskinas (Switzerland), Juraj Madaric1 (Slovakia), Blandine Maurel (France), John William McEvoy (Ireland), Gil Meltzer (Israel), Borislava Mihaylova (United Kingdom), Richard Mindham (United Kingdom), Ioana Mozos (Romania), Jens Cosedis Nielsen (Denmark), Eva Prescott (Denmark), Amina Rakisheva (Kazakhstan), Barbara Rantner (Germany), Bianca Rocca (Italy), Xavier Rossello (Spain), Jean Paul Schmid (Switzerland), Daniel Staub (Switzerland), Sabine Steiner (Germany), Isabella Sudano (Switzerland), Martin Teraa (Netherlands), Ilonca Vaartjes (Netherlands), Rafael Vidal-Perez (Spain), Christiaan Vrints (Belgium), and Katja Zeppenfeld (Netherlands).
ESC National Cardiac Societies actively involved in the review process of the 2024 ESC Guidelines for the management of peripheral arterial and aortic diseases: Algeria: Algerian Society of Cardiology, Mohammed El Amine Bouzid; Armenia: Armenian Cardiologists Association, Arsen A. Tsaturyan; Austria: Austrian Society of Cardiology, Georg Delle Karth; Azerbaijan: Azerbaijan Society of Cardiology, Fuad Samadov; Belgium: Belgian Society of Cardiology, Antoine Bondue; Bosnia and Herzegovina: Association of Cardiologists of Bosnia and Herzegovina, Alden Begić; Bulgaria: Bulgarian Society of Cardiology, Ivo Petrov; Croatia: Croatian Cardiac Society, Majda Vrkic Kirhmajer; Cyprus: Cyprus Society of Cardiology, Georgios P. Georghiou; Czechia: Czech Society of Cardiology, Pavel Procházka; Denmark: Danish Society of Cardiology, Torsten B. Rasmussen; Egypt: Egyptian Society of Cardiology, Yasser A. Sadek; Estonia: Estonian Society of Cardiology, Jaagup Truusalu; Finland: Finnish Cardiac Society, Petri Saari; France: French Society of Cardiology, Guillaume Jondeau; Germany: German Cardiac Society, Christiane Tiefenbacher; Greece: Hellenic Society of Cardiology, Kimon Stamatelopoulos; Hungary: Hungarian Society of Cardiology, Endre Kolossváry; Iceland: Icelandic Society of Cardiology, Elín Hanna Laxdal; Ireland: Irish Cardiac Society, Monica Monaghan; Israel: Israel Heart Society, Jonathan Koslowsky; Italy: Italian Federation of Cardiology, Ciro Indolfi; Kazakhstan: Association of Cardiologists of Kazakhstan, Nursultan Kospanov; Kosovo (Republic of): Kosovo Society of Cardiology, Pranvera Ibrahimi; Kyrgyzstan: Kyrgyz Society of Cardiology, Olga Lunegova; Latvia: Latvian Society of Cardiology, Ainars Rudzitis; Lithuania: Lithuanian Society of Cardiology, Andrius Berūkštis; Luxembourg: Luxembourg Society of Cardiology, Katja Lottermoser; Malta: Maltese Cardiac Society, Maryanne Caruana; Morocco: Moroccan Society of Cardiology, Raissuni Zainab; North Macedonia: National Society of Cardiology of North Macedonia, Marijan Bosevski; Norway: Norwegian Society of Cardiology, Stein Samstad; Portugal: Portuguese Society of Cardiology, Ana Teresa Timoteo; Romania: Romanian Society of Cardiology, Ovidiu Dragomir Chioncel; San Marino: San Marino Society of Cardiology, Pier Camillo Pavesi; Slovakia: Slovak Society of Cardiology, Maria Rasiova; Slovenia: Slovenian Society of Cardiology, Borut Jug; Spain: Spanish Society of Cardiology, Ariana González Gomez; Sweden: Swedish Society of Cardiology, Stefan James; Switzerland: Swiss Society of Cardiology, Marc Righini; Tunisia: Tunisian Society of Cardiology and Cardio-Vascular Surgery, Amine Tarmiz; Turkey: Turkish Society of Cardiology, Eralp Tutar; and Ukraine: Ukrainian Association of Cardiology, Maksym Sokolov. ESC Clinical Practice Guidelines (CPG) Committee: Eva Prescott (Chairperson) (Denmark), Stefan James (Co-Chairperson) (Sweden), Elena Arbelo (Spain), Colin Baigent (United Kingdom), Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.126
Michael A. Borger (Germany), Sergio Buccheri (Sweden), Borja Ibanez (Spain), Lars Køber (Denmark), Konstantinos C. Koskinas (Switzerland), John William McEvoy (Ireland), Borislava Mihaylova (United Kingdom), Richard Mindham (United Kingdom), Lis Neubeck (United Kingdom), Jens Cosedis Nielsen (Denmark), Agnes A. Pasquet (Belgium), Amina Rakisheva (Kazakhstan), Bianca Rocca (Italy), Xavier Rossello (Spain), Ilonca Vaartjes (Netherlands), Christiaan Vrints (Belgium), Adam Witkowski (Poland), and Katja Zeppenfeld (Netherlands).
20 References
1. van Kuijk JP, Flu WJ, Welten GM, Hoeks SE, Chonchol M, Vidakovic R, et al. Long-term prognosis of patients with peripheral arterial disease with or without polyvascular atherosclerotic disease. Eur Heart J 2010;31:992–9. https://doi.org/10.1093/eurheartj/ ehp553 2. Dolmaci OB, El Mathari S, Driessen AHG, Klautz RJM, Poelmann RE, Lindeman JHN, et al. Are thoracic aortic aneurysm patients at increased risk for cardiovascular diseases? J Clin Med 2023;12:272. https://doi.org/10.3390/jcm12010272 3. Tully L, Gianos E, Vani A, Guo Y, Balakrishnan R, Schwartzbard A, et al. Suboptimal risk factor control in patients undergoing elective coronary or peripheral percutaneous intervention. Am Heart J 2014;168:310–6.e3. https://doi.org/10.1016/j.ahj.2014.05.011 4. Saratzis A, Jaspers NEM, Gwilym B, Thomas O, Tsui A, Lefroy R, et al. Observational study of the medical management of patients with peripheral artery disease. Br J Surg 2019;106:1168–77. https://doi.org/10.1002/bjs.11214 5. McDermott MM, Mandapat AL, Moates A, Albay M, Chiou E, Celic L, et al. Knowledge and attitudes regarding cardiovascular disease risk and prevention in patients with coronary or peripheral arterial disease. Arch Intern Med 2003;163:2157–62. https://doi. org/10.1001/archinte.163.18.2157 6. Grayson PC, Ponte C, Suppiah R, Robson JC, Gribbons KB, Judge A, et al. 2022 American College of Rheumatology/EULAR classification criteria for Takayasu arteritis. Ann Rheum Dis 2022;81:1654–60. https://doi.org/10.1136/ard-2022-223482 7. Hellmich B, Agueda A, Monti S, Buttgereit F, de Boysson H, Brouwer E, et al. 2018 update of the EULAR recommendations for the management of large vessel vasculitis. Ann Rheum Dis 2020;79:19–30. https://doi.org/10.1136/annrheumdis-2019-215672 8. Ponte C, Grayson PC, Robson JC, Suppiah R, Gribbons KB, Judge A, et al. 2022 American College of Rheumatology/EULAR classification criteria for giant cell arteritis. Ann Rheum Dis 2022;81:1647–53. https://doi.org/10.1136/ard-2022-223480 9. Stone JR, Bruneval P, Angelini A, Bartoloni G, Basso C, Batoroeva L, et al. Consensus statement on surgical pathology of the aorta from the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology: I. Inflammatory diseases. Cardiovasc Pathol 2015;24:267–78. https://doi.org/10. 1016/j.carpath.2015.05.001 10. Diseases GBD, Injuries C. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease study 2019. Lancet 2020;396:1204–22. https://doi.org/10.1016/S0140- 6736(20)30925-9 11. Lin J, Chen Y, Jiang N, Li Z, Xu S. Burden of peripheral artery disease and its attributable risk factors in 204 countries and territories from 1990 to 2019. Front Cardiovasc Med 2022;9:868370. https://doi.org/10.3389/fcvm.2022.868370 12. GBD 2019 Peripheral Artery Disease Collaborators. Global burden of peripheral artery disease and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease study 2019. Lancet Glob Health 2023;11:e1553–65. https://doi.org/10.1016/ S2214-109X(23)00355-8 13. Liu W, Yang C, Chen, Lei F, Qin J-J, Liu H, et al. Global death burden and attributable risk factors of peripheral artery disease by age, sex, SDI regions, and countries from 1990 to 2030: results from the Global Burden of Disease study 2019. Atherosclerosis 2022;347:17–27. https://doi.org/10.1016/j.atherosclerosis.2022.03.002 14. Roth GA, Mensah GA, Johnson CO, Addolorato G, Ammirati E, Baddour LM, et al. Global burden of cardiovascular diseases and risk factors, 1990–2019: update from the GBD 2019 study. J Am Coll Cardiol 2020;76:2982–3021. https://doi.org/10.1016/j. jacc.2020.11.010 15. Pu L, Wang L, Zhang R, Zhao T, Jiang Y, Han L. Projected global trends in ischemic stroke incidence, deaths and disability-adjusted life years from 2020 to 2030. Stroke 2023;54:1330–9. https://doi.org/10.1161/STROKEAHA.122.040073 16. Summers KL, Kerut EK, Sheahan CM, Sheahan MG, III. Evaluating the prevalence of abdominal aortic aneurysms in the United States through a national screening database. J Vasc Surg 2021;73:61–8. https://doi.org10.1016/j.jvs.2020.03.046 17. Behrendt CA, Thomalla G, Rimmele DL, Petersen EL, Twerenbold R, Debus ES, et al. Editor’s choice—prevalence of peripheral arterial disease, abdominal aortic aneurysm, and risk factors in the Hamburg city health study: a cross sectional analysis. Eur J Vasc Endovasc Surg 2023;65:590–8. https://doi.org/10.1016/j.ejvs.2023.01.002 18. Rossello X, Dorresteijn JA, Janssen A, Lambrinou E, Scherrenberg M, Bonnefoy-Cudraz E, et al. Risk prediction tools in cardiovascular disease prevention: a report from the ESC Prevention of CVD programme led by the European Association of Preventive Cardiology (EAPC) in collaboration with the Acute Cardiovascular Care Association (ACCA) and the Association of Cardiovascular Nursing and Allied Professions (ACNAP). Eur Heart J Acute Cardiovasc Care 2020;9: 522–32. https://doi.org/10.1177/2048872619858285 19. Visseren FLJ, Mach F, Smulders YM, Carballo D, Koskinas KC, Bäck M, et al. 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice. Eur Heart J 2021; 42:3227–337. https://doi.org/10.1093/eurheartj/ehab484 20. Aday AW, Matsushita K. Epidemiology of peripheral artery disease and polyvascular disease. Circ Res 2021;128:1818–32. https://doi.org/10.1161/CIRCRESAHA.121. 318535 21. Pabon M, Cheng S, Altin SE, Sethi SS, Nelson MD, Moreau KL, et al. Sex differences in peripheral artery disease. Circ Res 2022;130:496–511. https://doi.org/10.1161/ CIRCRESAHA.121.320702 22. Khawaja T, Janus SE, Tashtish N, Janko M, Baeza C, Gilkeson R, et al. Prevalence of thoracic aortic aneurysm in patients referred for no/low-charge coronary artery calcium scoring: insights from the CLARIFY registry. Am J Prev Cardiol 2022;12:100378. https://doi.org/10.1016/j.ajpc.2022.100378 23. Obel LM, Diederichsen AC, Steffensen FH, Frost L, Lambrechtsen J, Busk M, et al. Population-based risk factors for ascending, arch, descending, and abdominal aortic dilations for 60-74-year-old individuals. J Am Coll Cardiol 2021;78:201–11. https://doi.org/ 10.1016/j.jacc.2021.04.094 24. Bossone E, Eagle KA. Epidemiology and management of aortic disease: aortic aneurysms and acute aortic syndromes. Nat Rev Cardiol 2021;18:331–48. https://doi.org/ 10.1038/s41569-020-00472-6 25. Verhagen JMA, Kempers M, Cozijnsen L, Bouma BJ, Duijnhouwer AL, Post JG, et al. Expert consensus recommendations on the cardiogenetic care for patients with thoracic aortic disease and their first-degree relatives. Int J Cardiol 2018;258:243–8. https:// doi.org/10.1016/j.ijcard.2018.01.145 26. Burger PM, Pradhan AD, Dorresteijn JAN, Koudstaal S, Teraa M, de Borst GJ, et al. C-reactive protein and risk of cardiovascular events and mortality in patients with various cardiovascular disease locations. Am J Cardiol 2023;197:13–23. https://doi.org/10. 1016/j.amjcard.2023.03.025 27. Nidorf SM, Fiolet ATL, Mosterd A, Eikelboom JW, Schut A, Opstal TSJ, et al. Colchicine in patients with chronic coronary disease. N Engl J Med 2020;383:1838–47. https://doi. org/10.1056/NEJMoa2021372 28. Tardif JC, Kouz S, Waters DD, Bertrand OF, Diaz R, Maggioni AP, et al. Efficacy and safety of low-dose colchicine after myocardial infarction. N Engl J Med 2019;381: 2497–505. https://doi.org/10.1056/NEJMoa1912388 29. Parkkila K, Kiviniemi A, Tulppo M, Perkiömäki J, Kesäniemi YA, Ukkola O. Carotid and femoral bruits as cardiovascular risk indicators in a middle-aged Finnish population: a 20-year prospective study. PLoS One 2022;17:e0278901. https://doi.org/10.1371/ journal.pone.0278901 30. Pickett CA, Jackson JL, Hemann BA, Atwood JE. Carotid bruits as a prognostic indicator of cardiovascular death and myocardial infarction: a meta-analysis. Lancet 2008; 371:1587–94. https://doi.org/10.1016/s0140-6736(08)60691-1 31. Charry D, Gouskova N, Meyer ML, Ring K, Nambi V, Heiss G, et al. Arterial stiffness and contralateral differences in blood pressure: the Atherosclerosis Risk in Communities (ARIC) study. J Clin Hypertens (Greenwich) 2022;24:878–84. https://doi. org/10.1111/jch.14493 32. Aboyans V, Criqui MH, McDermott MM, Allison MA, Denenberg JO, Shadman R, et al. The vital prognosis of subclavian stenosis. J Am Coll Cardiol 2007;49:1540–5. https://doi. org/10.1016/j.jacc.2006.09.055 33. Marcovina SM, Shapiro MD. Measurement of lipoprotein(a): a once in a lifetime opportunity. J Am Coll Cardiol 2022;79:629–31. https://doi.org/10.1016/j.jacc.2021.11. 053 34. Arndt H, Nordanstig J, Bertges DJ, Budtz-Lilly J, Venermo M, Espada CL, et al. A Delphi consensus on patient reported outcomes for registries and trials including patients with intermittent claudication: recommendations and reporting standard. Eur J Vasc Endovasc Surg 2022;64:526–33. https://doi.org/10.1016/j.ejvs.2022.08.011 35. Rymer JA, Narcisse D, Cosiano M, Tanaka J, McDermott MM, Treat-Jacobson DJ, et al. Patient-reported outcome measures in symptomatic, non-limb-threatening peripheral artery disease: a state-of-the-art review. Circ Cardiovasc Interv 2022;15:e011320. https://doi.org/10.1161/circinterventions.121.011320 36. Raja A, Spertus J, Yeh RW, Secemsky EA. Assessing health-related quality of life among patients with peripheral artery disease: a review of the literature and focus on patientreported outcome measures. Vasc Med 2021;26:317–25. https://doi.org/10.1177/ 1358863x20977016 37. Treat-Jacobson D, McDermott MM, Bronas UG, Campia U, Collins TC, Criqui MH, et al. Optimal exercise programs for patients with peripheral artery disease: a scientific statement from the American Heart Association. Circulation 2019;139:e10–33. https:// doi.org/10.1161/cir.0000000000000623 38. Poku E, Duncan R, Keetharuth A, Essat M, Phillips P, Woods HB, et al. Patient-reported outcome measures in patients with peripheral arterial disease: a systematic review of
ESC Guidelines 3663
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.127
psychometric properties. Health Qual Life Outcomes 2016;14:161. https://doi.org/10. 1186/s12955-016-0563-y 39. Mays RJ, Casserly IP, Kohrt WM, Ho PM, Hiatt WR, Nehler MR, et al. Assessment of functional status and quality of life in claudication. J Vasc Surg 2011;53:1410–21. https:// doi.org/10.1016/j.jvs.2010.11.092 40. Regensteiner JG, Hiatt WR, Coll JR, Criqui MH, Treat-Jacobson D, McDermott MM, et al. The impact of peripheral arterial disease on health-related quality of life in the peripheral arterial disease awareness, risk, and treatment: new resources for survival (PARTNERS) program. Vasc Med 2008;13:15–24. https://doi.org/10.1177/ 1358863x07084911 41. Harwood AE, King S, Totty J, Smith GE, Vanicek N, Chetter IC. A systematic review of muscle morphology and function in intermittent claudication. J Vasc Surg 2017;66: 1241–57. https://doi.org/10.1016/j.jvs.2017.05.106 42. Schieber MN, Hasenkamp RM, Pipinos II, Johanning JM, Stergiou N, DeSpiegelaere HK, et al. Muscle strength and control characteristics are altered by peripheral artery disease. J Vasc Surg 2017;66:178–86.e12. https://doi.org/10.1016/j.jvs.2017.01.051 43. Gohil RA, Mockford KA, Mazari F, Khan J, Vanicek N, Chetter IC, et al. Balance impairment, physical ability, and its link with disease severity in patients with intermittent claudication. Ann Vasc Surg 2013;27:68–74. https://doi.org/10.1016/j.avsg.2012.05.005 44. Mockford KA, Mazari FA, Jordan AR, Vanicek N, Chetter IC, Coughlin PA. Computerized dynamic posturography in the objective assessment of balance in patients with intermittent claudication. Ann Vasc Surg 2011;25:182–90. https://doi.org/ 10.1016/j.avsg.2010.07.021 45. Gardner AW, Montgomery PS. Impaired balance and higher prevalence of falls in subjects with intermittent claudication. J Gerontol A Biol Sci Med Sci 2001;56:M454–8. https://doi.org/10.1093/gerona/56.7.m454 46. McDermott MM, Ferrucci L, Liu K, Guralnik JM, Tian Lu, Liao Y, et al. Leg symptom categories and rates of mobility decline in peripheral arterial disease. J Am Geriatr Soc 2010;58:1256–62. https://doi.org/10.1111/j.1532-5415.2010.02941.x 47. McDermott MM, Liu K, Greenland P, Guralnik JM, Criqui MH, Chan C, et al. Functional decline in peripheral arterial disease: associations with the ankle brachial index and leg symptoms. JAMA 2004;292:453–61. https://doi.org/10.1001/jama.292.4.453 48. McDermott MM, Greenland P, Guralnik JM, Guralnik JM, Criqui MH, Chan C, et al. Depressive symptoms and lower extremity functioning in men and women with peripheral arterial disease. J Gen Intern Med 2003;18:461–7. https://doi.org/10.1046/j. 1525-1497.2003.20527.x 49. Ramirez JL, Drudi LM, Grenon SM. Review of biologic and behavioral risk factors linking depression and peripheral artery disease. Vasc Med 2018;23:478–88. https://doi. org/10.1177/1358863X18773161 50. Golledge J, Leicht AS, Yip L, Rowbotham SE, Pinchbeck J, Jenkins JS, et al. Relationship between disease specific quality of life measures, physical performance, and activity in people with intermittent claudication caused by peripheral artery disease. Eur J Vasc Endovasc Surg 2020;59:957–64. https://doi.org/10.1016/j.ejvs.2020.02.006 51. Gardner AW, Montgomery PS, Wang M, Xu C. Predictors of health-related quality of life in patients with symptomatic peripheral artery disease. J Vasc Surg 2018;68: 1126–34. https://doi.org/10.1016/j.jvs.2017.12.074 52. McDermott MM, Tian L, Liu K, Guralnik JM, Ferrucci L, Tan J, et al. Prognostic value of functional performance for mortality in patients with peripheral artery disease. J Am Coll Cardiol 2008;51:1482–9. https://doi.org/10.1016/j.jacc.2007.12.034 53. McDermott MM, Guralnik JM, Tian L, Ferrucci L, Liu K, Liao Y, et al. Baseline functional performance predicts the rate of mobility loss in persons with peripheral arterial disease. J Am Coll Cardiol 2007;50:974–82. https://doi.org/10.1016/j.jacc.2007.05.030 54. Sprengers RW, Teraa M, Moll FL, de Wit GA, van der Graaf Y, Verhaar MC. Quality of life in patients with no-option critical limb ischemia underlines the need for new effective treatment. J Vasc Surg 2010;52:843–9.e1. https://doi.org/10.1016/j.jvs.2010.04.057 55. Rose GA. The diagnosis of ischaemic heart pain and intermittent claudication in field surveys. Bull World Health Organ 1962;27:645–58 . 56. Leng GC, Fowkes FG. The Edinburgh claudication questionnaire: an improved version of the WHO/Rose questionnaire for use in epidemiological surveys. J Clin Epidemiol 1992;45:1101–9. https://doi.org/10.1016/0895-4356(92)90150-l 57. Birkett ST, Harwood AE, Caldow E, Ibeggazene S, Ingle L, Pymer S. A systematic review of exercise testing in patients with intermittent claudication: a focus on test standardisation and reporting quality in randomised controlled trials of exercise interventions. PLoS One 2021;16:e0249277. https://doi.org/10.1371/journal.pone.0249277 58. Harwood AE, Pymer S, Ingle L, Doherty P, Chetter IC, Parmenter B. Exercise training for intermittent claudication: a narrative review and summary of guidelines for practitioners. BMJ Open Sport Exerc Med 2020;6:e000897. https://doi.org/10.1136/bmjsem- 2020-000897 59. Treat-Jacobson D, McDermott MM, Beckman JA, Burt MA, Creager MA, Ehrman JK, et al. Implementation of supervised exercise therapy for patients with symptomatic peripheral artery disease: a science advisory from the American Heart Association. Circulation 2019;140:e700–10. https://doi.org/10.1161/cir.0000000000000727 60. Hiatt WR, Rogers RK, Brass EP. The treadmill is a better functional test than the 6-minute walk test in therapeutic trials of patients with peripheral artery disease. Circulation 2014;130:69–78. https://doi.org/10.1161/circulationaha.113.007003 61. Nicolaï SP, Viechtbauer W, Kruidenier LM, Candel MJJM, Prins MH, Teijink JAW. Reliability of treadmill testing in peripheral arterial disease: a meta-regression analysis. J Vasc Surg 2009;50:322–9. https://doi.org/10.1016/j.jvs.2009.01.042 62. Mazzolai L, Belch J, Venermo M, Aboyans V, Brodmann M, Bura-Rivière A, et al. Exercise therapy for chronic symptomatic peripheral artery disease. Eur Heart J 2024;45:1303–21. https://doi.org/10.1093/eurheartj/ehad734 63. McDermott MM, Guralnik JM, Criqui MH, Liu K, Kibbe MR, Ferrucci L. Six-minute walk is a better outcome measure than treadmill walking tests in therapeutic trials of patients with peripheral artery disease. Circulation 2014;130:61–8. https://doi.org/10. 1161/circulationaha.114.007002 64. McDermott MM, Ades PA, Dyer A, Guralnik JM, Kibbe M, Criqui MH. Corridor-based functional performance measures correlate better with physical activity during daily life than treadmill measures in persons with peripheral arterial disease. J Vasc Surg 2008; 48:1231–7.e1. https://doi.org/10.1016/j.jvs.2008.06.050 65. ATS Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories. ATS statement: guidelines for the six-minute walk test. Am J Respir Crit Care Med 2002;166:111–7. https://doi.org/10.1164/ajrccm.166.1.at1102 66. Verdijk LB, van Loon L, Meijer K, Savelberg HH. One-repetition maximum strength test represents a valid means to assess leg strength in vivo in humans. J Sports Sci 2009;27:59–68. https://doi.org/10.1080/02640410802428089 67. Ritti-Dias RM, Basyches M, Câmara L, Puech-Leao P, Battistella L, Wolosker N. Test-retest reliability of isokinetic strength and endurance tests in patients with intermittent claudication. Vasc Med 2010;15:275–8. https://doi.org/10.1177/ 1358863x10371415 68. Guralnik JM, Simonsick EM, Ferrucci L, Glynn RJ, Berkman LF, Blazer DG, et al. A short physical performance battery assessing lower extremity function: association with selfreported disability and prediction of mortality and nursing home admission. J Gerontol 1994;49:M85–94. https://doi.org/10.1093/geronj/49.2.m85 69. Guralnik JM, Ferrucci L, Simonsick EM, Salive ME, Wallace RB. Lower-extremity function in persons over the age of 70 years as a predictor of subsequent disability. N Engl J Med 1995;332:556–62. https://doi.org/10.1056/nejm199503023320902 70. Isselbacher EM, Preventza O, Hamilton Black J III, Augoustides JG, Beck AW, Bolen MA, et al. 2022 ACC/AHA Guideline for the diagnosis and management of aortic disease: a report of the American Heart Association/American College of Cardiology Joint Committee on clinical practice guidelines. J Am Coll Cardiol 2022;80:e223–393. https://doi.org/10.1016/j.jacc.2022.08.004 71. Pelliccia A, Sharma S, Gati S, Bäck M, Börjesson M, Caselli S, et al. 2020 ESC Guidelines on sports cardiology and exercise in patients with cardiovascular disease. Eur Heart J 2021;42:17–96. https://doi.org/10.1093/eurheartj/ehaa605 72. de Heer F, Gökalp AL, Kluin J, Takkenberg JJM. Measuring what matters to the patient: health related quality of life after aortic valve and thoracic aortic surgery. Gen Thorac Cardiovasc Surg 2019;67:37–43. https://doi.org/10.1007/s11748-017-0830-9 73. Chaddha A, Kline-Rogers E, Braverman AC, Erickson SR, Jackson EA, Franklin BA, et al. Survivors of aortic dissection: activity, mental health, and sexual function. Clin Cardiol 2015;38:652–9. https://doi.org/10.1002/clc.22418 74. Andonian C, Freilinger S, Achenbach S, Ewert P, Gundlach U, Kaemmerer H, et al. Quality of life in patients with Marfan syndrome: a cross-sectional study of 102 adult patients. Cardiovasc Diagn Ther 2021;11:602–10. https://doi.org/10.21037/cdt-20-692 75. Vanem TT, Rand-Hendriksen S, Brunborg C, Geiran OR, Røe C. Health-related quality of life in Marfan syndrome: a 10-year follow-up. Health Qual Life Outcomes 2020;18: 376. https://doi.org/10.1186/s12955-020-01633-4 76. Cervin A, Wanhainen A, Björck M. Popliteal aneurysms are common among men with screening detected abdominal aortic aneurysms, and prevalence correlates with the diameters of the common iliac arteries. Eur J Vasc Endovasc Surg 2020;59:67–72. https://doi.org/10.1016/j.ejvs.2019.07.042 77. Aboyans V, Ricco JB, Bartelink MEL, Björck M, Brodmann M, Cohnert T, et al. 2017 ESC Guidelines on the diagnosis and treatment of peripheral arterial diseases, in collaboration with the European Society for Vascular Surgery (ESVS): document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries. Endorsed by: the European Stroke Organization (ESO), the task force for the diagnosis and treatment of peripheral arterial diseases of the European Society of Cardiology (ESC) and of the European Society for Vascular Surgery (ESVS). Eur Heart J 2018;39:763–816. https://doi.org/ 10.1093/eurheartj/ehx095 78. Ichihashi S, Desormais I, Hashimoto T, Magne J, Kichikawa K, Aboyans V. Accuracy and reliability of the ankle brachial index measurement using a multicuff oscillometric device versus the Doppler method. Eur J Vasc Endovasc Surg 2020;60:462–8. https://doi. org/10.1016/j.ejvs.2020.06.013 79. Aboyans V, Criqui MH, Abraham P, Allison MA, Creager MA, Diehm C, et al. Measurement and interpretation of the ankle-brachial index: a scientific statement from the American Heart Association. Circulation 2012;126:2890–909. https://doi. org/10.1161/CIR.0b013e318276fbcb 80. Høyer C, Strandberg J, Overvad Jordansen MK, Zacho HD. The ability of the toe-brachial index to predict the outcome of treadmill exercise testing in patients with a normal resting ankle-brachial index. Ann Vasc Surg 2020;64:263–9. https://doi. org/10.1016/j.avsg.2019.10.041 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.128
81. Godet R, Bruneau A, Vielle B, Vincent F, Le Tourneau T, Carre F, et al. Post-exercise ankle blood pressure and ankle to brachial index after heavy load bicycle exercise. Scand J Med Sci Sports 2018;28:2144–52. https://doi.org/10.1111/sms.13234 82. van Langen H, van Gurp J, Rubbens L. Interobserver variability of ankle-brachial index measurements at rest and post exercise in patients with intermittent claudication. Vasc Med 2009;14:221–6. https://doi.org/10.1177/1358863x08101017 83. Stein R, Hriljac I, Halperin JL, Gustavson SM, Teodorescu V, Olin JW, Limitation of the resting ankle-brachial index in symptomatic patients with peripheral arterial disease. Vasc Med 2006;11:29–33. https://doi.org/10.1191/1358863x06vm663oa 84. Abraham P, Desvaux B, Saumet JL. Ankle-brachial index after maximum exercise in treadmill and cycle ergometers in athletes. Clin Physiol 1998;18:321–6. https://doi. org/10.1046/j.1365-2281.1998.00100.x 85. Stoffers HE, Kester AD, Kaiser V, Rinkens PELM, Kitslaar PJEHM, Knottnerus JA, The diagnostic value of the measurement of the ankle-brachial systolic pressure index in primary health care. J Clin Epidemiol 1996;49:1401–5. https://doi.org/10.1016/s0895- 4356(96)00275-2 86. Ouriel K, McDonnell AE, Metz CE, Zarins CK. Critical evaluation of stress testing in the diagnosis of peripheral vascular disease. Surgery 1982;91:686–93 . 87. Laing S, Greenhalgh RM. The detection and progression of asymptomatic peripheral arterial disease. Br J Surg 2005;70:628–30. https://doi.org/10.1002/bjs.1800701017 88. Ankle Brachial Index Collaboration; Fowkes FG, Murray GD, Butcher I, Heald CL, Lee RJ, et al. Ankle brachial index combined with Framingham risk score to predict cardiovascular events and mortality: a meta-analysis. JAMA 2008;300:197–208. https://doi. org/10.1001/jama.300.2.197 89. Criqui MH, McClelland RL, McDermott MM, McDermott MM, Allison MA, Blumenthal RS, et al. The ankle-brachial index and incident cardiovascular events in the MESA (multi-ethnic study of atherosclerosis). J Am Coll Cardiol 2010;56:1506–12. https:// doi.org/10.1016/j.jacc.2010.04.060 90. Herraiz-Adillo Á, Cavero-Redondo I, Álvarez-Bueno C, Pozuelo-Carrascosa DP, Solera-Martínez M. The accuracy of toe brachial index and ankle brachial index in the diagnosis of lower limb peripheral arterial disease: a systematic review and meta-analysis. Atherosclerosis 2020;315:81–92. https://doi.org/10.1016/j. atherosclerosis.2020.09.026 91. Tehan PE, Santos D, Chuter VH. A systematic review of the sensitivity and specificity of the toe-brachial index for detecting peripheral artery disease. Vasc Med 2016;21: 382–9. https://doi.org/10.1177/1358863x16645854 92. Fukui M, Tanaka M, Hamaguchi M, Senmaru T, Sakabe K, Asano M, et al. Toe-brachial index is associated more strongly with albuminuria or glomerular filtration rate than ankle-brachial index in patients with type 2 diabetes. Hypertens Res 2012;35:745–9. https://doi.org/10.1038/hr.2012.16 93. Dachun X, Jue L, Liling Z, Xu Y, Hu D, Pagoto SL, et al. Sensitivity and specificity of the ankle—brachial index to diagnose peripheral artery disease: a structured review. Vasc Med 2010;15:361–9. https://doi.org/10.1177/1358863x10378376 94. Morimoto S, Nakajima F, Yurugi T, Morita T, Jo F, Nishikawa M, et al. Risk factors of normal ankle-brachial index and low toe-brachial index in hemodialysis patients. Ther Apher Dial 2009;13:103–7. https://doi.org/10.1111/j.1744-9987.2009.00663.x 95. Young MJ, Adams JE, Anderson GF, Boulton AJ, Cavanagh PR. Medial arterial calcification in the feet of diabetic patients and matched non-diabetic control subjects. Diabetologia 1993;36:615–21. https://doi.org/10.1007/bf00404070 96. Carter SA, Lezack JD. Digital systolic pressures in the lower limb in arterial disease. Circulation 1971;43:905–14. https://doi.org/10.1161/01.cir.43.6.905 97. Watanabe Y, Masaki H, Kojima K, Tanemoto K. Toe-brachial index in the second toe: substitutability to toe-brachial index in the great toe and ankle-brachial index. Ann Vasc Dis 2016;9:300–6. https://doi.org/10.3400/avd.oa.16-00078 98. Pérez-Martin A, Meyer G, Demattei C, Böge G, Laroche J-P, Quéré I, et al. Validation of a fully automatic photoplethysmographic device for toe blood pressure measurement. Eur J Vasc Endovasc Surg 2010;40:515–20. https://doi.org/10.1016/j.ejvs.2010.06.008 99. Hoyer C, Sandermann J, Petersen LJ. The toe-brachial index in the diagnosis of peripheral arterial disease. J Vasc Surg 2013;58:231–8. https://doi.org/10.1016/j.jvs.2013.03. 044 100. Monti M, Calanca L, Alatri A, Mazzolai L. Accuracy of in-patients ankle-brachial index measurement by medical students. Vasa 2016;45:43–8. https://doi.org/10.1024/0301- 1526/a000494 101. Kaiser V, Kester AD, Stoffers HE, Kitslaar PJ, Knottnerus JA. The influence of experience on the reproducibility of the ankle-brachial systolic pressure ratio in peripheral arterial occlusive disease. Eur J Vasc Endovasc Surg 1999;18:25–9. https://doi.org/10. 1053/ejvs.1999.0843 102. Ray SA, Srodon PD, Taylor RS, Dormandy JA. Reliability of ankle:brachial pressure index measurement by junior doctors. Br J Surg 1994;81:188–90. https://doi.org/10. 1002/bjs.1800810208 103. Gerhard-Herman MD, Gornik HL, Barrett C, Barshes NR, Corriere MA, Drachman DE, et al. 2016 AHA/ACC Guideline on the management of patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/ American Heart Association task force on clinical practice guidelines. Circulation 2017;135:e726–79. https://doi.org/10.1161/CIR.0000000000000471 104. Stivalet O, Paisant A, Belabbas D, Omarjee L, Le Faucheur A, Landreau P, et al. Exercise testing criteria to diagnose lower extremity peripheral artery disease assessed by computed-tomography angiography. PLoS One 2019;14:e0219082. https://doi.org/10. 1371/journal.pone.0219082 105. Abraham P, Picquet J, Vielle B, Sigaudo-Roussel D, Paisant-Thouveny F, Enon B, et al. Transcutaneous oxygen pressure measurements on the buttocks during exercise to detect proximal arterial ischemia: comparison with arteriography. Circulation 2003; 107:1896–900. https://doi.org/10.1161/01.Cir.0000060500.60646.E0 106. Yamamoto K, Miyata T, Onozuka A, Koyama H, Ohtsu H, Nagawa H. Plantar flexion as an alternative to treadmill exercise for evaluating patients with intermittent claudication. Eur J Vasc Endovasc Surg 2007;33:325–9. https://doi.org/10.1016/j.ejvs. 2006.10.012 107. Maufus M, Sevestre-Pietri MA, Sessa C, Pignon B, Egelhofer H, Dupas S, et al. Critical limb ischaemia and the response to bone marrow-derived cell therapy according to tcPO(2) measurement. Vasa 2017;46:23–8. https://doi.org/10.1024/0301-1526/ a000590 108. Leenstra B, Wijnand J, Verhoeven B, Koning O, Teraa M, Verhaar MC, et al. Applicability of transcutaneous oxygen tension measurement in the assessment of chronic limb-threatening ischemia. Angiology 2020;71:208–16. https://doi.org/10. 1177/0003319719866958 109. Ott A. Inflammation and transcutaneous measurement of oxygen pressure in dermatology. Adv Exp Med Biol 1987;220:79–82. https://doi.org/10.1007/978-1- 4613-1927-6_14 110. Woo Y, Suh YJ, Lee H, Jeong E, Park SC, Yun SS, et al. TcPO2 value can predict wound healing time in clinical practice of CLTI patients. Ann Vasc Surg 2023;91:249–56. https:// doi.org/10.1016/j.avsg.2022.11.020 111. Wang Z, Hasan R, Firwana B, Elraiyah T, Tsapas A, Prokop L, et al. A systematic review and meta-analysis of tests to predict wound healing in diabetic foot. J Vasc Surg 2016; 63:29S–36S.e2. https://doi.org/10.1016/j.jvs.2015.10.004 112. Yamada T, Ohta T, Ishibashi H, Sugimoto I, Iwata H, Takahashi M, et al. Clinical reliability and utility of skin perfusion pressure measurement in ischemic limbs—comparison with other noninvasive diagnostic methods. J Vasc Surg 2008;47:318–23. https://doi. org/10.1016/j.jvs.2007.10.045 113. Noori N, Haruno L, Schroeder I, Vrahas M, Little M, Moon C, et al. Preoperative transcutaneous oxygen perfusion measurements in predicting atraumatic wound healing after major lower extremity amputation. Orthopedics 2022;45:174–80. https://doi. org/10.3928/01477447-20220128-05 114. Nishio H, Minakata K, Kawaguchi A, Kumagai M, Ikeda T, Shimizu A, et al. Transcutaneous oxygen pressure as a surrogate index of lower limb amputation. Int Angiol 2016;35:565–72. 115. Sarin S, Shami S, Shields DA, Scurr JH, Smith PD. Selection of amputation level: a review. Eur J Vasc Surg 1991;5:611–20. https://doi.org/10.1016/s0950-821x(05)80894-1 116. Abraham P, Ramondou P, Hersant J, Sempore WY, Feuilloy M, Henni S. Investigation of arterial claudication with transcutaneous oxygen pressure at exercise: interests and limits. Trends Cardiovasc Med 2021;31:218–23. https://doi.org/10. 1016/j.tcm.2020.03.003 117. Abraham P, Gu Y, Guo L, Kroeger K, Ouedraogo N, Wennberg P, et al. Clinical application of transcutaneous oxygen pressure measurements during exercise. Atherosclerosis 2018;276:117–23. https://doi.org/10.1016/j.atherosclerosis.2018. 07.023 118. Colas-Ribas C, Signolet I, Henni S, Feuillloy M, Gagnadoux F, Abraham P. High prevalence of known and unknown pulmonary diseases in patients with claudication during exercise oximetry: a retrospective analysis. Medicine (Baltimore) 2016;95:e4888. https://doi.org/10.1097/md.0000000000004888 119. Frank U, Nikol S, Belch J, Boc V, Brodmann M, Carpentier PH, et al. ESVM guideline on peripheral arterial disease. Vasa 2019;48:1–79. https://doi.org/10.1024/0301-1526/ a000834 120. Schlager O, Francesconi M, Haumer M, Dick P, Sabeti S, Amighi J, et al. Duplex sonography versus angiography for assessment of femoropopliteal arterial disease in a ‘real-world’ setting. J Endovasc Ther 2007;14:452–9. https://doi.org/10.1177/ 152660280701400404 121. Collins R, Burch J, Cranny G, Aguiar-Ibáñez R, Craig D, Wright K, et al. Duplex ultrasonography, magnetic resonance angiography, and computed tomography angiography for diagnosis and assessment of symptomatic, lower limb peripheral arterial disease: systematic review. BMJ 2007;334:1257. https://doi.org/10.1136/bmj.39217. 473275.55 122. Sprynger M, Rigo F, Moonen M, Aboyans V, Edvardsen T, de Alcantara ML, et al. Focus on echovascular imaging assessment of arterial disease: complement to the ESC Guidelines (PARTIM 1) in collaboration with the working group on aorta and peripheral vascular diseases. Eur Heart J Cardiovasc Imaging 2018;19:1195–221. https://doi. org/10.1093/ehjci/jey103 123. Collins R, Cranny G, Burch J, Aguiar-Ibáñez R, Craig D, Wright K, et al. A systematic review of duplex ultrasound, magnetic resonance angiography and computed tomography angiography for the diagnosis and assessment of symptomatic, lower limb peripheral arterial disease. Health Technol Assess 2007;11:iii–iv, xi-xiii, 1–184. https://doi. org/10.3310/hta11200
ESC Guidelines 3665
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.129
124. Rodway AD, Cheal D, Allan C, Pazos-Casal F, Hanna L, Field BCT, et al. Ankle Doppler for cuffless ankle brachial index estimation and peripheral artery disease diagnosis independent of diabetes. J Clin Med 2022;12:97. https://doi.org/10.3390/ jcm12010097 125. Katsanos K, Tepe G, Tsetis D, Fanelli F. Standards of practice for superficial femoral and popliteal artery angioplasty and stenting. Cardiovasc Intervent Radiol 2014;37: 592–603. https://doi.org/10.1007/s00270-014-0876-3 126. Coffi SB, Ubbink DT, Zwiers I, van Gurp JA, Legemate DA. Improved assessment of the hemodynamic significance of borderline iliac stenoses with use of hyperemic duplex scanning. J Vasc Surg 2002;36:575–80. https://doi.org/10.1067/mva.2002.126086 127. Elsman BH, Legemate DA, de Vos HJ, Mali WP, Eikelboom BC. Hyperaemic colour duplex scanning for the detection of aortoiliac stenoses. a comparative study with intra-arterial pressure measurement. Eur J Vasc Endovasc Surg 1997;14:462–7. https://doi.org/10.1016/s1078-5884(97)80125-6 128. Venermo M, Sprynger M, Desormais I, Björck M, Brodmann M, Cohnert T, et al. Follow-up of patients after revascularisation for peripheral arterial diseases: a consensus document from the European Society of Cardiology working group on aorta and peripheral vascular diseases and the European Society for Vascular Surgery. Eur J Prev Cardiol 2019;26:1971–84. https://doi.org/10.1177/2047487319846999 129. Golemati S, Cokkinos DD. Recent advances in vascular ultrasound imaging technology and their clinical implications. Ultrasonics 2022;119:106599. https://doi.org/10.1016/j. ultras.2021.106599 130. Itoga NK, Minami HR, Chelvakumar M, Pearson K, Mell MM, Bendavid E, et al. Cost-effectiveness analysis of asymptomatic peripheral artery disease screening with the ABI test. Vasc Med 2018;23:97–106. https://doi.org/10.1177/1358863X17745371 131. Xu D, Zou L, Xing Y, Hou L, Wei Y, Zhang J, et al. Diagnostic value of ankle-brachial index in peripheral arterial disease: a meta-analysis. Can J Cardiol 2013;29:492–8. https://doi.org/10.1016/j.cjca.2012.06.014 132. Hashimoto T, Ichihashi S, Iwakoshi S, Kichikawa K. Combination of pulse volume recording (PVR) parameters and ankle-brachial index (ABI) improves diagnostic accuracy for peripheral arterial disease compared with ABI alone. Hypertens Res 2016;39:430–4. https://doi.org/10.1038/hr.2016.13 133. Tehan PE, Bray A, Chuter VH. Non-invasive vascular assessment in the foot with diabetes: sensitivity and specificity of the ankle brachial index, toe brachial index and continuous wave Doppler for detecting peripheral arterial disease. J Diabetes Complications 2016;30:155–60. https://doi.org/10.1016/j.jdiacomp.2015.07.019 134. Loukas M, Bilinsky E, Bilinsky S, Blaak C, Tubbs RS, Anderson RH. The anatomy of the aortic root. Clin Anat 2014;27:748–56. https://doi.org/10.1002/ca.22295 135. Dagenais F. Anatomy of the thoracic aorta and of its branches. Thorac Surg Clin 2011; 21:219–27, viii. https://doi.org/10.1016/j.thorsurg.2010.12.004 136. Lombardi JV, Hughes GC, Appoo JJ, Bavaria JE, Beck AW, Cambria RP, et al. Society for Vascular Surgery (SVS) and Society of Thoracic Surgeons (STS) reporting standards for type B aortic dissections. Ann Thorac Surg 2020;109:959–81. https://doi.org/10.1016/j. athoracsur.2019.10.005 137. Rodríguez-Palomares JF, Teixidó-Tura G, Galuppo V, Cuéllar H, Laynez A, Gutiérrez L, et al. Multimodality assessment of ascending aortic diameters: comparison of different measurement methods. J Am Soc Echocardiogr 2016;29:819–26.e4. https://doi.org/10. 1016/j.echo.2016.04.006 138. Saura D, Dulgheru R, Caballero L, Bernard A, Kou S, Gonjilashvili N, et al. Two-dimensional transthoracic echocardiographic normal reference ranges for proximal aorta dimensions: results from the EACVI NORRE study. Eur Heart J Cardiovasc Imaging 2017;18:167–79. https://doi.org/10.1093/ehjci/jew053 139. Bons LR, Duijnhouwer AL, Boccalini S, van den Hoven AT, van der Vlugt MJ, Chelu RG, et al. Intermodality variation of aortic dimensions: how, where and when to measure the ascending aorta. Int J Cardiol 2019;276:230–5. https://doi.org/10.1016/j.ijcard.2018. 08.067 140. Amsallem M, Ou P, Milleron O, Henry-Feugeas M-C, Detaint D, Arnoult F, et al. Comparative assessment of ascending aortic aneurysms in Marfan patients using ECG-gated computerized tomographic angiography versus trans-thoracic echocardiography. Int J Cardiol 2015;184:22–7. https://doi.org/10.1016/j.ijcard.2015.01.086 141. Matthews EO, Pinchbeck J, Elmore K, Jones RE, Moxon JV, Golledge J. The reproducibility of measuring maximum abdominal aortic aneurysm diameter from ultrasound images. Ultrasound J 2021;13:13. https://doi.org/10.1186/s13089-021-00211-z 142. Bonnafy T, Lacroix P, Desormais I, Labrunie A, Marin B, Leclerc A, et al. Reliability of the measurement of the abdominal aortic diameter by novice operators using a pocket-sized ultrasound system. Arch Cardiovasc Dis 2013;106:644–50. https://doi. org/10.1016/j.acvd.2013.08.004 143. Fitzgerald BT, Kwon A, Scalia GM. The new dimension in aortic measurements—use of the inner edge measurement for the thoracic aorta in Australian patients. Heart Lung Circ 2015;24:1104–10. https://doi.org/10.1016/j.hlc.2015.05.001 144. Burman ED, Keegan J, Kilner PJ. Aortic root measurement by cardiovascular magnetic resonance: specification of planes and lines of measurement and corresponding normal values. Circ Cardiovasc Imaging 2008;1:104–13. https://doi.org/10.1161/ circimaging.108.768911 145. Muraru D, Maffessanti F, Kocabay G, Peluso D, Bianco LD, Piasentini E, et al. Ascending aorta diameters measured by echocardiography using both leading edge-to-leading edge and inner edge-to-inner edge conventions in healthy volunteers. Eur Heart J Cardiovasc Imaging 2014;15:415–22. https://doi.org/10.1093/ehjci/jet173 146. Vis JC, Rodríguez-Palomares JF, Teixidó-Tura G, Galian-Gay L, Granato C, Guala A, et al. Implications of asymmetry and valvular morphotype on echocardiographic measurements of the aortic root in bicuspid aortic valve. J Am Soc Echocardiogr 2019;32: 105–12. https://doi.org/10.1016/j.echo.2018.08.004 147. Ghulam Ali S, Fusini L, Dalla Cia A, Tamborini G, Gripari P, Muratori M, et al. Technological advancements in echocardiographic assessment of thoracic aortic dilatation: head to head comparison among multidetector computed tomography, 2-dimensional, and 3-dimensional echocardiography measurements. J Thorac Imaging 2018;33:232–9. https://doi.org/10.1097/rti.0000000000000330 148. Mendoza DD, Kochar M, Devereux RB, Basson CT, Min JK, Holmes K, et al. Impact of image analysis methodology on diagnostic and surgical classification of patients with thoracic aortic aneurysms. Ann Thorac Surg 2011;92:904–12. https://doi.org/10.1016/ j.athoracsur.2011.03.130 149. Campens L, Demulier L, De Groote K, Vandekerckhove K, De Wolf D, Roman MJ, et al. Reference values for echocardiographic assessment of the diameter of the aortic root and ascending aorta spanning all age categories. Am J Cardiol 2014;114:914–20. https://doi.org/10.1016/j.amjcard.2014.06.024 150. Pedersen OM, Aslaksen A, Vik-Mo H. Ultrasound measurement of the luminal diameter of the abdominal aorta and iliac arteries in patients without vascular disease. J Vasc Surg 1993;17:596–601. https://doi.org/10.1067/mva.1993.39525 151. Kim H, Kwon TW, Choi E, Jeong S, Kim H-K, Han Y, et al. Aortoiliac diameter and length in a healthy cohort. PLoS One 2022;17:e0268077. https://doi.org/10.1371/ journal.pone.0268077 152. Evangelista A, Flachskampf FA, Erbel R, Antonini-Canterin F, Vlachopoulos C, Rocchi G, et al. Echocardiography in aortic diseases: EAE recommendations for clinical practice. Eur J Echocardiogr 2010;11:645–58. https://doi.org/10.1093/ejechocard/jeq056 153. Zafar MA, Li Y, Rizzo JA, Charilaou P, Saeyeldin A, Velasquez CA, et al. Height alone, rather than body surface area, suffices for risk estimation in ascending aortic aneurysm. J Thorac Cardiovasc Surg 2018;155:1938–50. https://doi.org/10.1016/j.jtcvs.2017.10.140 154. Masri A, Kalahasti V, Svensson LG, Roselli EE, Johnston D, Hammer D, et al. Aortic cross-sectional area/height ratio and outcomes in patients with a trileaflet aortic valve and a dilated aorta. Circulation 2016;134:1724–37. https://doi.org/10.1161/ circulationaha.116.022995 155. Wu J, Zafar MA, Li Y, Saeyeldin A, Huang Y, Zhao R, et al. Ascending aortic length and risk of aortic adverse events: the neglected dimension. J Am Coll Cardiol 2019;74: 1883–94. https://doi.org/10.1016/j.jacc.2019.07.078 156. Pham MHC, Ballegaard C, de Knegt MC, Sigvardsen PE, Sørgaard MH, Fuchs A, et al. Normal values of aortic dimensions assessed by multidetector computed tomography in the Copenhagen general population study. Eur Heart J Cardiovasc Imaging 2019;20: 939–48. https://doi.org/10.1093/ehjci/jez012 157. Davis AE, Lewandowski AJ, Holloway CJ, Ntusi NAB, Banerjee R, Nethononda R, et al. Observational study of regional aortic size referenced to body size: production of a cardiovascular magnetic resonance nomogram. J Cardiovasc Magn Reson 2014;16:9. https://doi.org/10.1186/1532-429x-16-9 158. Braley KT, Tang X, Makil ES, Borroughs-Ray D, Collins RT. The impact of body weight on the diagnosis of aortic dilation—misdiagnosis in overweight and underweight groups. Echocardiography 2017;34:1029–34. https://doi.org/10.1111/echo.13565 159. Evangelista A, Sitges M, Jondeau G, Nijveldt R, Pepi M, Cuellar H, et al. Multimodality imaging in thoracic aortic diseases: a clinical consensus statement from the European Association of Cardiovascular Imaging and the European Society of Cardiology working group on aorta and peripheral vascular diseases. Eur Heart J Cardiovasc Imaging 2023;24:e65–85. https://doi.org/10.1093/ehjci/jead024 160. Macdonald DB, Hurrell C, Costa AF, McInnes MDF, O’Malley ME, Barrett B, et al. Canadian Association of Radiologists Guidance on contrast associated acute kidney injury. Can Assoc Radiol J 2022;73:499–514. https://doi.org/10.1177/ 08465371221083970 161. Committee opinion no. 723: guidelines for diagnostic imaging during pregnancy and lactation. Obstet Gynecol 2017;130:e210–6. https://doi.org/10.1097/AOG.000000000 0002355 162. von Kodolitsch Y, Nienaber CA, Dieckmann C, Schwartz AG, Hofmann T, Brekenfeld C, et al. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med 2004; 116:73–7. https://doi.org/10.1016/j.amjmed.2003.08.030 163. Nazerian P, Pivetta E, Veglia S, Cavigli E, Mueller C, de Matos Soeiro A, et al. Integrated use of conventional chest radiography cannot rule out acute aortic syndromes in emergency department patients at low clinical probability. Acad Emerg Med 2019; 26:1255–65. https://doi.org/10.1111/acem.13819 164. Hartnell GG, Wakeley CJ, Tottle A, Papouchado M, Wilde RP. Limitations of chest radiography in discriminating between aortic dissection and myocardial infarction: implications for thrombolysis. J Thorac Imaging 1993;8:152–5. https://doi.org/10.1097/ 00005382-199321000-00008 165. Evangelista A, Avegliano G, Aguilar R, Cuellar H, Igual A, Gonzalez-Alujas T, et al. Impact of contrast-enhanced echocardiography on the diagnostic algorithm of acute aortic dissection. Eur Heart J 2010;31:472–9. https://doi.org/10.1093/eurheartj/ehp505 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.130
166. Litmanovich D, Bankier AA, Cantin L, Raptopoulos V, Boiselle PM. CT and MRI in diseases of the aorta. AJR Am J Roentgenol 2009;193:928–40. https://doi.org/10.2214/ajr. 08.2166 167. Pennell DJ, Sechtem UP, Higgins CB, Manning W, Pohost G, Rademakers F, et al. Clinical indications for cardiovascular magnetic resonance (CMR): consensus panel report. J Cardiovasc Magn Reson 2004;6:727–65. https://doi.org/10.1081/jcmr- 200038581 168. Yoshioka K, Tanaka R. MRI and MRA of aortic disease. Ann Vasc Dis 2010;3:196–201. https://doi.org/10.3400/avd.sasdi10003 169. Fadel BM, Mohty D, Kazzi BE, Alamro B, Arshi F, Mustafa M, et al. Ultrasound imaging of the abdominal aorta: a comprehensive review. J Am Soc Echocardiogr 2021;34:1119–36. https://doi.org/10.1016/j.echo.2021.06.012 170. Bhave NM, Nienaber CA, Clough RE, Eagle KA. Multimodality imaging of thoracic aortic diseases in adults. JACC Cardiovasc Imaging 2018;11:902–19. https://doi.org/10.1016/ j.jcmg.2018.03.009 171. Goldstein SA, Evangelista A, Abbara S, Arai A, Asch FM, Badano LP, et al. Multimodality imaging of diseases of the thoracic aorta in adults: from the American Society of Echocardiography and the European Association of Cardiovascular Imaging: endorsed by the Society of Cardiovascular Computed Tomography and Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr 2015;28:119–82. https:// doi.org/10.1016/j.echo.2014.11.015 172. Erbel R, Aboyans V, Boileau C, Bossone E, Bartolomeo RD, Eggebrecht H, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases: document covering acute and chronic aortic diseases of the thoracic and abdominal aorta of the adult. The task force for the diagnosis and treatment of aortic diseases of the European Society of Cardiology (ESC). Eur Heart J 2014;35:2873–926. https://doi.org/10.1093/eurheartj/ ehu281 173. Bossone E, Czerny M, Lerakis S, Rodríguez-Palomares J, Kukar N, Ranieri B, et al. Imaging and biomarkers in acute aortic syndromes: diagnostic and prognostic implications. Curr Probl Cardiol 2021;46:100654. https://doi.org/10.1016/j.cpcardiol.2020. 100654 174. Bossone E, LaBounty TM, Eagle KA. Acute aortic syndromes: diagnosis and management, an update. Eur Heart J 2018;39:739–49d. https://doi.org/10.1093/eurheartj/ ehx319 175. Vardhanabhuti V, Nicol E, Morgan-Hughes G, Roobottom CA, Roditi G, Hamilton MCK, et al. Recommendations for accurate CT diagnosis of suspected acute aortic syndrome (AAS)—on behalf of the British Society of Cardiovascular Imaging (BSCI)/ British Society of Cardiovascular CT (BSCCT). Br J Radiol 2016;89:20150705. https://doi.org/10.1259/bjr.20150705 176. Carstensen M, Keer D, Rempel J, Jeon P, Barrett B. Prevalence of risk factors for contrast-induced nephrotoxicity in outpatients undergoing intravenous contrast-enhanced computed tomography studies. Can Assoc Radiol J 2012;63: 177–82. https://doi.org/10.1016/j.carj.2010.12.004 177. Brenner DJ, Hall EJ. Computed tomography—an increasing source of radiation exposure. N Engl J Med 2007;357:2277–84. https://doi.org/10.1056/NEJMra072149 178. Barra L, Kanji T, Malette J, Pagnoux C. Imaging modalities for the diagnosis and disease activity assessment of Takayasu’s arteritis: a systematic review and meta-analysis. Autoimmun Rev 2018;17:175–87. https://doi.org/10.1016/j.autrev.2017.11.021 179. Dyverfeldt P, Bissell M, Barker AJ, Bolger AF, Carlhäll C-J, Ebbers T, et al. 4D flow cardiovascular magnetic resonance consensus statement. J Cardiovasc Magn Reson 2015; 17:72. https://doi.org/10.1186/s12968-015-0174-5 180. Rodriguez-Palomares JF. Genetics of bicuspid aortic valve: ready for clinical use? Heart 2022;108:1078–9. https://doi.org/10.1136/heartjnl-2021-320742 181. Guala A, Teixido-Tura G, Dux-Santoy L, Granato C, Ruiz-Muñoz A, Valente F, et al. Decreased rotational flow and circumferential wall shear stress as early markers of descending aorta dilation in Marfan syndrome: a 4D flow CMR study. J Cardiovasc Magn Reson 2019;21:63. https://doi.org/10.1186/s12968-019-0572-1 182. Horowitz MJ, Kupsky DF, El-Said HG, Alshawabkeh L, Kligerman SJ, Hsiao A. 4D flow MRI quantification of congenital shunts: comparison to invasive catheterization. Radiol Cardiothorac Imaging 2021;3:e200446. https://doi.org/10.1148/ryct.2021200446 183. Rizk J. 4D flow MRI applications in congenital heart disease. Eur Radiol 2021;31: 1160–74. https://doi.org/10.1007/s00330-020-07210-z 184. Gupta SK, Ya’qoub L, Wimmer AP, Fisher S, Saeed IM. Safety and clinical impact of MRI in patients with non-MRI-conditional cardiac devices. Radiol Cardiothorac Imaging 2020; 2:e200086. https://doi.org/10.1148/ryct.2020200086 185. Munawar DA, Chan JEZ, Emami M, Kadhim K, Khokhar K, O’Shea C, et al. Magnetic resonance imaging in non-conditional pacemakers and implantable cardioverterdefibrillators: a systematic review and meta-analysis. Europace 2020;22:288–98. https://doi.org/10.1093/europace/euz343 186. Nienaber CA. The role of imaging in acute aortic syndromes. Eur Heart J Cardiovasc Imaging 2013;14:15–23. https://doi.org/10.1093/ehjci/jes215 187. van der Geest KSM, Treglia G, Glaudemans A, Brouwer E, Sandovici M, Jamar F, et al. Diagnostic value of [18F]FDG-PET/CT for treatment monitoring in large vessel vasculitis: a systematic review and meta-analysis. Eur J Nucl Med Mol Imaging 2021;48: 3886–902. https://doi.org/10.1007/s00259-021-05362-8 188. Dejaco C, Ramiro S, Duftner C, Besson FL, Bley TA, Blockmans D, et al. EULAR recommendations for the use of imaging in large vessel vasculitis in clinical practice. Ann Rheum Dis 2018;77:636–43. https://doi.org/10.1136/annrheumdis-2017-212649 189. Forsythe RO, Dweck MR, McBride OMB, Vesey AT, Semple SI, Shah ASV, et al. (18) F-sodium fluoride uptake in abdominal aortic aneurysms: the SoFIA(3) study. J Am Coll Cardiol 2018;71:513–23. https://doi.org/10.1016/j.jacc.2017.11.053 190. Roque A, Pizzi MN. (18)F-FDG PET/CT: not only a promise for complex scenarioslet’s talk about aortic grafts. J Nucl Cardiol 2022;29:2949–51. https://doi.org/10.1007/ s12350-021-02888-0 191. Roque A, Pizzi MN, Fernández-Hidalgo N, Permanyer E, Cuellar-Calabria H, Romero-Farina G, et al. Morpho-metabolic post-surgical patterns of non-infected prosthetic heart valves by [18F]FDG PET/CTA: ‘normality’ is a possible diagnosis. Eur Heart J Cardiovasc Imaging 2020;21:24–33. https://doi.org/10.1093/ehjci/jez222 192. Pizzi MN, Roque A, Cuéllar-Calabria H, Fernández-Hidalgo N, Ferreira-González I, González-Alujas MT, et al. (18)F-FDG-PET/CTA of prosthetic cardiac valves and valvetube grafts: infective versus inflammatory patterns. JACC Cardiovasc Imaging 2016;9: 1224–7. https://doi.org/10.1016/j.jcmg.2016.05.013 193. Pizzi MN, Roque A, Fernández-Hidalgo N, Cuéllar-Calabria H, Ferreira-González I, Gonzàlez-Alujas MT, et al. Improving the diagnosis of infective endocarditis in prosthetic valves and intracardiac devices with 18F-fluordeoxyglucose positron emission tomography/computed tomography angiography: initial results at an infective endocarditis referral center. Circulation 2015;132:1113–26. https://doi.org/10.1161/ circulationaha.115.015316 194. Teraa M, Hazenberg CE, Houben IB, Trimarchi S, van Herwaarden JA. Important issues regarding planning and sizing for emergent TEVAR. J Cardiovasc Surg (Torino) 2020;61: 708–12. https://doi.org/10.23736/S0021-9509.20.11571-4 195. Lindholt JS, Sogaard R. Population screening and intervention for vascular disease in Danish men (VIVA): a randomised controlled trial. Lancet 2017;390:2256–65. https://doi.org/10.1016/S0140-6736(17)32250-X 196. Lin JS, Evans CV, Johnson E, Redmond N, Coppola EL, Smith N. Nontraditional risk factors in cardiovascular disease risk assessment: updated evidence report and systematic review for the US preventive services task force. JAMA 2018;320:281–97. https:// doi.org/10.1001/jama.2018.4242 197. Normahani P, Burgess L, Norrie J, Epstein DM, Kandiyil N, Saratzis A, et al. Study protocol for a multicentre comparative diagnostic accuracy study of tools to establish the presence and severity of peripheral arterial disease in people with diabetes mellitus: the DM PAD study. BMJ Open 2022;12:e066950. https://doi.org/10.1136/ bmjopen-2022-066950 198. Ueshima D, Barioli A, Nai Fovino L, D’Amico G, Fabris T, Brener SJ, et al. The impact of pre-existing peripheral artery disease on transcatheter aortic valve implantation outcomes: a systematic review and meta-analysis. Catheter Cardiovasc Interv 2020;95: 993–1000. https://doi.org/10.1002/ccd.28335 199. de Weerd M, Greving JP, Hedblad B, Lorenz MW, Mathiesen EB, O’Leary DH, et al. Prevalence of asymptomatic carotid artery stenosis in the general population: an individual participant data meta-analysis. Stroke 2010;41:1294–7. https://doi.org/10.1161/ STROKEAHA.110.581058 200. Krist AH, Davidson KW, Mangione CM, Barry MJ, Cabana M, Caughey AB, et al. Screening for asymptomatic carotid artery stenosis: US preventive services task force recommendation statement. JAMA 2021;325:476–81. https://doi.org/10.1001/jama. 2020.26988 201. AbuRahma AF, Avgerinos ED, Chang RW, Darling RC, Duncan AA, Forbes TL, et al. Society for Vascular Surgery clinical practice guidelines for management of extracranial cerebrovascular disease. J Vasc Surg 2022;75:4S–22S. https://doi.org/10.1016/j.jvs.2021. 04.073 202. Howard DPJ, Gaziano L, Rothwell PM. Risk of stroke in relation to degree of asymptomatic carotid stenosis: a population-based cohort study, systematic review, and meta-analysis. Lancet Neurol 2021;20:193–202. https://doi.org/10.1016/s1474- 4422(20)30484-1 203. Paraskevas KI, Spence JD, Mikhailidis DP, Antignani PL, Gloviczki P, Eckstein H-H, et al. Why do guidelines recommend screening for abdominal aortic aneurysms, but not for asymptomatic carotid stenosis? A plea for a randomized controlled trial. Int J Cardiol 2023;371:406–12. https://doi.org/10.1016/j.ijcard.2022.09.045 204. Kobo O, Saada M, von Birgelen C, Tonino PAL, Íñiguez-Romo A, Fröbert O, et al. Impact of multisite artery disease on clinical outcomes after percutaneous coronary intervention: an analysis from the e-Ultimaster registry. Eur Heart J Qual Care Clin Outcomes 2023;9:417–26. https://doi.org/10.1093/ehjqcco/qcac043 205. Steffel J, Eikelboom JW, Anand SS, Shestakovska O, Yusuf S, Fox KAA. The COMPASS trial: net clinical benefit of low-dose rivaroxaban plus aspirin as compared with aspirin in patients with chronic vascular disease. Circulation 2020;142:40–8. https://doi.org/10. 1161/CIRCULATIONAHA.120.046048 206. Del Giorno R, Reveilhac M, Stauffer I, Berthoud M, Mazzolai L, Depairon M, et al. A new score for improving cardiovascular risk prediction and prevention. Nutr Metab Cardiovasc Dis 2023;33:1546–55. https://doi.org/10.1016/j.numecd.2023.04.019 207. Mehta A, Rigdon J, Tattersall MC, German CA, Barringer TA, Joshi PH, et al. Association of carotid artery plaque with cardiovascular events and incident coronary
ESC Guidelines 3667
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.131
artery calcium in individuals with absent coronary calcification: the MESA. Circ Cardiovasc Imaging 2021;14:e011701. https://doi.org/10.1161/circimaging.120.011701 208. Gepner AD, Young R, Delaney JA, Budoff MJ, Polak JF, Blaha MJ, et al. Comparison of carotid plaque score and coronary artery calcium score for predicting cardiovascular disease events: the multi-ethnic study of atherosclerosis. J Am Heart Assoc 2017;6: e005179. https://doi.org/10.1161/jaha.116.005179 209. Laclaustra M, Casasnovas JA, Fernández-Ortiz A, Fuster V, León-Latre M, Jiménez-Borreguero LJ, et al. Femoral and carotid subclinical atherosclerosis association with risk factors and coronary calcium: the AWHS study. J Am Coll Cardiol 2016;67:1263–74. https://doi.org/10.1016/j.jacc.2015.12.056 210. Jacobowitz GR, Rockman CB, Gagne PJ, Adelman MA, Lamparello PJ, Landis R, et al. A model for predicting occult carotid artery stenosis: screening is justified in a selected population. J Vasc Surg 2003;38:705–9. https://doi.org/10.1016/s0741- 5214(03)00730-4 211. Rockman CB, Jacobowitz GR, Gagne PJ, Adelman MA, Lamparello PJ, Landis R, et al. Focused screening for occult carotid artery disease: patients with known heart disease are at high risk. J Vasc Surg 2004;39:44–50. https://doi.org/10.1016/j.jvs.2003.07.008 212. Yuo TH, Sidaoui J, Marone LK, Makaroun MS, Chaer RA. Revascularization of asymptomatic carotid stenosis is not appropriate in patients on dialysis. J Vasc Surg 2015;61: 670–4. https://doi.org/10.1016/j.jvs.2014.10.002 213. Ramos MJ, González-Fajardo JA, Vaquero-Puerta C, Vallina-Victorero M, Vicente-Santiago M, Vaquero-Lorenzo F, et al. Asymptomatic carotid stenosis in patients with intermittent claudication: epidemiological study. J Cardiovasc Surg (Torino) 2011;52:761–8 . 214. Aboyans V, Lacroix P, Guilloux J, Rollé F, Le Guyader A, Cautrès M, et al. A predictive model for screening cerebrovascular disease in patient undergoing coronary artery bypass grafting. Interact Cardiovasc Thorac Surg 2005;4:90–5. https://doi.org/10.1510/icvts. 2004.092262 215. Cornily JC, Le Saux D, Vinsonneau U, Bezon E, Le Ven F, Le Gal G, et al. Assessment of carotid artery stenosis before coronary artery bypass surgery. Is it always necessary? Arch Cardiovasc Dis 2011;104:77–83. https://doi.org/10.1016/j.acvd.2010.11.008 216. Johansson EP, Wester P. Carotid bruits as predictor for carotid stenoses detected by ultrasonography: an observational study. BMC Neurol 2008;8:23. https://doi.org/10. 1186/1471-2377-8-23 217. Carmody BJ, Arora S, Avena R, Curry KM, Simpkins J, Cosby K, et al. Accelerated carotid artery disease after high-dose head and neck radiotherapy: is there a role for routine carotid duplex surveillance? J Vasc Surg 1999;30:1045–51. https://doi.org/10.1016/ s0741-5214(99)70042-x 218. Song P, Rudan D, Zhu Y, Fowkes FJI, Rahimi K, Fowkes FGR, et al. Global, regional, and national prevalence and risk factors for peripheral artery disease in 2015: an updated systematic review and analysis. Lancet Glob Health 2019;7:e1020–30. https://doi.org/10. 1016/s2214-109x(19)30255-4 219. Campia U, Gerhard-Herman M, Piazza G, Goldhaber SZ. Peripheral artery disease: past, present, and future. Am J Med 2019;132:1133–41. https://doi.org/10.1016/j. amjmed.2019.04.043 220. Søgaard R, Lindholt JS. Cost-effectiveness of population-based vascular disease screening and intervention in men from the Viborg Vascular (VIVA) trial. Br J Surg 2018;105: 1283–93. https://doi.org/10.1002/bjs.10872 221. Lindholt JS, Juul S, Fasting H, Henneberg EW. Screening for abdominal aortic aneurysms: single centre randomised controlled trial. BMJ 2005;330:750. https://doi.org/ 10.1136/bmj.38369.620162.82 222. Norman PE, Jamrozik K, Lawrence-Brown MM, Le MT, Spencer CA, Tuohy RJ, et al. Population based randomised controlled trial on impact of screening on mortality from abdominal aortic aneurysm. BMJ 2004;329:1259. https://doi.org/10.1136/bmj. 38272.478438.55 223. Ashton HA, Buxton MJ, Day NE, Kim LG, Marteau TM, Scott RA, et al. The multicentre aneurysm screening study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet 2002;360: 1531–9. https://doi.org/10.1016/s0140-6736(02)11522-4 224. Scott RA, Wilson NM, Ashton HA, Kay DN. Influence of screening on the incidence of ruptured abdominal aortic aneurysm: 5-year results of a randomized controlled study. Br J Surg 1995;82:1066–70. https://doi.org/10.1002/bjs.1800820821 225. Duncan A, Maslen C, Gibson C, Hartshorne T, Farooqi A, Saratzis A, et al. Ultrasound screening for abdominal aortic aneurysm in high-risk women. Br J Surg 2021;108: 1192–8. https://doi.org/10.1093/bjs/znab220 226. Lindholt JS, Sogaard R, Rasmussen LM, Mejldal A, Lambrechtsen J, Steffensen FH, et al. Five-year outcomes of the Danish cardiovascular screening (DANCAVAS) trial. N Engl J Med 2022;387:1385–94. https://doi.org/10.1056/NEJMoa2208681 227. Howard DP, Banerjee A, Fairhead JF, Handa A, Silver LE, Rothwell PM. Population-based study of incidence of acute abdominal aortic aneurysms with projected impact of screening strategy. J Am Heart Assoc 2015;4:e001926. https://doi. org/10.1161/JAHA.115.001926 228. Howard DP, Banerjee A, Fairhead JF, Handa A, Silver LE, Rothwell PM. Age-specific incidence, risk factors and outcome of acute abdominal aortic aneurysms in a defined population. Br J Surg 2015;102:907–15. https://doi.org/10.1002/bjs.9838 229. Sprynger M, Willems M, Van Damme H, Drieghe B, Wautrecht JC, Moonen M. Screening program of abdominal aortic aneurysm. Angiology 2019;70:407–13. https:// doi.org/10.1177/0003319718824940 230. Larsson E, Granath F, Swedenborg J, Hultgren R. A population-based case-control study of the familial risk of abdominal aortic aneurysm. J Vasc Surg 2009;49:47–50; discussion 51. https://doi.org/10.1016/j.jvs.2008.08.012 231. Linné A, Forsberg J, Lindström D, Ideskog E, Hultgren R. Age at detection of abdominal aortic aneurysms in siblings of patients with abdominal aortic aneurysms. J Vasc Surg 2016;63:883–7. https://doi.org/10.1016/j.jvs.2015.10.057 232. Aboyans V, Bataille V, Bliscaux P, Ederhy S, Filliol D, Honton B, et al. Effectiveness of screening for abdominal aortic aneurysm during echocardiography. Am J Cardiol 2014;114:1100–4. https://doi.org/10.1016/j.amjcard.2014.07.024 233. Hicks CW, Al-Qunaibet A, Ding N, Kwak L, Folsom AR, Tanaka H, et al. Symptomatic and asymptomatic peripheral artery disease and the risk of abdominal aortic aneurysm: the Atherosclerosis Risk in Communities (ARIC) study. Atherosclerosis 2021;333:32–8. https://doi.org/10.1016/j.atherosclerosis.2021.08.016 234. Benson RA, Poole R, Murray S, Moxey P, Loftus IM. Screening results from a large United Kingdom abdominal aortic aneurysm screening center in the context of optimizing United Kingdom National Abdominal Aortic Aneurysm Screening Programme protocols. J Vasc Surg 2016;63:301–4. https://doi.org/10.1016/j.jvs.2015.08.091 235. Sciria CT, Osorio B, Wang J, Lu DY, Amin N, Vohra A, et al. Sex-based disparities in outcomes with abdominal aortic aneurysms. Am J Cardiol 2021;155:135–48. https:// doi.org/10.1016/j.amjcard.2021.06.023 236. Carter JL, Morris DR, Sherliker P, Clack R, Lam KBH, Halliday A, et al. Sex-specific associations of vascular risk factors with abdominal aortic aneurysm: findings from 1.5 million women and 0.8 million men in the United States and United Kingdom. J Am Heart Assoc 2020;9:e014748. https://doi.org/10.1161/JAHA.119.014748 237. Wanhainen A, Lundkvist J, Bergqvist D, Bjorck M. Cost-effectiveness of screening women for abdominal aortic aneurysm. J Vasc Surg 2006;43:908–14; discussion 914. https://doi.org/10.1016/j.jvs.2005.12.064 238. Sofi F, Abbate R, Gensini GF, Casini A. Accruing evidence on benefits of adherence to the Mediterranean diet on health: an updated systematic review and meta-analysis. Am J Clin Nutr 2010;92:1189–96. https://doi.org/10.3945/ajcn.2010.29673 239. Mente A, Dehghan M, Rangarajan S, O’Donnell M, Hu W, Dagenais G, et al. Diet, cardiovascular disease, and mortality in 80 countries. Eur Heart J 2023;44:2560–79. https://doi.org/10.1093/eurheartj/ehad269 240. Wan D, Dehghan M, de Souza RJ, Ramasundarahettige C, Eikelboom JW, Bosch J, et al. Dietary intake and cardiovascular outcomes in patients with chronic vascular disease: insights from the COMPASS trial cohort. Eur J Prev Cardiol 2023;30:709–18. https://doi. org/10.1093/eurjpc/zwad062 241. Adegbola A, Behrendt CA, Zyriax BC, Windler E, Kreutzburg T. The impact of nutrition on the development and progression of peripheral artery disease: a systematic review. Clin Nutr 2022;41:49–70. https://doi.org/10.1016/j.clnu.2021.11.005 242. Mach F, Baigent C, Catapano AL, Koskinas KC, Casula M, Badimon L, et al. 2019 ESC/ EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. Eur Heart J 2020;41:111–88. https://doi.org/10.1093/eurheartj/ehz455 243. Amarenco P, Kim JS, Labreuche J, Charles H, Giroud M, Lee B-C, et al. Benefit of targeting a LDL (low-density lipoprotein) cholesterol <70 mg/dL during 5 years after ischemic stroke. Stroke 2020;51:1231–9. https://doi.org/10.1161/strokeaha.119.028718 244. Aung PP, Maxwell HG, Jepson RG, Price JF, Leng GC. Lipid-lowering for peripheral arterial disease of the lower limb. Cochrane Database Syst Rev 2007;4:CD000123. https:// doi.org/10.1002/14651858.CD000123.pub2 245. Heart Protection Study Collaborative Group. Randomized trial of the effects of cholesterol-lowering with simvastatin on peripheral vascular and other major vascular outcomes in 20,536 people with peripheral arterial disease and other high-risk conditions. J Vasc Surg 2007;45:645–54; discussion 653–644. https://doi.org/10.1016/j.jvs. 2006.12.054 246. Baigent C, Keech A, Kearney PM, Blackwell L, Buck G, Pollicino C, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005;366:1267–78. https://doi.org/10.1016/S0140-6736(05)67394-1 247. Bonaca MP, Gutierrez JA, Cannon C, Giugliano R, Blazing M, Park J-G, et al. Polyvascular disease, type 2 diabetes, and long-term vascular risk: a secondary analysis of the IMPROVE-IT trial. Lancet Diabetes Endocrinol 2018;6:934–43. https://doi.org/10. 1016/s2213-8587(18)30290-0 248. Yu E, Malik VS, Hu FB. Cardiovascular disease prevention by diet modification: JACC health promotion series. J Am Coll Cardiol 2018;72:914–26. https://doi.org/10.1016/j. jacc.2018.02.085 249. López-Laguna N, Martínez-González MA, Toledo E, Babio N, Sorlí JV, Ros E, et al. Risk of peripheral artery disease according to a healthy lifestyle score: the PREDIMED study. Atherosclerosis 2018;275:133–40. https://doi.org/10.1016/j.atherosclerosis. 2018.05.049 250. Kaluza J, Stackelberg O, Harris HR, Akesson A, Björck M, Wolk A. Mediterranean diet is associated with reduced risk of abdominal aortic aneurysm in smokers: results of two prospective cohort studies. Eur J Vasc Endovasc Surg 2021;62:284–93. https:// doi.org/10.1016/j.ejvs.2021.04.017 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.132
251. Liu L, Yang Y. Nutritional management mode of early cardiac rehabilitation in patients with Stanford type A aortic dissection. Comput Math Methods Med 2022;2022: 2124636. https://doi.org/10.1155/2022/2124636 252. Lauret GJ, Fokkenrood HJ, Bendermacher BL, Scheltinga MR, Teijink JA. Physical activity monitoring in patients with intermittent claudication. Eur J Vasc Endovasc Surg 2014; 47:656–63. https://doi.org/10.1016/j.ejvs.2014.03.001 253. Gardner AW, Addison O, Katzel LI, Montgomery PS, Prior SJ, Serra MC, et al. Association between physical activity and mortality in patients with claudication. Med Sci Sports Exerc 2021;53:732–9. https://doi.org/10.1249/mss.0000000000002526 254. Gardner AW, Montgomery PS, Parker DE. Physical activity is a predictor of all-cause mortality in patients with intermittent claudication. J Vasc Surg 2008;47:117–22. https:// doi.org/10.1016/j.jvs.2007.09.033 255. Gardner AW, Montgomery PS, Wang M, Shen B, Zhang S, Pomilla WA. Association between meeting physical activity time-intensity guidelines with ambulation, quality of life, and inflammation in claudication. J Cardiopulm Rehabil Prev 2022;42:E82–9. https://doi.org/10.1097/hcr.0000000000000686 256. Thijssen CGE, Bons LR, Gökalp AL, Van Kimmenade RRJ, Mokhles MM, Pelliccia A, et al. Exercise and sports participation in patients with thoracic aortic disease: a review. Expert Rev Cardiovasc Ther 2019;17:251–66. https://doi.org/10.1080/14779072.2019. 1585807 257. Delsart P, Maldonado-Kauffmann P, Bic M, Boudghene-Stambouli F, Sobocinski J, Juthier F, et al. Post aortic dissection: gap between activity recommendation and real life patients aerobic capacities. Int J Cardiol 2016;219:271–6. https://doi.org/10. 1016/j.ijcard.2016.06.026 258. Chaddha A, Eagle KA, Braverman AC, Kline-Rogers E, Hirsch AT, Brook R, et al. Exercise and physical activity for the post-aortic dissection patient: the clinician’s conundrum. Clin Cardiol 2015;38:647–51. https://doi.org/10.1002/clc.22481 259. Chaddha A, Kline-Rogers E, Woznicki EM, Brook R, Housholder-Hughes S, Braverman AC, et al. Cardiology patient page. Activity recommendations for postaortic dissection patients. Circulation 2014;130:e140–2. https://doi.org/10.1161/circulationaha.113. 005819 260. Katsiki N, Papadopoulou SK, Fachantidou AI, Mikhailidis DP. Smoking and vascular risk: are all forms of smoking harmful to all types of vascular disease? Public Health 2013; 127:435–41. https://doi.org/10.1016/j.puhe.2012.12.021 261. Wu CW, Chuang HY, Watanabe K, Wu P-S, Pan H-C, Wang C-L, et al. Association between secondhand smoke and peripheral arterial disease: a meta-analysis of crosssectional studies. Int Arch Occup Environ Health 2022;95:1091–101. https://doi.org/10. 1007/s00420-022-01837-9 262. Sode BF, Nordestgaard BG, Gronbaek M, Dahl M. Tobacco smoking and aortic aneurysm: two population-based studies. Int J Cardiol 2013;167:2271–7. https://doi.org/10. 1016/j.ijcard.2012.06.003 263. Altobelli E, Rapacchietta L, Profeta VF, Fagnano R. Risk factors for abdominal aortic aneurysm in population-based studies: a systematic review and meta-analysis. Int J Environ Res Public Health 2018;15:2805. https://doi.org/10.3390/ijerph15122805 264. Lederle FA, Nelson DB, Joseph AM. Smokers’ relative risk for aortic aneurysm compared with other smoking-related diseases: a systematic review. J Vasc Surg 2003;38: 329–34. https://doi.org/10.1016/s0741-5214(03)00136-8 265. Teo KK, Ounpuu S, Hawken S, Pandey MR, Valentin V, Hunt D, et al. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: a case-control study. Lancet 2006;368:647–58. https://doi.org/10.1016/S0140-6736(06)69249-0 266. Mahtta D, Ramsey D, Krittanawong C, Al Rifai M, Khurram N, Samad Z, et al. Recreational substance use among patients with premature atherosclerotic cardiovascular disease. Heart 2021;107:650–6. https://doi.org/10.1136/heartjnl-2020-318119 267. Anthonisen NR, Skeans MA, Wise RA, Manfreda J, Kanner RE, Connett JE. The effects of a smoking cessation intervention on 14.5-year mortality: a randomized clinical trial. Ann Intern Med 2005;142:233–9. https://doi.org/10.7326/0003-4819-142- 4-200502150-00005 268. Suissa K, Lariviere J, Eisenberg MJ, Eberg M, Gore GC, Grad R, et al. Efficacy and safety of smoking cessation interventions in patients with cardiovascular disease: a network meta-analysis of randomized controlled trials. Circ Cardiovasc Qual Outcomes 2017;10: e002458. https://doi.org/10.1161/CIRCOUTCOMES.115.002458 269. Livingstone-Banks J, Fanshawe TR, Thomas KH, Theodoulou A, Hajizadeh A, Hartman L, et al. Nicotine receptor partial agonists for smoking cessation. Cochrane Database Syst Rev 2023;5:CD006103. https://doi.org/10.1002/14651858.CD006103.pub8 270. Rose JJ, Krishnan-Sarin S, Exil VJ, Hamburg NM, Fetterman JL, Ichinose F, et al. Cardiopulmonary impact of electronic cigarettes and vaping products: a scientific statement from the American Heart Association. Circulation 2023;148:703–28. https://doi.org/10.1161/CIR.0000000000001160 271. Lindson N, Butler AR, McRobbie H, Bullen C, Hajek P, Begh R, et al. Electronic cigarettes for smoking cessation. Cochrane Database Syst Rev 2024;1:CD010216. https://doi. org/10.1002/14651858.CD010216.pub8 272. Travis N, Knoll M, Cadham CJ, Cook S, Warner KE, Fleischer NL, et al. Health effects of electronic cigarettes: an umbrella review and methodological considerations. Int J Environ Res Public Health 2022;19:9054. https://doi.org/10.3390/ijerph19159054 273. Abbott AJ, Reibel YG, Arnett MC, Marka N, Drake MA. Oral and systemic health implications of electronic cigarette usage as compared to conventional tobacco cigarettes: a review of the literature. J Dent Hyg 2023;97:21–35. 274. Hamann SL, Kungskulniti N, Charoenca N, Kasemsup V, Ruangkanchanasetr S, Jongkhajornpong P. Electronic cigarette harms: aggregate evidence shows damage to biological systems. Int J Environ Res Public Health 2023;20:6808. https://doi.org/10. 3390/ijerph20196808 275. Kavousi M, Pisinger C, Barthelemy JC, De Smedt D, Koskinas K, Marques-Vidal P, et al. Electronic cigarettes and health with special focus on cardiovascular effects: position paper of the European Association of Preventive Cardiology (EAPC). Eur J Prev Cardiol 2021;28:1552–66. https://doi.org/10.1177/2047487320941993 276. Goldman RE, Parker DR, Eaton CB, Borkan JM, Gramling R, Cover RT, et al. Patients’ perceptions of cholesterol, cardiovascular disease risk, and risk communication strategies. Ann Fam Med 2006;4:205–12. https://doi.org/10.1370/afm.534 277. Howarth M, Lister C. Social prescribing in cardiology: rediscovering the nature within us. Br J Card Nurs 2019;14:1–9. https://doi.org/10.12968/bjca.2019.0036 278. Nichols LO, Martindale-Adams J, Burns R, Graney MJ, Zuber J. Translation of a dementia caregiver support program in a health care system—REACH VA. Arch Intern Med 2011;171:353–9. https://doi.org/10.1001/archinternmed.2010.548 279. Martire LM, Schulz R, Keefe FJ, Rudy TE, Starz TW. Couple-oriented education and support intervention for osteoarthritis: effects on spouses’ support and responses to patient pain. Fam Syst Health 2008;26:185–95. https://doi.org/10.1037/1091-7527. 26.2.185 280. Morris SM, King C, Turner M, Payne S. Family carers providing support to a person dying in the home setting: a narrative literature review. Palliat Med 2015;29:487–95. https://doi.org/10.1177/0269216314565706 281. Ventura AD, Burney S, Brooker J, Fletcher J, Ricciardelli L. Home-based palliative care: a systematic literature review of the self-reported unmet needs of patients and carers. Palliat Med 2014;28:391–402. https://doi.org/10.1177/0269216313511141 282. Reynolds CF, III, Jeste DV, Sachdev PS, Blazer DG. Mental health care for older adults: recent advances and new directions in clinical practice and research. World Psychiatry 2022;21:336–63. https://doi.org/10.1002/wps.20996 283. Katch H. The role of self-efficacy in cardiovascular disease self-management: a review of effective programs. Patient Intelligence 2010;2:33–4. doi: https://doi.org/10.2147/PI. S12624] 284. Ohman EM, Bhatt DL, Steg PG, Goto S, Hirsch AT, Liau C-S, et al. The REduction of Atherothrombosis for Continued Health (REACH) registry: an international, prospective, observational investigation in subjects at risk for atherothrombotic events– study design. Am Heart J 2006;151:786.e1–10. https://doi.org/10.1016/j.ahj.2005.11. 004 285. Simons PC, Algra A, van de Laak MF, Grobbee DE, van der Graaf Y. Second manifestations of ARTerial disease (SMART) study: rationale and design. Eur J Epidemiol 1999;15: 773–81. https://doi.org/10.1023/a:1007621514757 286. Dorresteijn JA, Visseren FL, Wassink AM, Gondrie MJA, Steyerberg EW, Ridker PM, et al. Development and validation of a prediction rule for recurrent vascular events based on a cohort study of patients with arterial disease: the SMART risk score. Heart 2013;99:866–72. https://doi.org/10.1136/heartjnl-2013-303640 287. Kaasenbrood L, Bhatt DL, Dorresteijn JAN, Wilson PWF, D’Agostino RB, Massaro JM, et al. Estimated life expectancy without recurrent cardiovascular events in patients with vascular disease: the SMART-REACH model. J Am Heart Assoc 2018;7: e009217. https://doi.org/10.1161/JAHA.118.009217 288. Hageman SHJ, McKay AJ, Ueda P, Gunn LH, Jernberg T, Hagström E, et al. Estimation of recurrent atherosclerotic cardiovascular event risk in patients with established cardiovascular disease: the updated SMART2 algorithm. Eur Heart J 2022;43:1715–27. https://doi.org/10.1093/eurheartj/ehac056 289. van Trier TJ, Snaterse M, Boekholdt SM, Scholte Op Reimer WJM, Hageman SHJ, Visseren FLJ, et al. Validation of systematic coronary risk evaluation 2 (SCORE2) and SCORE2-older persons in the EPIC Norfolk prospective population cohort. Eur J Prev Cardiol 2024;31:182–9. https://doi.org/10.1093/eurjpc/zwad318 290. Wan D, Li V, Banfield L, Azab S, de Souza RJ, Anand SS, et al. Diet and nutrition in peripheral artery disease: a systematic review. Can J Cardiol 2022;38:672–80. https://doi. org/10.1016/j.cjca.2022.01.021 291. Sesso HD, Rist PM, Aragaki AK, Rautiainen S, Johnson LG, Friedenberg G, et al. Multivitamins in the prevention of cancer and cardiovascular disease: the COcoa Supplement and Multivitamin Outcomes Study (COSMOS) randomized clinical trial. Am J Clin Nutr 2022;115:1501–10. https://doi.org/10.1093/ajcn/nqac056 292. Bondonno NP, Murray K, Cassidy A, Bondonno CP, Lewis JR, Croft KD, et al. Higher habitual flavonoid intakes are associated with a lower risk of peripheral artery disease hospitalizations. Am J Clin Nutr 2021;113:187–99. https://doi.org/10.1093/ajcn/ nqaa300 293. Bapir M, Untracht GR, Cooke D, McVey JH, Skene SS, Campagnolo P, et al. Cocoa flavanol consumption improves lower extremity endothelial function in healthy individuals and people with type 2 diabetes. Food Funct 2022;13:10439–48. https://doi. org/10.1039/d2fo02017c 294. Fassora M, Calanca L, Jaques C, Mazzolai L, Kayser B, Lanzi S. Intensity-dependent effects of exercise therapy on walking performance and aerobic fitness in
ESC Guidelines 3669
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.133
symptomatic patients with lower-extremity peripheral artery disease: a systematic review and meta-analysis. Vasc Med 2022;27:158–70. https://doi.org/10.1177/ 1358863x211034577 295. O’Connor EA, Evans CV, Rushkin MC, Redmond N, Lin JS. Behavioral counseling to promote a healthy diet and physical activity for cardiovascular disease prevention in adults with cardiovascular risk factors: updated evidence report and systematic review for the US preventive services task force. JAMA 2020;324:2076–94. https://doi.org/10. 1001/jama.2020.17108 296. Hartmann-Boyce J, McRobbie H, Lindson N, Bullen C, Begh R, Theodoulou A, et al. Electronic cigarettes for smoking cessation. Cochrane Database Syst Rev 2021;4: CD010216. https://doi.org/10.1002/14651858.CD010216.pub5 297. Krabbe B, Espinola-Klein C, Malyar N, Brodmann M, Mazzolai L, Belch JJF, et al. Health effects of e-cigarettes and their use for smoking cessation from a vascular perspective. Vasa 2023;52:81–5. https://doi.org/10.1024/0301-1526/a001056 298. Garber CE, Blissmer B, Deschenes MR, Franklin BA, Lamonte MJ, Lee I-M, et al. American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise. Med Sci Sports Exerc 2011;43:1334–59. https://doi.org/10.1249/MSS.0b013e318213fefb 299. Twine CP, Kakkos SK, Aboyans V, Baumgartner I, Behrendt C-A, Bellmunt-Montoya S, et al. Editor’s choice—European Society for Vascular Surgery (ESVS) 2023 clinical practice guidelines on antithrombotic therapy for vascular diseases. Eur J Vasc Endovasc Surg 2023;65:627–89. https://doi.org/10.1016/j.ejvs.2023.03.042 300. McEvoy JW, Touyz RM, McCarthy CP, Bruno RM, Brouwers S, Canavan MD, et al. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J 2024. https://doi.org/10.1093/eurheartj/ehae178 301. Blood Pressure Lowering Treatment Trialists’ Collaboration. Age-stratified and blood-pressure-stratified effects of blood-pressure-lowering pharmacotherapy for the prevention of cardiovascular disease and death: an individual participant-level data meta-analysis. Lancet 2021;398:1053–64. https://doi.org/10.1016/S0140- 6736(21)01921-8 302. Ettehad D, Emdin CA, Kiran A, Anderson SG, Callender T, Emberson J, et al. Blood pressure lowering for prevention of cardiovascular disease and death: a systematic review and meta-analysis. Lancet 2016;387:957–67. https://doi.org/10.1016/s0140- 6736(15)01225-8 303. Williamson JD, Supiano MA, Applegate WB, Berlowitz DR, Campbell RC, Chertow GM, et al. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 years: a randomized clinical trial. JAMA 2016;315:2673–82. https://doi.org/10.1001/jama.2016.7050 304. Zhang W, Zhang S, Deng Y, Wu S, Ren J, Sun G, et al. Trial of intensive blood-pressure control in older patients with hypertension. N Engl J Med 2021;385:1268–79. https:// doi.org/10.1056/NEJMoa2111437 305. Thomopoulos C, Parati G, Zanchetti A. Effects of blood pressure lowering on outcome incidence in hypertension. 1. Overview, meta-analyses, and meta-regression analyses of randomized trials. J Hypertens 2014;32:2285–95. https://doi.org/10.1097/ hjh.0000000000000378 306. Wright JT, Jr, Williamson JD, Whelton PK, Snyder JK, Sink KM, Rocco MV, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med 2015; 373:2103–16. https://doi.org/10.1056/NEJMoa1511939 307. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in highrisk patients. N Engl J Med 2000;342:145–53. https://doi.org/10.1056/ nejm200001203420301 308. Bavry AA, Anderson RD, Gong Y, Denardo SJ, Cooper-DeHoff RM, Handberg EM, et al. Outcomes among hypertensive patients with concomitant peripheral and coronary artery disease: findings from the INternational VErapamil-SR/Trandolapril STudy. Hypertension 2010;55:48–53. https://doi.org/10.1161/hypertensionaha.109.142240 309. Fudim M, Hopley CW, Huang Z, Kavanagh S, Rockhold FW, Baumgartner I, et al. Association of hypertension and arterial blood pressure on limb and cardiovascular outcomes in symptomatic peripheral artery disease: the EUCLID trial. Circ Cardiovasc Qual Outcomes 2020;13:e006512. https://doi.org/10.1161/circoutcomes. 120.006512 310. Thomas Manapurathe D, Krishna SM, Dewdney B, Moxon JV, Biros E, Golledge J, Effect of blood pressure lowering medications on leg ischemia in peripheral artery disease patients: a meta-analysis of randomised controlled trials. PLoS One 2017;12: e0178713. https://doi.org/10.1371/journal.pone.0178713 311. Lu Y, Ballew SH, Tanaka H, Szklo M, Heiss G, Coresh J, et al. 2017 ACC/AHA blood pressure classification and incident peripheral artery disease: the Atherosclerosis Risk in Communities (ARIC) study. Eur J Prev Cardiol 2020;27:51–9. https://doi.org/10.1177/ 2047487319865378 312. Yusuf S, Teo KK, Pogue J, Dyal L, Copland I, Schumacher H, et al. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med 2008;358:1547–59. https://doi.org/10.1056/NEJMoa0801317 313. Ostergren J, Sleight P, Dagenais G, Danisa K, Bosch J, Qilong Y, et al. Impact of ramipril in patients with evidence of clinical or subclinical peripheral arterial disease. Eur Heart J 2004;25:17–24. https://doi.org/10.1016/j.ehj.2003.10.033 314. Paravastu SC, Mendonca DA, Da Silva A. Beta blockers for peripheral arterial disease. Cochrane Database Syst Rev 2013;9:CD005508. https://doi.org/10.1002/14651858. CD005508.pub3 315. Kray JE, Dombrovskiy VY, Vogel TR. Use of angiotensin-converting enzyme inhibitors and freedom from amputation after lower extremity revascularization. Vasc Health Risk Manag 2017;13:269–74. https://doi.org/10.2147/vhrm.S137698 316. Høgh A, Lindholt JS, Nielsen H, Jensen LP, Johnsen SP. Use of angiotensin-converting enzyme inhibitors and cardiovascular outcomes following primary vascular surgery: a nationwide propensity score matched follow-up study. Vasc Endovascular Surg 2012; 46:515–23. https://doi.org/10.1177/1538574412455229 317. Armstrong EJ, Chen DC, Singh GD, Amsterdam EA, Laird JR. Angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use is associated with reduced major adverse cardiovascular events among patients with critical limb ischemia. Vasc Med 2015;20:237–44. https://doi.org/10.1177/1358863x15574321 318. Aronow WS, Ahn C. Effect of beta blockers on incidence of new coronary events in older persons with prior myocardial infarction and symptomatic peripheral arterial disease. Am J Cardiol 2001;87:1284–6. https://doi.org/10.1016/s0002-9149(01) 01521-1 319. Soga Y, Iida O, Takahara M, Hirano K, Suzuki K, Kawasaki D. Beta-blocker treatment does not worsen critical limb ischemia in patients receiving endovascular therapy. J Atheroscler Thromb 2015;22:481–9. https://doi.org/10.5551/jat.27359 320. Carey RM, Wright JT, Jr, Taler SJ, Whelton PK. Guideline-driven management of hypertension: an evidence-based update. Circ Res 2021;128:827–46. https://doi.org/ 10.1161/circresaha.121.318083 321. Evans KL, Tuttle KR, Folt DA, Dawson T, Haller ST, Brewster PS, et al. Use of renin-angiotensin inhibitors in people with renal artery stenosis. Clin J Am Soc Nephrol 2014;9:1199–206. https://doi.org/10.2215/cjn.11611113 322. Hackam DG, Duong-Hua ML, Mamdani M, Li Ping, Tobe SW, Spence JD, et al. Angiotensin inhibition in renovascular disease: a population-based cohort study. Am Heart J 2008;156:549–55. https://doi.org/10.1016/j.ahj.2008.05.013 323. Solomon SD, Rice MM, Jablonski KA, Jose P, Domanski M, Sabatine M, et al. Renal function and effectiveness of angiotensin-converting enzyme inhibitor therapy in patients with chronic stable coronary disease in the Prevention of Events with ACE inhibition (PEACE) trial. Circulation 2006;114:26–31. https://doi.org/10.1161/circulationaha.105. 592733 324. Cooper CJ, Murphy TP, Cutlip DE, Jamerson K, Henrich W, Reid DM, et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med 2014;370: 13–22. https://doi.org/10.1056/NEJMoa1310753 325. Mayr NP, Hapfelmeier A, Martin K, Kurz A, van der Starre P, Babik B, et al. Comparison of sedation and general anaesthesia for transcatheter aortic valve implantation on cerebral oxygen saturation and neurocognitive outcomedagger. Br J Anaesth 2016; 116:90–9. https://doi.org/10.1093/bja/aev294 326. Singh K, Bønaa KH, Jacobsen BK, Bjørk L, Solberg S. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study: the Tromsø study. Am J Epidemiol 2001;154:236–44. https://doi.org/10.1093/aje/154.3.236 327. Vogel TR, Dombrovskiy VY, Galiñanes EL, Kruse RL. Preoperative statins and limb salvage after lower extremity revascularization in the Medicare population. Circ Cardiovasc Interv 2013;6:694–700. https://doi.org/10.1161/circinterventions.113. 000274 328. Kumbhani DJ, Steg PG, Cannon CP, Eagle KA, Smith SC, Goto S, et al. Statin therapy and long-term adverse limb outcomes in patients with peripheral artery disease: insights from the REACH registry. Eur Heart J 2014;35:2864–72. https://doi.org/10. 1093/eurheartj/ehu080 329. Pastori D, Farcomeni A, Milanese A, Del Sole F, Menichelli D, Hiatt WR, et al. Statins and major adverse limb events in patients with peripheral artery disease: a systematic review and meta-analysis. Thromb Haemost 2020;120:866–75. https://doi.org/10.1055/ s-0040-1709711 330. Su Z, Guo J, Gu Y. Pharmacotherapy in clinical trials for abdominal aortic aneurysms: a systematic review and meta-analysis. Clin Appl Thromb Hemost 2022;28: 10760296221120423. https://doi.org/10.1177/10760296221120423 331. Cannon CP, Blazing MA, Giugliano RP, McCagg A, White JA, Theroux P, et al. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J Med 2015;372:2387–97. https://doi.org/10.1056/NEJMoa1410489 332. Kaasenbrood L, Boekholdt SM, van der Graaf Y, Ray KK, Peters RJG, Kastelein JJP, et al. Distribution of estimated 10-year risk of recurrent vascular events and residual risk in a secondary prevention population. Circulation 2016;134:1419–29. https://doi.org/10. 1161/CIRCULATIONAHA.116.021314 333. Clavijo LC, Caro J, Choi J, Caro JA, Tun H, Rowe V, et al. The addition of evolocumab to maximal tolerated statin therapy improves walking performance in patients with peripheral arterial disease and intermittent claudication (Evol-PAD study). Cardiovasc Revasc Med 2023;55:1–5. https://doi.org/10.1016/j.carrev.2023.04.020 334. Cholesterol Treatment Trialists Collaboration; Fulcher J, O’Connell R, Voysey M, Emberson J, Blackwell L, et al. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. Lancet 2015;385:1397–405. https://doi.org/10.1016/S0140-6736(14) 61368-4 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.134
335. Murphy SA, Cannon CP, Blazing MA, Giugliano RP, White JA, Lokhnygina Y, et al. Reduction in total cardiovascular events with ezetimibe/simvastatin post-acute coronary syndrome: the IMPROVE-IT trial. J Am Coll Cardiol 2016;67:353–61. https://doi.org/ 10.1016/j.jacc.2015.10.077 336. Sabatine MS, Giugliano RP, Keech AC, Honarpour N, Wiviott SD, Murphy SA, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med 2017;376:1713–22. https://doi.org/10.1056/NEJMoa1615664 337. Westin GG, Armstrong EJ, Bang H, Yeo K-K, Anderson D, Dawson DL, et al. Association between statin medications and mortality, major adverse cardiovascular event, and amputation-free survival in patients with critical limb ischemia. J Am Coll Cardiol 2014;63:682–90. https://doi.org/10.1016/j.jacc.2013.09.073 338. Belch JJF, Brodmann M, Baumgartner I, Binder CJ, Casula M, Heiss C, et al. Lipid-lowering and anti-thrombotic therapy in patients with peripheral arterial disease. Vasa 2021;50:401–11. https://doi.org/10.1024/0301-1526/a000969 339. Momsen AH, Jensen MB, Norager CB, Madsen MR, Vestersgaard-Andersen T, Lindholt JS. Drug therapy for improving walking distance in intermittent claudication: a systematic review and meta-analysis of robust randomised controlled studies. Eur J Vasc Endovasc Surg 2009;38:463–74. https://doi.org/10.1016/j.ejvs.2009.06.002 340. Flint AC, Conell C, Ren X, Kamel H, Chan SL, Rao VA, et al. Statin adherence is associated with reduced recurrent stroke risk in patients with or without atrial fibrillation. Stroke 2017;48:1788–94. https://doi.org/10.1161/strokeaha.117.017343 341. Merwick Á, Albers GW, Arsava EM, Ay H, Calvet D, Coutts SB, et al. Reduction in early stroke risk in carotid stenosis with transient ischemic attack associated with statin treatment. Stroke 2013;44:2814–20. https://doi.org/10.1161/strokeaha.113.001576 342. Amarenco P, Labreuche J. Lipid management in the prevention of stroke: review and updated meta-analysis of statins for stroke prevention. Lancet Neurol 2009;8:453–63. https://doi.org/10.1016/s1474-4422(09)70058-4 343. Amarenco P, Bogousslavsky J, Callahan A, III, Goldstein LB, Hennerici M, Rudolph AE, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med 2006;355:549–59. https://doi.org/10.1056/NEJMoa061894 344. Hackam DG, Wu F, Li P, Austin PC, Tobe SW, Mamdani MM, et al. Statins and renovascular disease in the elderly: a population-based cohort study. Eur Heart J 2011;32: 598–610. https://doi.org/10.1093/eurheartj/ehq452 345. Peng M, Dong H, Jiang X, Che W, Zou Y, Zhang Y, et al. A randomized unblinded trial to compare effects of intensive versus conventional lipid-lowering therapy in patients undergoing renal artery stenting. J Cardiol 2019;74:443–50. https://doi.org/10.1016/j. jjcc.2019.04.010 346. Vashist A, Heller EN, Brown EJ, Jr, Alhaddad IA. Renal artery stenosis: a cardiovascular perspective. Am Heart J 2002;143:559–64. https://doi.org/10.1067/mhj.2002.120769 347. Pan Z, Cui H, Wu N, Zhang H. Effect of statin therapy on abdominal aortic aneurysm growth rate and mortality: a systematic review and meta-analysis. Ann Vasc Surg 2020; 67:503–10. https://doi.org/10.1016/j.avsg.2020.03.036 348. Salata K, Syed M, Hussain MA, de Mestral C, Greco E, Mamdani M, et al. Statins reduce abdominal aortic aneurysm growth, rupture, and perioperative mortality: a systematic review and meta-analysis. J Am Heart Assoc 2018;7:e008657. https://doi.org/10.1161/ jaha.118.008657 349. Takagi H, Yamamoto H, Iwata K, Goto S, Umemoto T. Effects of statin therapy on abdominal aortic aneurysm growth: a meta-analysis and meta-regression of observational comparative studies. Eur J Vasc Endovasc Surg 2012;44:287–92. https://doi.org/10.1016/ j.ejvs.2012.06.021 350. Stein LH, Berger J, Tranquilli M, Elefteraides JA. Effect of statin drugs on thoracic aortic aneurysms. Am J Cardiol 2013;112:1240–5. https://doi.org/10.1016/j.amjcard.2013.05. 081 351. Jovin IS, Duggal M, Ebisu K, Paek H, Oprea AD, Tranquilli M, et al. Comparison of the effect on long-term outcomes in patients with thoracic aortic aneurysms of taking versus not taking a statin drug. Am J Cardiol 2012;109:1050–4. https://doi.org/10.1016/j. amjcard.2011.11.038 352. Skovbo Kristensen JS, Krasniqi L, Obel LM, Kavaliunaite E, Liisberg M, Lindholt JS. Exploring drug repurposing for treatment of abdominal aortic aneurysms: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2024;67:570–82. https://doi.org/10. 1016/j.ejvs.2023.11.037 353. Rahman MN, Khan JA, Mazari FA, Mockford K, McCollum PT, Chetter IC. A randomized placebo controlled trial of the effect of preoperative statin use on matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases in areas of low and peak wall stress in patients undergoing elective open repair of abdominal aortic aneurysm. Ann Vasc Surg 2011;25:32–8. https://doi.org/10.1016/j.avsg.2010.06.006 354. Periard D, Guessous I, Mazzolai L, Haesler E, Monney P, Hayoz D. Reduction of small infrarenal abdominal aortic aneurysm expansion rate by statins. Vasa 2012;41:35–42. https://doi.org/10.1024/0301-1526/a000161 355. Angeloni E, Vitaterna A, Pirelli M, Refice S. Effects of statin therapy on ascending aorta aneurysms growth: a propensity-matched analysis. Int J Cardiol 2015;191:52–5. https:// doi.org/10.1016/j.ijcard.2015.05.001 356. Rowbotham SE, Krishna SM, Moran CS, Golledge J. Fenofibrate and telmisartan in the management of abdominal aortic aneurysm. Curr Drug Targets 2018;19:1241–6. https:// doi.org/10.2174/1389450119666171227224655 357. Pinchbeck JL, Moxon JV, Rowbotham SE, Bourke M, Lazzaroni S, Morton SK, et al. Randomized placebo-controlled trial assessing the effect of 24-week fenofibrate therapy on circulating markers of abdominal aortic aneurysm: outcomes from the FAME-2 trial. J Am Heart Assoc 2018;7:e009866. https://doi.org/10.1161/JAHA.118.009866 358. Lamb YN. Inclisiran: first approval. Drugs 2021;81:389–95. https://doi.org/10.1007/ s40265-021-01473-6 359. Ray KK, Bays HE, Catapano AL, Lalwani ND, Bloedon LT, Sterling LR, et al. Safety and efficacy of bempedoic acid to reduce LDL cholesterol. N Engl J Med 2019;380: 1022–32. https://doi.org/10.1056/NEJMoa1803917 360. Ballantyne CM, Banach M, Mancini GBJ, Lepor NE, Hanselman JC, Zhao X, et al. Efficacy and safety of bempedoic acid added to ezetimibe in statin-intolerant patients with hypercholesterolemia: a randomized, placebo-controlled study. Atherosclerosis 2018; 277:195–203. https://doi.org/10.1016/j.atherosclerosis.2018.06.002 361. Nissen SE, Lincoff AM, Brennan D, Ray KK, Mason D, Kastelein JJP, et al. Bempedoic acid and cardiovascular outcomes in statin-intolerant patients. N Engl J Med 2023; 388:1353–64. https://doi.org/10.1056/NEJMoa2215024 362. Balling M, Afzal S, Davey Smith G, Varbo A, Langsted A, Kamstrup PR, et al. Elevated LDL triglycerides and atherosclerotic risk. J Am Coll Cardiol 2023;81:136–52. https:// doi.org/10.1016/j.jacc.2022.10.019 363. Gao JW, Hao QY, Gao M, Zhang K, Li X-Z, Wang J-F, et al. Triglyceride-glucose index in the development of peripheral artery disease: findings from the Atherosclerosis Risk in Communities (ARIC) study. Cardiovasc Diabetol 2021;20:126. https://doi.org/10. 1186/s12933-021-01319-1 364. Britton KA, Mukamal KJ, Ix JH, Siscovick DS, Newman AB, de Boer IH, et al. Insulin resistance and incident peripheral artery disease in the cardiovascular health study. Vasc Med 2012;17:85–93. https://doi.org/10.1177/1358863X11436195 365. Pande RL, Perlstein TS, Beckman JA, Creager MA. Association of insulin resistance and inflammation with peripheral arterial disease: the National Health and Nutrition Examination Survey, 1999 to 2004. Circulation 2008;118:33–41. https://doi.org/10. 1161/CIRCULATIONAHA.107.721878 366. Wang D, Liu B, Tao W, Hao Z, Liu M. Fibrates for secondary prevention of cardiovascular disease and stroke. Cochrane Database Syst Rev 2015;10:CD009580. https://doi. org/10.1002/14651858.CD009580.pub2 367. Meade T, Zuhrie R, Cook C, Cooper J. Bezafibrate in men with lower extremity arterial disease: randomised controlled trial. BMJ 2002;325:1139. https://doi.org/10.1136/ bmj.325.7373.1139 368. Bhatt DL, Steg PG, Miller M, Brinton EA, Jacobson TA, Ketchum SB, et al. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med 2019;380:11–22. https://doi.org/10.1056/NEJMoa1812792 369. Bhatt DS, Steg PG, Miller M, Brinton E, Jacobson T, Tardif J-C, et al. Abstract 10627: benefits of icosapent ethyl in patients with prior peripheral artery disease: REDUCE-IT PAD. Circulation 2021;144:A10627. https://doi.org/10.1161/circ.144. suppl_1.10627 370. Kobayashi Y, Fujikawa T, Haruna A, Kawano R, Ozawa M, Haze T, et al. Omega-3 fatty acids reduce remnant-like lipoprotein cholesterol and improve the ankle-brachial index of hemodialysis patients with dyslipidemia: a pilot study. Medicina (Kaunas) 2024;60:75. https://doi.org/10.3390/medicina60010075 371. Dopheide JF, Veit J, Ramadani H, Adam L, Papac L, Vonbank A, et al. Adherence to statin therapy favours survival of patients with symptomatic peripheral artery disease. Eur Heart J Cardiovasc Pharmacother 2021;7:263–70. https://doi.org/10.1093/ehjcvp/ pvz081 372. Bonaca MP, Nault P, Giugliano RP, Keech AC, Pineda AL, Kanevsky E, et al. Low-density lipoprotein cholesterol lowering with evolocumab and outcomes in patients with peripheral artery disease: insights from the FOURIER trial (further cardiovascular outcomes research with PCSK9 inhibition in subjects with elevated risk). Circulation 2018;137:338–50. https://doi.org/10.1161/circulationaha.117.032235 373. Oyama K, Giugliano RP, Tang M, Bonaca MP, Saver JL, Murphy SA, et al. Effect of evolocumab on acute arterial events across all vascular territories: results from the FOURIER trial. Eur Heart J 2021;42:4821–9. https://doi.org/10.1093/eurheartj/ ehab604 374. Marx N, Federici M, Schutt K, Müller-Wieland D, Ajjan RA, Antunes MJ, et al. 2023 ESC Guidelines for the management of cardiovascular disease in patients with diabetes. Eur Heart J 2023;44:4043–140. https://doi.org/10.1093/eurheartj/ehad192 375. Lazzarini PA, Cramb SM, Golledge J, Morton JI, Magliano DJ, Van Netten JJ. Global trends in the incidence of hospital admissions for diabetes-related foot disease and amputations: a review of national rates in the 21st century. Diabetologia 2023;66:267–87. https://doi.org/10.1007/s00125-022-05845-9 376. Armstrong PA. Visceral duplex scanning: evaluation before and after artery intervention for chronic mesenteric ischemia. Perspect Vasc Surg Endovasc Ther 2007;19: 386–92; discussion 393–384. https://doi.org/10.1177/1531003507311802 377. Criqui MH, Aboyans V. Epidemiology of peripheral artery disease. Circ Res 2015;116: 1509–26. https://doi.org/10.1161/CIRCRESAHA.116.303849 378. McGurnaghan SJ, McKeigue PM, Read SH, Franzen S, Svensson A-M, Colombo M, et al. Development and validation of a cardiovascular risk prediction model in type 1 diabetes. Diabetologia 2021;64:2001–11. https://doi.org/10.1007/s00125-021-05478-4
ESC Guidelines 3671
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.135
379. Armstrong DG, Boulton AJM, Bus SA. Diabetic foot ulcers and their recurrence. N Engl J Med 2017;376:2367–75. https://doi.org/10.1056/NEJMra1615439 380. Malyar NM, Freisinger E, Meyborg M, Lüders F, Gebauer K, Reinecke H, et al. Amputations and mortality in in-hospital treated patients with peripheral artery disease and diabetic foot syndrome. J Diabetes Complications 2016;30:1117–22. https:// doi.org/10.1016/j.jdiacomp.2016.03.033 381. Verma S, Al-Omran M, Leiter LA, Mazer CD, Rasmussen S, Saevereid HA, et al. Cardiovascular efficacy of liraglutide and semaglutide in individuals with diabetes and peripheral artery disease. Diabetes Obes Metab 2022;24:1288–99. https://doi.org/10. 1111/dom.14700 382. Verma S, Mazer CD, Al-Omran M, Inzucchi SE, Fitchett D, Hehnke U, et al. Cardiovascular outcomes and safety of empagliflozin in patients with type 2 diabetes mellitus and peripheral artery disease: a subanalysis of EMPA-REG OUTCOME. Circulation 2018;137:405–7. https://doi.org/10.1161/circulationaha.117.032031 383. American Diabetes Association. Standards of care in diabetes–2023 abridged for primary care providers. Clin Diabetes 2022;41:4–31. https://doi.org/10.2337/cd23-as01 384. Sattar N, McGuire DK. Prevention of CV outcomes in antihyperglycaemic drug-naive patients with type 2 diabetes with, or at elevated risk of, ASCVD: to start or not to start with metformin. Eur Heart J 2021;42:2574–6. https://doi.org/10. 1093/eurheartj/ehaa879 385. Mahaffey KW, Neal B, Perkovic V, de Zeeuw D, Fulcher G, Erondu N, et al. Canagliflozin for primary and secondary prevention of cardiovascular events: results from the CANVAS program (canagliflozin cardiovascular assessment study). Circulation 2018;137:323–34. https://doi.org/10.1161/CIRCULATIONAHA.117. 032038 386. Neal B, Perkovic V, Mahaffey KW, de Zeeuw D, Fulcher G, Erondu N, et al. Canagliflozin and cardiovascular and renal events in type 2 diabetes. N Engl J Med 2017;377:644–57. https://doi.org/10.1056/NEJMoa1611925 387. Goldenberg RM, Cheng AYY, Fitzpatrick T, Gilbert JD, Verma S, Hopyan JJ. Benefits of GLP-1 (glucagon-like peptide 1) receptor agonists for stroke reduction in type 2 diabetes: a call to action for neurologists. Stroke 2022;53:1813–22. https://doi.org/10. 1161/STROKEAHA.121.038151 388. Malhotra K, Katsanos AH, Lambadiari V, Goyal N, Palaiodimou L, Kosmidou M, et al. GLP-1 receptor agonists in diabetes for stroke prevention: a systematic review and meta-analysis. J Neurol 2020;267:2117–22. https://doi.org/10.1007/s00415-020- 09813-4 389. Tsai WH, Chuang SM, Liu SC, Lee C-C, Chien M-N, Leung C-H, et al. Effects of SGLT2 inhibitors on stroke and its subtypes in patients with type 2 diabetes: a systematic review and meta-analysis. Sci Rep 2021;11:15364. https://doi.org/10.1038/ s41598-021-94945-4 390. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:854–65 . 391. Kooy A, de Jager J, Lehert P, Bets D, Wulffelé MG, Donker AJM, et al. Long-term effects of metformin on metabolism and microvascular and macrovascular disease in patients with type 2 diabetes mellitus. Arch Intern Med 2009;169:616–25. https://doi.org/ 10.1001/archinternmed.2009.20 392. Tan S, Goudot G, Arnoux A, Tran Y, Maissoro H, Poenou G, et al. Occurrence of major local lower limb events in type 2 diabetic patients with lower extremity arterial disease: impact of metformin. Ann Vasc Surg 2023;90:153–61. https://doi.org/10.1016/j. avsg.2022.09.064 393. Ferrannini G, Gerstein H, Colhoun HM, Dagenais GR, Diaz R, Dyal L, et al. Similar cardiovascular outcomes in patients with diabetes and established or high risk for coronary vascular disease treated with dulaglutide with and without baseline metformin. Eur Heart J 2021;42:2565–73. https://doi.org/10.1093/eurheartj/ehaa777 394. Zoungas S, Arima H, Gerstein HC, Holman RR, Woodward M, Reaven P, et al. Effects of intensive glucose control on microvascular outcomes in patients with type 2 diabetes: a meta-analysis of individual participant data from randomised controlled trials. Lancet Diabetes Endocrinol 2017;5:431–7. https://doi.org/10.1016/S2213-8587(17) 30104-3 395. Group AC, Patel A, MacMahon S, Chalmers J, Neal B, Billot L, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes. N Engl J Med 2008;358:2560–72. https://doi.org/10.1056/NEJMoa0802987 396. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:837–53. https:// doi.org/10.1016/S0140-6736(98)07019-6 397. Diabetes Control and Complications Trial Research Group; Nathan DM, Genuth S, Lachin J, Cleary P, Crofford O, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993;329:977–86. https://doi.org/10.1056/ NEJM199309303291401 398. McGuire DK, Shih WJ, Cosentino F, Charbonnel B, Cherney DZI, Dagogo-Jack S, et al. Association of SGLT2 inhibitors with cardiovascular and kidney outcomes in patients with type 2 diabetes: a meta-analysis. JAMA Cardiol 2021;6:148–58. https://doi.org/10. 1001/jamacardio.2020.4511 399. Bhatt DL, Szarek M, Steg PG, Cannon CP, Leiter LA, McGuire DK, et al. Sotagliflozin in patients with diabetes and recent worsening heart failure. N Engl J Med 2021;384: 117–28. https://doi.org/10.1056/NEJMoa2030183 400. Bhatt DL, Szarek M, Pitt B, Cannon CP, Leiter LA, McGuire DK, et al. Sotagliflozin in patients with diabetes and chronic kidney disease. N Engl J Med 2021;384:129–39. https://doi.org/10.1056/NEJMoa2030186 401. Wiviott SD, Raz I, Bonaca MP, Mosenzon O, Kato ET, Cahn A, et al. Dapagliflozin and cardiovascular outcomes in type 2 diabetes. N Engl J Med 2019;380:347–57. https://doi. org/10.1056/NEJMoa1812389 402. Zinman B, Wanner C, Lachin JM, Fitchett D, Bluhmki E, Hantel S, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med 2015;373: 2117–28. https://doi.org/10.1056/NEJMoa1504720 403. Sattar N, Lee MMY, Kristensen SL, Branch KRH, Del Prato S, Khurmi NS, et al. Cardiovascular, mortality, and kidney outcomes with GLP-1 receptor agonists in patients with type 2 diabetes: a systematic review and meta-analysis of randomised trials. Lancet Diabetes Endocrinol 2021;9:653–62. https://doi.org/10.1016/S2213-8587(21) 00203-5 404. Gerstein HC, Sattar N, Rosenstock J, Ramasundarahettige C, Pratley R, Lopes RD, et al. Cardiovascular and renal outcomes with efpeglenatide in type 2 diabetes. N Engl J Med 2021;385:896–907. https://doi.org/10.1056/NEJMoa2108269 405. Gerstein HC, Colhoun HM, Dagenais GR, Diaz R, Lakshmanan M, Pais P, et al. Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a doubleblind, randomised placebo-controlled trial. Lancet 2019;394:121–30. https://doi.org/ 10.1016/S0140-6736(19)31149-3 406. Marso SP, Daniels GH, Brown-Frandsen K, Kristensen P, Mann JFE, Nauck MA, et al. Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med 2016;375: 311–22. https://doi.org/10.1056/NEJMoa1603827 407. Marso SP, Bain SC, Consoli A, Eliaschewitz FG, Jódar E, Leiter LA, et al. Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. N Engl J Med 2016; 375:1834–44. https://doi.org/10.1056/NEJMoa1607141 408. International Hypoglycaemia Study Group. Hypoglycaemia, cardiovascular disease, and mortality in diabetes: epidemiology, pathogenesis, and management. Lancet Diabetes Endocrinol 2019;7:385–96. https://doi.org/10.1016/S2213-8587(18)30315-2 409. Zoungas S, Chalmers J, Ninomiya T, Li Q, Cooper ME, Colagiuri S, et al. Association of HbA1c levels with vascular complications and death in patients with type 2 diabetes: evidence of glycaemic thresholds. Diabetologia 2012;55:636–43. https://doi.org/10. 1007/s00125-011-2404-1 410. Currie CJ, Peters JR, Tynan A, Evans M, Heine RJ, Bracco OL, et al. Survival as a function of HbA(1c) in people with type 2 diabetes: a retrospective cohort study. Lancet 2010; 375:481–9. https://doi.org/10.1016/S0140-6736(09)61969-3 411. Control G, Turnbull FM, Abraira C, Anderson RJ, Byington RP, Chalmers JP, et al. Intensive glucose control and macrovascular outcomes in type 2 diabetes. Diabetologia 2009;52:2288–98. https://doi.org/10.1007/s00125-009-1470-0 412. Caturano A, Galiero R, Pafundi PC, Cesaro A, Vetrano E, Palmiero G, et al. Does a strict glycemic control during acute coronary syndrome play a cardioprotective effect? Pathophysiology and clinical evidence. Diabetes Res Clin Pract 2021;178:108959. https://doi.org/10.1016/j.diabres.2021.108959 413. Soehnlein O, Libby P. Targeting inflammation in atherosclerosis—from experimental insights to the clinic. Nat Rev Drug Discov 2021;20:589–610. https://doi.org/10.1038/ s41573-021-00198-1 414. Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med 2017;377:1119–31. https://doi.org/10.1056/NEJMoa1707914 415. Samuel M, Tardif JC, Bouabdallaoui N, Khairy P, Dubé M-P, Blondeau L, et al. Colchicine for secondary prevention of cardiovascular disease: a systematic review and meta-analysis of randomized controlled trials. Can J Cardiol 2021;37:776–85. https://doi.org/10.1016/j.cjca.2020.10.006 416. Antonopoulos AS, Papanikolaou E, Vogiatzi G, Oikonomou E, Tousoulis D. Anti-inflammatory agents in peripheral arterial disease. Curr Opin Pharmacol 2018; 39:1–8. https://doi.org/10.1016/j.coph.2017.11.001 417. Mills JL, Sr, Conte MS, Armstrong DG, Pomposelli FB, Schanzer A, Sidawy AN, et al. The Society for Vascular Surgery lower extremity threatened limb classification system: risk stratification based on wound, ischemia, and foot infection (WIfI). J Vasc Surg 2014;59:220–34.e1–2. https://doi.org/10.1016/j.jvs.2013.08.003 418. Fowkes FG, Aboyans V, Fowkes FJ, McDermott MM, Sampson UKA, Criqui MH, Peripheral artery disease: epidemiology and global perspectives. Nat Rev Cardiol 2017;14:156–70. https://doi.org/10.1038/nrcardio.2016.179 419. Diehm C, Allenberg JR, Pittrow D, Mahn M, Tepohl G, Haberl RL, et al. Mortality and vascular morbidity in older adults with asymptomatic versus symptomatic peripheral artery disease. Circulation 2009;120:2053–61. https://doi.org/10.1161/circulationaha. 109.865600 420. McDermott MM, Greenland P, Liu K, Guralnik JM, Criqui MH, Dolan NC, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA 2001;286:1599–606. https://doi.org/10.1001/jama.286.13.1599 421. Sigvant B, Wiberg-Hedman K, Bergqvist D, Rolandsson O, Andersson B, Persson E, et al. A population-based study of peripheral arterial disease prevalence with special Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.136
focus on critical limb ischemia and sex differences. J Vasc Surg 2007;45:1185–91. https://doi.org/10.1016/j.jvs.2007.02.004 422. Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FGR, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). Eur J Vasc Endovasc Surg 2007;33:S1–75. https://doi.org/10.1016/j.ejvs.2006.09.024 423. Buso G, Aboyans V, Mazzolai L. Lower extremity artery disease in patients with type 2 diabetes. Eur J Prev Cardiol 2019;26:114–24. https://doi.org/10.1177/20474873198 80044 424. Porras CP, Bots ML, Teraa M, van Doorn S, Vernooij RWM. Differences in symptom presentation in women and men with confirmed lower limb peripheral artery disease: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2022;63:602–12. https://doi.org/10.1016/j.ejvs.2021.12.039 425. Fereydooni A, Gorecka J, Dardik A. Using the epidemiology of critical limb ischemia to estimate the number of patients amenable to endovascular therapy. Vasc Med 2020; 25:78–87. https://doi.org/10.1177/1358863X19878271 426. Conte MS, Bradbury AW, Kolh P, White JV, Dick F, Fitridge R, et al. Global vascular guidelines on the management of chronic limb-threatening ischemia. Eur J Vasc Endovasc Surg 2019;58:S1–109.e33. https://doi.org/10.1016/j.ejvs.2019.05.006 427. Sigvant B, Lundin F, Wahlberg E. The risk of disease progression in peripheral arterial disease is higher than expected: a meta-analysis of mortality and disease progression in peripheral arterial disease. Eur J Vasc Endovasc Surg 2016;51:395–403. https://doi.org/ 10.1016/j.ejvs.2015.10.022 428. Hageman SHJ, de Borst GJ, Dorresteijn JAN, Bots ML, Westerink J, Asselbergs FW, et al. Cardiovascular risk factors and the risk of major adverse limb events in patients with symptomatic cardiovascular disease. Heart 2020;106:1686–92. https://doi.org/10. 1136/heartjnl-2019-316088 429. Anand SS, Caron F, Eikelboom JW, Bosch J, Dyal L, Aboyans V, et al. Major adverse limb events and mortality in patients with peripheral artery disease: the COMPASS trial. J Am Coll Cardiol 2018;71:2306–15. https://doi.org/10.1016/j.jacc.2018.03.008 430. Eikelboom JW, Connolly SJ, Bosch J, Dagenais GR, Hart RG, Shestakovska O, et al. Rivaroxaban with or without aspirin in stable cardiovascular disease. N Engl J Med 2017;377:1319–30. https://doi.org/10.1056/NEJMoa1709118 431. Agnelli G, Belch JJF, Baumgartner I, Giovas P, Hoffmann U. Morbidity and mortality associated with atherosclerotic peripheral artery disease: a systematic review. Atherosclerosis 2020;293:94–100. https://doi.org/10.1016/j.atherosclerosis.2019. 09.012 432. Wijnand JGJ, van Koeverden ID, Teraa M, Spreen MI, Mali WPTM, van Overhagen H, et al. Validation of randomized controlled trial-derived models for the prediction of postintervention outcomes in chronic limb-threatening ischemia. J Vasc Surg 2020; 71:869–79. https://doi.org/10.1016/j.jvs.2019.06.195 433. Jaramillo EA, Smith EJT, Matthay ZA, Sanders KM, Hiramoto JS, Gasper WJ, et al. Racial and ethnic disparities in major adverse limb events persist for chronic limb threatening ischemia despite presenting limb threat severity after peripheral vascular intervention. J Vasc Surg 2023;77:848–57.e2. https://doi.org/10.1016/j.jvs.2022.10.043 434. Brizuela Sanz JA, Gonzalez Fajardo JA, Taylor JH, Río Solá L, Muñoz Moreno MF, Vaquero Puerta C, et al. Design of a new risk score in critical limb ischaemia: the ERICVA model. Eur J Vasc Endovasc Surg 2016;51:90–9. https://doi.org/10.1016/j.ejvs. 2015.09.025 435. Kreutzburg T, Peters F, Kuchenbecker J, Marschall U, Lee R, Kriston L, et al. Editor’s choice—the GermanVasc score: a pragmatic risk score predicts five year amputation free survival in patients with peripheral arterial occlusive disease. Eur J Vasc Endovasc Surg 2021;61:248–56. https://doi.org/10.1016/j.ejvs.2020.11.013 436. Niazi K, Khan TH, Easley KA. Diagnostic utility of the two methods of ankle brachial index in the detection of peripheral arterial disease of lower extremities. Catheter Cardiovasc Interv 2006;68:788–92. https://doi.org/10.1002/ccd.20906 437. Crawford F, Welch K, Andras A, Chappell FM. Ankle brachial index for the diagnosis of lower limb peripheral arterial disease. Cochrane Database Syst Rev 2016;9:CD010680. https://doi.org/10.1002/14651858.CD010680.pub2 438. Aday AW, Kinlay S, Gerhard-Herman MD. Comparison of different exercise ankle pressure indices in the diagnosis of peripheral artery disease. Vasc Med 2018;23: 541–8. https://doi.org/10.1177/1358863X18781723 439. Tehan PE, Barwick AL, Sebastian M, Chuter VH. Diagnostic accuracy of the postexercise ankle-brachial index for detecting peripheral artery disease in suspected claudicants with and without diabetes. Vasc Med 2018;23:116–25. https://doi.org/10.1177/ 1358863X17751259 440. Manu CA, Freedman B, Rashid H, Winkley K, Edmonds ME. Peripheral arterial disease located in the feet of patients with diabetes and foot ulceration demands a new approach to the assessment of ischemia. Int J Low Extrem Wounds 2022;21:397–404. https://doi.org/10.1177/1534734620947979 441. Salaun P, Desormais I, Lapébie FX, Rivière AB, Aboyans V, Lacroix P, et al. Comparison of ankle pressure, systolic toe pressure, and transcutaneous oxygen pressure to predict major amputation after 1 year in the copart cohort. Angiology 2019;70:229–36. https://doi.org/10.1177/0003319718793566 442. Fowkes FG, Murray GD, Butcher I, Folsom AR, Hirsch AT, Couper DJ, et al. Development and validation of an ankle brachial index risk model for the prediction of cardiovascular events. Eur J Prev Cardiol 2014;21:310–20. https://doi.org/10.1177/ 2047487313516564 443. Wang FM, Yang C, Ballew SH, Kalbaugh CA, Meyer ML, Tanaka H, et al. Ankle-brachial index and subsequent risk of incident and recurrent cardiovascular events in older adults: the Atherosclerosis Risk in Communities (ARIC) study. Atherosclerosis 2021; 336:39–47. https://doi.org/10.1016/j.atherosclerosis.2021.09.028 444. Cull DL, Manos G, Hartley MC, Taylor SM, Langan EM, Eidt JF, et al. An early validation of the Society for Vascular Surgery lower extremity threatened limb classification system. J Vasc Surg 2014;60:1535–42. https://doi.org/10.1016/j.jvs.2014.08.107 445. Liette MD, Crisologo PA, Masadeh S, Yang SH, Bergmann CB, Caldwell CC, et al. A prospective analysis of the SVS WIfI classification system to stratify immediate and 1-year patient outcomes. J Foot Ankle Surg 2023;62:661–5. https://doi.org/10.1053/j. jfas.2023.02.003 446. van Reijen NS, Ponchant K, Ubbink DT, Koelemay MJW. Editor’s choice—the prognostic value of the WIfI classification in patients with chronic limb threatening ischaemia: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2019;58:362–71. https://doi.org/10.1016/j.ejvs.2019.03.040 447. Eiberg JP, Gronvall Rasmussen JB, Hansen MA, Schroeder TV. Duplex ultrasound scanning of peripheral arterial disease of the lower limb. Eur J Vasc Endovasc Surg 2010;40: 507–12. https://doi.org/10.1016/j.ejvs.2010.06.002 448. Met R, Bipat S, Legemate DA, Reekers JA, Koelemay MJ. Diagnostic performance of computed tomography angiography in peripheral arterial disease: a systematic review and meta-analysis. JAMA 2009;301:415–24. https://doi.org/10.1001/jama.301.4.415 449. Itoga NK, Kim T, Sailer AM, Fleischmann D, Mell MW. Lower extremity computed tomography angiography can help predict technical success of endovascular revascularization in the superficial femoral and popliteal artery. J Vasc Surg 2017;66:835–43.e1. https://doi.org/10.1016/j.jvs.2017.02.031 450. Selvin E, Hirsch AT. Contemporary risk factor control and walking dysfunction in individuals with peripheral arterial disease: NHANES 1999–2004. Atherosclerosis 2008; 201:425–33. https://doi.org/10.1016/j.atherosclerosis.2008.02.002 451. Pande RL, Perlstein TS, Beckman JA, Creager MA. Secondary prevention and mortality in peripheral artery disease: National Health and Nutrition Examination Study, 1999 to 2004. Circulation 2011;124:17–23. https://doi.org/10.1161/circulationaha.110.003954 452. Krishnamurthy V, Munir K, Rectenwald JE, Mansour A, Hans S, Eliason JL, et al. Contemporary outcomes with percutaneous vascular interventions for peripheral critical limb ischemia in those with and without poly-vascular disease. Vasc Med 2014;19:491–9. https://doi.org/10.1177/1358863x14552013 453. Penin-Grandes S, Lopez-Ortiz S, Maroto-Izquierdo S, Menéndez H, Pinto-Fraga J, Martín-Hernández J, et al. Winners do what they fear: exercise and peripheral arterial disease–an umbrella review. Eur J Prev Cardiol 2024;31:380–388. https://doi.org/10. 1093/eurjpc/zwad261 454. Gardner AW, Poehlman ET. Exercise rehabilitation programs for the treatment of claudication pain. A meta-analysis. JAMA 1995;274:975–80. 455. Parmenter BJ, Raymond J, Dinnen P, Singh MA. A systematic review of randomized controlled trials: walking versus alternative exercise prescription as treatment for intermittent claudication. Atherosclerosis 2011;218:1–12. https://doi.org/10.1016/j. atherosclerosis.2011.04.024 456. Fakhry F, van de Luijtgaarden KM, Bax L, den Hoed PT, Hunink MGGM, Rouwet EV, et al. Supervised walking therapy in patients with intermittent claudication. J Vasc Surg 2012;56:1132–42. https://doi.org/10.1016/j.jvs.2012.04.046 457. Parmenter BJ, Dieberg G, Smart NA. Exercise training for management of peripheral arterial disease: a systematic review and meta-analysis. Sports Med 2015;45:231–44. https://doi.org/10.1007/s40279-014-0261-z 458. Lane R, Harwood A, Watson L, Leng GC. Exercise for intermittent claudication. Cochrane Database Syst Rev 2017;12:CD000990. https://doi.org/10.1002/14651858. CD000990.pub4 459. Parmenter BJ, Mavros Y, Ritti Dias R, King S, Fiatarone Singh M. Resistance training as a treatment for older persons with peripheral artery disease: a systematic review and meta-analysis. Br J Sports Med 2020;54:452–61. https://doi.org/10.1136/bjsports- 2018-100205 460. Perks J, Zaccardi F, Paterson C, Houghton JSM, Nickinson ATO, Pepper CJ, et al. Effect of high-pain versus low-pain structured exercise on walking ability in people with intermittent claudication: meta-analysis. Br J Surg 2022;109:686–94. https://doi.org/10. 1093/bjs/znac134 461. Guidon M, McGee H. Exercise-based interventions and health-related quality of life in intermittent claudication: a 20-year (1989–2008) review. Eur J Cardiovasc Prev Rehabil 2010;17:140–54. https://doi.org/10.1097/HJR.0b013e3283377f08 462. Parmenter BJ, Dieberg G, Phipps G, Smart NA. Exercise training for health-related quality of life in peripheral artery disease: a systematic review and meta-analysis. Vasc Med 2015;20:30–40. https://doi.org/10.1177/1358863x14559092 463. Gommans LN, Fokkenrood HJ, van Dalen HC, Scheltinga MRM, Teijink JAW, Peters RJG. Safety of supervised exercise therapy in patients with intermittent claudication. J Vasc Surg 2015;61:512–8.e2. https://doi.org/10.1016/j.jvs.2014.08.070 464. Harwood AE, Pymer S, Ibeggazene S, Ingle L, Caldow E, Birkett ST. Provision of exercise services in patients with peripheral artery disease in the United Kingdom. Vascular 2022;30:874–81. https://doi.org/10.1177/17085381211035259
ESC Guidelines 3673
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.137
465. Lanzi S, Belch J, Brodmann M, Madaric J, Bura-Riviere A, Visonà A, et al. Supervised exercise training in patients with lower extremity peripheral artery disease. Vasa 2022; 51:267–74. https://doi.org/10.1024/0301-1526/a001024 466. Gommans LN, Saarloos R, Scheltinga MR, Houterman S, de Bie RA, Fokkenrood HJP, et al. Editor’s choice—the effect of supervision on walking distance in patients with intermittent claudication: a meta-analysis. Eur J Vasc Endovasc Surg 2014;48:169–84. https://doi.org/10.1016/j.ejvs.2014.04.019 467. Vemulapalli S, Dolor RJ, Hasselblad V, Schmit K, Banks A, Heidenfelder B, et al. Supervised vs unsupervised exercise for intermittent claudication: a systematic review and meta-analysis. Am Heart J 2015;169:924–37.e3. https://doi.org/10.1016/j. ahj.2015.03.009 468. Hageman D, Fokkenrood HJ, Gommans LN, van den Houten MM, Teijink JA. Supervised exercise therapy versus home-based exercise therapy versus walking advice for intermittent claudication. Cochrane Database Syst Rev 2018;4:CD005263. https://doi.org/10.1002/14651858.CD005263.pub4 469. Pymer S, Ibeggazene S, Palmer J, Tew GA, Ingle L, Smith GE, et al. An updated systematic review and meta-analysis of home-based exercise programs for individuals with intermittent claudication. J Vasc Surg 2021;74:2076–85.e20. https://doi.org/10.1016/j. jvs.2021.03.063 470. Waddell A, Seed S, Broom DR, McGregor G, Birkett ST, Harwood AE. Safety of homebased exercise for people with intermittent claudication: a systematic review. Vasc Med 2022;27:186–92. https://doi.org/10.1177/1358863x211060388 471. Golledge J, Singh TP, Alahakoon C, Pinchbeck J, Yip L, Moxon JV, et al. Meta-analysis of clinical trials examining the benefit of structured home exercise in patients with peripheral artery disease. Br J Surg 2019;106:319–31. https://doi.org/10.1002/bjs.11101 472. Bulmer AC, Coombes JS. Optimising exercise training in peripheral arterial disease. Sports Med 2004;34:983–1003. https://doi.org/10.2165/00007256-200434140-00004 473. Ehrman JK, Gardner AW, Salisbury D, Lui K, Treat-Jacobson D. Supervised exercise therapy for symptomatic peripheral artery disease: a review of current experience and practice-based recommendations. J Cardiopulm Rehabil Prev 2023;43:15–21. https://doi.org/10.1097/hcr.0000000000000723 474. McDermott MM, Spring B, Tian L, Treat-Jacobson D, Ferrucci L, Lloyd-Jones D, et al. Effect of low-intensity vs high-intensity home-based walking exercise on walk distance in patients with peripheral artery disease: the LITE randomized clinical trial. JAMA 2021; 325:1266–76. https://doi.org/10.1001/jama.2021.2536 475. Jansen SC, Abaraogu UO, Lauret GJ, Fakhry F, Fokkenrood HJP, Teijink JAW. Modes of exercise training for intermittent claudication. Cochrane Database Syst Rev 2020;8: CD009638. https://doi.org/10.1002/14651858.CD009638.pub3 476. Gardner AW, Parker DE, Montgomery PS, Blevins SM. Diabetic women are poor responders to exercise rehabilitation in the treatment of claudication. J Vasc Surg 2014; 59:1036–43. https://doi.org/10.1016/j.jvs.2013.10.058 477. Gommans LN, Scheltinga MR, van Sambeek MR, Maas AHEM, Bendermacher BLW, Teijink JAW. Gender differences following supervised exercise therapy in patients with intermittent claudication. J Vasc Surg 2015;62:681–8. https://doi.org/10.1016/j. jvs.2015.03.076 478. Dipnarine K, Barak S, Martinez CA, Carmeli E, Stopka CB. Pain-free treadmill exercise for patients with intermittent claudication: are there gender differences? Vascular 2016; 24:304–14. https://doi.org/10.1177/1708538115592800 479. Gardner AW, Parker DE, Montgomery PS. Sex-specific predictors of improved walking with step-monitored, home-based exercise in peripheral artery disease. Vasc Med 2015;20:424–31. https://doi.org/10.1177/1358863x15596237 480. Ney B, Lanzi S, Calanca L, Mazzolai L. Multimodal supervised exercise training is effective in improving long term walking performance in patients with symptomatic lower extremity peripheral artery disease. J Clin Med 2021;10:2057.https://doi.org/10.3390/ jcm10102057 481. Lanzi S, Pousaz A, Calanca L, Mazzolai L. Sex-based differences in supervised exercise therapy outcomes for symptomatic peripheral artery disease. Vasc Med 2023;28: 147–9. https://doi.org/10.1177/1358863x221149454 482. Fakhry F, Spronk S, van der Laan L, Wever JJ, Teijink JAW, Hoffmann WH, et al. Endovascular revascularization and supervised exercise for peripheral artery disease and intermittent claudication: a randomized clinical trial. JAMA 2015;314:1936–44. https://doi.org/10.1001/jama.2015.14851 483. Pandey A, Banerjee S, Ngo C, Mody P, Marso SP, Brilakis ES, et al. Comparative efficacy of endovascular revascularization versus supervised exercise training in patients with intermittent claudication: meta-analysis of randomized controlled trials. JACC Cardiovasc Interv 2017;10:712–24. https://doi.org/10.1016/j.jcin.2017.01.027 484. Dorn A, Dorweiler B, Ahmad W, Mylonas S, Becker I, Majd P. Low and high ankle-brachial index are both associated with mortality in German nursing home residents–the five-year follow-up of the ‘allo-study’ Cohort. J Clin Med 2023;12:4411. https://doi.org/10.3390/jcm12134411 485. Fowkes FG, Price JF, Stewart MC, Butcher I, Leng GC, Pell AC, et al. Aspirin for prevention of cardiovascular events in a general population screened for a low ankle brachial index: a randomized controlled trial. JAMA 2010;303:841–8. https://doi.org/10. 1001/jama.2010.221 486. Belch J, MacCuish A, Campbell I, Cobbe S, Taylor R, Prescott R, et al. The prevention of progression of arterial disease and diabetes (POPADAD) trial: factorial randomised placebo controlled trial of aspirin and antioxidants in patients with diabetes and asymptomatic peripheral arterial disease. BMJ 2008;337:a1840. https://doi.org/10.1136/bmj. a1840 487. Bowman L, Mafham M, Wallendszus K, Stevens W, Buck G, Barton J, et al. Effects of aspirin for primary prevention in persons with diabetes mellitus. N Engl J Med 2018; 379:1529–39. https://doi.org/10.1056/NEJMoa1804988 488. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71–86. https://doi.org/10.1136/bmj.324.7329.71 489. De Carlo M, Di Minno G, Sayre T, Fazeli MS, Siliman G, Cimminiello C. Efficacy and safety of antiplatelet therapies in symptomatic peripheral artery disease: a systematic review and network meta-analysis. Curr Vasc Pharmacol 2021;19:542–55. https://doi. org/10.2174/1570161118666200820141131 490. Willems LH, Maas D, Kramers K, Reijnen MMPJ, Riksen NP, Ten Cate H, et al. Antithrombotic therapy for symptomatic peripheral arterial disease: a systematic review and network meta-analysis. Drugs 2022;82:1287–302. https://doi.org/10.1007/ s40265-022-01756-6 491. Katsanos K, Spiliopoulos S, Saha P, Diamantopoulos A, Karunanithy N, Krokidis M, et al. Comparative efficacy and safety of different antiplatelet agents for prevention of major cardiovascular events and leg amputations in patients with peripheral arterial disease: a systematic review and network meta-analysis. PLoS One 2015;10:e0135692. https://doi.org/10.1371/journal.pone.0135692 492. Basili S, Raparelli V, Vestri A, Di Tanna GL, Violi F. Comparison of efficacy of antiplatelet treatments for patients with claudication. A meta-analysis. Thromb Haemost 2010; 103:766–73. https://doi.org/10.1160/th09-09-0635 493. CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet 1996;348:1329–39. https://doi.org/10.1016/s0140-6736(96)09457-3 494. Berger JS, Krantz MJ, Kittelson JM, Hiatt WR. Aspirin for the prevention of cardiovascular events in patients with peripheral artery disease: a meta-analysis of randomized trials. JAMA 2009;301:1909–19. https://doi.org/10.1001/jama.2009.623 495. Hiatt WR, Fowkes FG, Heizer G, Berger JS, Baumgartner I, Held P, et al. Ticagrelor versus clopidogrel in symptomatic peripheral artery disease. N Engl J Med 2017;376: 32–40. https://doi.org/10.1056/NEJMoa1611688 496. Bhatt DL, Fox KA, Hacke W, Berger PB, Black HR, Boden WE, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med 2006;354:1706–17. https://doi.org/10.1056/NEJMoa060989 497. Bhatt DL, Flather MD, Hacke W, Berger PB, Black HR, Boden WE, et al. Patients with prior myocardial infarction, stroke, or symptomatic peripheral arterial disease in the CHARISMA trial. J Am Coll Cardiol 2007;49:1982–8. https://doi.org/10.1016/j.jacc. 2007.03.025 498. Kaplovitch E, Eikelboom JW, Dyal L, Aboyans V, Abola MT, Verhamme P, et al. Rivaroxaban and aspirin in patients with symptomatic lower extremity peripheral artery disease: a subanalysis of the COMPASS randomized clinical trial. JAMA Cardiol 2021;6:21–9. https://doi.org/10.1001/jamacardio.2020.4390 499. Anand SS, Bosch J, Eikelboom JW, Connolly SJ, Diaz R, Widimsky P, et al. Rivaroxaban with or without aspirin in patients with stable peripheral or carotid artery disease: an international, randomised, double-blind, placebo-controlled trial. Lancet 2018;391: 219–29. https://doi.org/10.1016/s0140-6736(17)32409-1 500. Strobl FF, Brechtel K, Schmehl J, Zeller T, Reiser MF, Claussen CD, et al. Twelve-month results of a randomized trial comparing mono with dual antiplatelet therapy in endovascularly treated patients with peripheral artery disease. J Endovasc Ther 2013;20: 699–706. https://doi.org/10.1583/13-4275mr.1 501. Tsai SY, Li YS, Lee CH, Cha S-W, Wang Y-C, Su T-W, et al. Mono or dual antiplatelet therapy for treating patients with peripheral artery disease after lower extremity revascularization: a systematic review and meta-analysis. Pharmaceuticals (Basel) 2022; 15:596. https://doi.org/10.3390/ph15050596 502. Thott O, Granath F, Malmstedt J, Wahlgren CM. Editor’s choice—dual antiplatelet therapy improves outcome in diabetic patients undergoing endovascular femoropopliteal stenting for critical limb ischaemia. Eur J Vasc Endovasc Surg 2017;53:403–10. https://doi.org/10.1016/j.ejvs.2016.12.014 503. Cho S, Lee YJ, Ko YG, Kang TS, Lim S-H, Hong S-J, et al. Optimal strategy for antiplatelet therapy after endovascular revascularization for lower extremity peripheral artery disease. JACC Cardiovasc Interv 2019;12:2359–70. https://doi.org/10.1016/j.jcin.2019.08. 006 504. Ipema J, Welling RHA, Bakker OJ, Bokkers RPH, de Vries J-PPM, Ünlü Ç. Short-term clinical outcomes of single versus dual antiplatelet therapy after infrainguinal endovascular treatment for peripheral arterial disease. J Clin Med 2020;9:3515. https://doi.org/ 10.3390/jcm9113515 505. Bonaca MP, Bauersachs RM, Anand SS, Debus ES, Nehler MR, Patel MR, et al. Rivaroxaban in peripheral artery disease after revascularization. N Engl J Med 2020; 382:1994–2004. https://doi.org/10.1056/NEJMoa2000052 506. Hiatt WR, Bonaca MP, Patel MR, Nehler MR, Debus ES, Anand SS, et al. Rivaroxaban and aspirin in peripheral artery disease lower extremity revascularization: impact of concomitant clopidogrel on efficacy and safety. Circulation 2020;142:2219–30. https://doi.org/10.1161/circulationaha.120.050465 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.138
507. Duff S, Mafilios MS, Bhounsule P, Hasegawa JT. The burden of critical limb ischemia: a review of recent literature. Vasc Health Risk Manag 2019;15:187–208. https://doi.org/ 10.2147/VHRM.S209241 508. Sarac TP, Huber TS, Back MR, Ozaki CK, Carlton LM, Flynn TC, et al. Warfarin improves the outcome of infrainguinal vein bypass grafting at high risk for failure. J Vasc Surg 1998;28:446–57. https://doi.org/10.1016/s0741-5214(98)70130-2 509. Efficacy of oral anticoagulants compared with aspirin after infrainguinal bypass surgery (the Dutch bypass oral anticoagulants or aspirin study): a randomised trial. Lancet 2000;355:346–51. https://doi.org/10.1016/S0140-6736(99)07199-8 510. Belch JJ, Dormandy J, Biasi GM, Cairols M, Diehm C, Eikelboom B, et al. Results of the randomized, placebo-controlled clopidogrel and acetylsalicylic acid in bypass surgery for peripheral arterial disease (CASPAR) trial. J Vasc Surg 2010;52:825–33.e2. https://doi.org/10.1016/j.jvs.2010.04.027 511. Brumberg RS, Back MR, Armstrong PA, Cuthbertson D, Shames ML, Johnson BL, et al. The relative importance of graft surveillance and warfarin therapy in infrainguinal prosthetic bypass failure. J Vasc Surg 2007;46:1160–6. https://doi.org/10.1016/j.jvs.2007.07. 046 512. Van Gelder IC, Kotecha D, Rienstra M, Bunting KV, Casado-Arroyo R, Caso V, et al. 2024 ESC Guidelines for the management of atrial fibrillation. Eur Heart J 2024. https://doi.org/10.1093/eurheartj/ehae176 513. Spiliopoulos S, Pastromas G, Katsanos K, Kitrou P, Karnabatidis D, Siablis D. Platelet responsiveness to clopidogrel treatment after peripheral endovascular procedures: the PRECLOP study: clinical impact and optimal cutoff value of on-treatment high platelet reactivity. J Am Coll Cardiol 2013;61:2428–34. https://doi.org/10.1016/j.jacc. 2013.03.036 514. Busch L, Stern M, Dannenberg L, Mourikis P, Gröne M, Özaslan G, et al. Impact of high on-treatment platelet reactivity after angioplasty in patients with peripheral arterial disease. Platelets 2021;32:391–7. https://doi.org/10.1080/09537104.2020.1742314 515. Cosmi B, Conti E, Coccheri S. Anticoagulants (heparin, low molecular weight heparin and oral anticoagulants) for intermittent claudication. Cochrane Database Syst Rev 2014;5:CD001999. https://doi.org/10.1002/14651858.CD001999.pub2 516. Bagger JP, Helligsoe P, Randsbaek F, Kimose HH, Jensen BS. Effect of verapamil in intermittent claudication. A randomized, double-blind, placebo-controlled, cross-over study after individual dose-response assessment. Circulation 1997;95:411–4. https:// doi.org/10.1161/01.cir.95.2.411 517. Gargiulo G, Giugliano G, Brevetti L, Sannino A, Schiattarella GG, Serino F, et al. Use of statins in lower extremity artery disease: a review. BMC Surg 2012;12:S15. https://doi. org/10.1186/1471-2482-12-s1-s15 518. McDermott MM, Guralnik JM, Greenland P, Pearce WH, Criqui MH, Liu K, et al. Statin use and leg functioning in patients with and without lower-extremity peripheral arterial disease. Circulation 2003;107:757–61. https://doi.org/10.1161/01.cir.0000050380. 64025.07 519. Robertson L, Andras A. Prostanoids for intermittent claudication. Cochrane Database Syst Rev 2013;4:CD000986. https://doi.org/10.1002/14651858.CD000986.pub3 520. Stevens JW, Simpson E, Harnan S, Squires H, Meng Y, Thomas S, et al. Systematic review of the efficacy of cilostazol, naftidrofuryl oxalate and pentoxifylline for the treatment of intermittent claudication. Br J Surg 2012;99:1630–8. https://doi.org/10.1002/ bjs.8895 521. Bedenis R, Stewart M, Cleanthis M, Robless P, Mikhailidis DP, Stansby G. Cilostazol for intermittent claudication. Cochrane Database Syst Rev 2014;10:CD003748. https://doi. org/10.1002/14651858.CD003748.pub4 522. Hiatt WR, Money SR, Brass EP. Long-term safety of cilostazol in patients with peripheral artery disease: the CASTLE study (cilostazol: a study in long-term effects). J Vasc Surg 2008;47:330–6. https://doi.org/10.1016/j.jvs.2007.10.009 523. Iida O, Yokoi H, Soga Y, Inoue N, Suzuki K, Yokoi Y, et al. Cilostazol reduces angiographic restenosis after endovascular therapy for femoropopliteal lesions in the sufficient treatment of peripheral intervention by cilostazol study. Circulation 2013;127: 2307–15. https://doi.org/10.1161/circulationaha.112.000711 524. de Backer TL, Vander Stichele R, Lehert P, Van Bortel L. Naftidrofuryl for intermittent claudication. Cochrane Database Syst Rev 2012;12:Cd001368. https://doi.org/10.1002/ 14651858.CD001368.pub4 525. Boccalon H, Lehert P, Mosnier M. Effect of naftidrofuryl on physiological walking distance in patients with intermittent claudication. Ann Cardiol Angeiol 2001;50:175–82. https://doi.org/10.1016/s0003-3928(01)00016-6 526. Broderick C, Forster R, Abdel-Hadi M, Salhiyyah K. Pentoxifylline for intermittent claudication. Cochrane Database Syst Rev 2020;10:Cd005262. https://doi.org/10.1002/ 14651858.CD005262.pub4 527. Nicolaï SP, Kruidenier LM, Bendermacher BL, Prins MH, Stokmans RA, Broos PPHL, et al. Ginkgo biloba for intermittent claudication. Cochrane Database Syst Rev 2013; 6:Cd006888. https://doi.org/10.1002/14651858.CD006888.pub3 528. Premaratne S, Newman J, Hobbs S, Garnham A, Wall M. Meta-analysis of direct surgical versus endovascular revascularization for aortoiliac occlusive disease. J Vasc Surg 2020;72:726–37. https://doi.org/10.1016/j.jvs.2019.12.035 529. Aboyans V, Björck M, Brodmann M, Collet J-P, Czerny M, De Carlo M, et al. Questions and answers on diagnosis and management of patients with peripheral arterial diseases: a companion document of the 2017 ESC Guidelines for the diagnosis and treatment of peripheral arterial diseases, in collaboration with the European Society for Vascular Surgery (ESVS): Endorsed by: the European Stroke Organisation (ESO), The Task Force for the Diagnosis and Treatment of Peripheral Arterial Diseases of the European Society of Cardiology (ESC) and of the European Society for Vascular Surgery (ESVS). Eur Heart J 2018;39:e35–41. https://doi.org/10.1093/eurheartj/ehx499 530. McQuade K, Gable D, Pearl G, Theune B, Black S. Four-year randomized prospective comparison of percutaneous ePTFE/nitinol self-expanding stent graft versus prosthetic femoral-popliteal bypass in the treatment of superficial femoral artery occlusive disease. J Vasc Surg 2010;52:584–91.e7. https://doi.org/10.1016/j.jvs.2010.03.071 531. Bosiers M, Deloose K, Callaert J, Moreels N, Keirse K, Verbist J, et al. Results of the Protégé EverFlex 200-mm-long nitinol stent (ev3) in TASC C and D femoropopliteal lesions. J Vasc Surg 2011;54:1042–50. https://doi.org/10.1016/j.jvs.2011.03.272 532. Farhan S, Enzmann FK, Bjorkman P, Kamran H, Zhang Z, Sartori S, et al. Revascularization strategies for patients with femoropopliteal peripheral artery disease. J Am Coll Cardiol 2023;81:358–70. https://doi.org/10.1016/j.jacc.2022.10.036 533. Katsanos K, Spiliopoulos S, Kitrou P, Krokidis M, Karnabatidis D. Risk of death following application of paclitaxel-coated balloons and stents in the femoropopliteal artery of the leg: a systematic review and meta-analysis of randomized controlled trials. J Am Heart Assoc 2018;7:e011245. https://doi.org/10.1161/jaha.118.011245 534. Ouriel K, Adelman MA, Rosenfield K, Scheinert D, Brodmann M, Peña C, et al. Safety of paclitaxel-coated balloon angioplasty for femoropopliteal peripheral artery disease. JACC Cardiovasc Interv 2019;12:2515–24. https://doi.org/10.1016/j.jcin.2019.08.025 535. Freisinger E, Koeppe J, Gerss J, Goerlich D, Malyar NM, Marschall U, et al. Mortality after use of paclitaxel-based devices in peripheral arteries: a real-world safety analysis. Eur Heart J 2020;41:3732–9. https://doi.org/10.1093/eurheartj/ehz698 536. Lyden SP, Brodmann M, Parikh SA, Krishnan P, Schroeder H, Werner M, et al. Four-year patient-level pooled mortality analysis of the ILLUMENATE US pivotal and EU randomized controlled trials. J Vasc Surg 2022;75:600–7. https://doi.org/10. 1016/j.jvs.2021.07.244 537. Secemsky EA, Song Y, Schermerhorn M, Yeh RW. Update from the longitudinal assessment of safety of femoropopliteal endovascular treatment with paclitaxel-coated devices among medicare beneficiaries: the SAFE-PAD study. Circ Cardiovasc Interv 2022;15:e012074. https://doi.org/10.1161/circinterventions.122.012074 538. Nordanstig J, James S, Andersson M, Andersson M, Danielsson P, Gillgren P, et al. Mortality with paclitaxel-coated devices in peripheral artery disease. N Engl J Med 2020;383:2538–46. https://doi.org/10.1056/NEJMoa2005206 539. Fashandi AZ, Mehaffey JH, Hawkins RB, Kron IL, Upchurch GR, Robinson WP. Major adverse limb events and major adverse cardiac events after contemporary lower extremity bypass and infrainguinal endovascular intervention in patients with claudication. J Vasc Surg 2018;68:1817–23. https://doi.org/10.1016/j.jvs.2018.06.193 540. Koelemay MJW, van Reijen NS, van Dieren S, Frans FA, Vermeulen EJG, Buscher HCJL, et al. Editor’s choice—randomised clinical trial of supervised exercise therapy vs. endovascular revascularisation for intermittent claudication caused by iliac artery obstruction: the SUPER study. Eur J Vasc Endovasc Surg 2022;63:421–9. https://doi.org/ 10.1016/j.ejvs.2021.09.042 541. Dormandy J, Mahir M, Ascady G, Balsano F, De Leeuw P, Blombery P, et al. Fate of the patient with chronic leg ischaemia. A review article. J Cardiovasc Surg (Torino) 1989;30: 50–7. 542. Jelnes R, Gaardsting O, Hougaard Jensen K, Baekgaard N, Tonnesen KH, Schroeder T. Fate in intermittent claudication: outcome and risk factors. BMJ 1986;293:1137–40. https://doi.org/10.1136/bmj.293.6555.1137 543. Leng GC, Lee AJ, Fowkes FG, Whiteman M, Dunbar J, Housley E, et al. Incidence, natural history and cardiovascular events in symptomatic and asymptomatic peripheral arterial disease in the general population. Int J Epidemiol 1996;25:1172–81. https:// doi.org/10.1093/ije/25.6.1172 544. Bloor K. Natural history of arteriosclerosis of the lower extremities: Hunterian lecture delivered at the Royal College of Surgeons of England on 22nd April 1960. Ann R Coll Surg Engl 1961;28:36–52. 545. Goode SD, Cleveland TJ, Gaines PA, Collaborators S. Randomized clinical trial of stents versus angioplasty for the treatment of iliac artery occlusions (STAG trial). Br J Surg 2013;100:1148–53. https://doi.org/10.1002/bjs.9197 546. Hajibandeh S, Hajibandeh S, Antoniou SA, Torella F, Antoniou GA. Covered vs uncovered stents for aortoiliac and femoropopliteal arterial disease: a systematic review and meta-analysis. J Endovasc Ther 2016;23:442–52. https://doi.org/10.1177/ 1526602816643834 547. Krankenberg H, Zeller T, Ingwersen M, Schmalstieg J, Gissler HM, Nikol S, et al. Self-expanding versus balloon-expandable stents for iliac artery occlusive disease: the randomized ICE trial. JACC Cardiovasc Interv 2017;10:1694–704. https://doi.org/ 10.1016/j.jcin.2017.05.015 548. Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease. Radiology 1997;204:87–96. https://doi.org/10.1148/radiology.204.1.9205227 549. Committee TS, Jaff MR, White CJ, Hiatt WR, Fowkes GR, Dormandy J, et al. An update on methods for revascularization and expansion of the TASC lesion classification to include below-the-knee arteries: a supplement to the inter-society consensus for
ESC Guidelines 3675
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.139
the management of peripheral arterial disease (TASC II). J Endovasc Ther 2015;22: 663–77. https://doi.org/10.1177/1526602815592206 550. Boc V, Kozak M, Erzen B, Božič Mijovski M, Boc A, Blinc A. Prognostic factors for restenosis of superficial femoral artery after endovascular treatment. J Clin Med 2023;12: 6343. https://doi.org/10.3390/jcm12196343 551. Alves-Cabratosa L, Comas-Cufi M, Ponjoan A, Garcia-Gil M, Martí-Lluch R, Blanch J, et al. Levels of ankle-brachial index and the risk of diabetes mellitus complications. BMJ Open Diabetes Res Care 2020;8:e000977. https://doi.org/10.1136/bmjdrc-2019- 000977 552. Heiss C, Olinic DM, Belch JJF, Brodmann M, Mazzolai L, Stanek A, et al. Management of chronic peripheral artery disease patients with indication for endovascular revascularization. Vasa 2022;51:121–37. https://doi.org/10.1024/0301-1526/a000998 553. Hajibandeh S, Hajibandeh S, Shah S, Child E, Antoniou GA, Torella F. Prognostic significance of ankle brachial pressure index: a systematic review and meta-analysis. Vascular 2017;25:208–24. https://doi.org/10.1177/1708538116658392 554. Meza-Torres B, Cunningham SG, Heiss C, Joy M, Feher M, Leese GP, et al. Adherence to general diabetes and foot care processes, with prompt referral, are associated with amputation-free survival in people with type 2 diabetes and foot ulcers: a Scottish national registry analysis. J Diabetes Res 2022;2022:7414258. https://doi.org/10.1155/ 2022/7414258 555. Shishehbor MH, White CJ, Gray BH, Menard MT, Lookstein R, Rosenfield K, et al. Critical limb ischemia: an expert statement. J Am Coll Cardiol 2016;68:2002–15. https://doi.org/10.1016/j.jacc.2016.04.071 556. Misra S, Shishehbor MH, Takahashi EA, Aronow HD, Brewster LP, Bunte MC, et al. Perfusion assessment in critical limb ischemia: principles for understanding and the development of evidence and evaluation of devices: a scientific statement from the American Heart Association. Circulation 2019;140:e657–72. https://doi.org/10.1161/ cir.0000000000000708 557. Sukul D, Grey SF, Henke PK, Gurm HS, Grossman PM. Heterogeneity of ankle-brachial indices in patients undergoing revascularization for critical limb ischemia. JACC Cardiovasc Interv 2017;10:2307–16. https://doi.org/10.1016/j.jcin.2017.08.026 558. Shishehbor MH, Hammad TA, Zeller T, Baumgartner I, Scheinert D, Rocha-Singh KJ. An analysis of IN.PACT DEEP randomized trial on the limitations of the societal guidelines–recommended hemodynamic parameters to diagnose critical limb ischemia. J Vasc Surg 2016;63:1311–7. https://doi.org/10.1016/j.jvs.2015.11.042 559. Randhawa MS, Reed GW, Grafmiller K, Gornik HL, Shishehbor MH. Prevalence of tibial artery and pedal arch patency by angiography in patients with critical limb ischemia and noncompressible ankle brachial index. Circ Cardiovasc Interv 2017;10:e004605. https://doi.org/10.1161/CIRCINTERVENTIONS.116.004605 560. Mustapha JA, Saab FA, Martinsen BJ, Pena CS, Zeller T, Driver VR, et al. Digital subtraction angiography prior to an amputation for critical limb ischemia (CLI): an expert recommendation statement from the CLI global society to optimize limb salvage. J Endovasc Ther 2020;27:540–6. https://doi.org/10.1177/1526602820928590 561. Menke J, Larsen J. Meta-analysis: accuracy of contrast-enhanced magnetic resonance angiography for assessing steno-occlusions in peripheral arterial disease. Ann Intern Med 2010;153:325–34. https://doi.org/10.7326/0003-4819-153-5-201009070-00007 562. Reinecke H, Unrath M, Freisinger E, Bunzemeier H, Meyborg M, Luders F, et al. Peripheral arterial disease and critical limb ischaemia: still poor outcomes and lack of guideline adherence. Eur Heart J 2015;36:932–8. https://doi.org/10.1093/ eurheartj/ehv006 563. Hess CN, Wang TY, Weleski Fu J, Gundrum J, Allen LaPointe NM, Rogers RK, et al. Long-term outcomes and associations with major adverse limb events after peripheral artery revascularization. J Am Coll Cardiol 2020;75:498–508. https://doi.org/10.1016/j. jacc.2019.11.050 564. Bradbury AW, Adam DJ, Bell J, Forbes JF, Fowkes FGR, Gillespie I, et al. Bypass versus angioplasty in severe ischaemia of the leg (BASIL) trial: a survival prediction model to facilitate clinical decision making. J Vasc Surg 2010;51:52s–68s. https://doi.org/10.1016/j. jvs.2010.01.077 565. Meltzer AJ, Graham A, Connolly PH, Meltzer EC, Karwowski JK, Bush HL, et al. The comprehensive risk assessment for bypass (CRAB) facilitates efficient perioperative risk assessment for patients with critical limb ischemia. J Vasc Surg 2013;57:1186–95. https://doi.org/10.1016/j.jvs.2012.09.083 566. van Netten JJ, Fortington LV, Hinchliffe RJ, Hijmans JM. Early post-operative mortality after major lower limb amputation: a systematic review of population and regional based studies. Eur J Vasc Endovasc Surg 2016;51:248–57. https://doi.org/10.1016/j. ejvs.2015.10.001 567. Farber A, Menard MT, Conte MS, Kaufman JA, Powell RJ, Choudhry NK, et al. Surgery or endovascular therapy for chronic limb-threatening ischemia. N Engl J Med 2022; 387:2305–16. https://doi.org/10.1056/NEJMoa2207899 568. Meza-Torres B, Carinci F, Heiss C, Joy M, de Lusignan S. Health service organisation impact on lower extremity amputations in people with type 2 diabetes with foot ulcers: systematic review and meta-analysis. Acta Diabetol 2021;58:735–47. https://doi. org/10.1007/s00592-020-01662-x 569. Peters EJ, Lipsky BA, Berendt AR, Embil JM, Lavery LA, Senneville E, et al. A systematic review of the effectiveness of interventions in the management of infection in the diabetic foot. Diabetes Metab Res Rev 2012;28:142–62. https://doi.org/10.1002/dmrr. 2247 570. Peters EJG, Lipsky BA, Senneville É, Abbas ZG, Aragón-Sánchez J, Diggle M, et al. Interventions in the management of infection in the foot in diabetes: a systematic review. Diabetes Metab Res Rev 2020;36:e3282. https://doi.org/10.1002/dmrr.3282 571. Dumville JC, Lipsky BA, Hoey C, Cruciani M, Fiscon M, Xia J. Topical antimicrobial agents for treating foot ulcers in people with diabetes. Cochrane Database Syst Rev 2017;6:CD011038. https://doi.org/10.1002/14651858.CD011038.pub2 572. Luo Y, Li L, Zhao P, Yang C, Zhang J. Effectiveness of silver dressings in the treatment of diabetic foot ulcers: a systematic review and meta-analysis. J Wound Care 2022;31: 979–86. https://doi.org/10.12968/jowc.2022.31.11.979 573. Shu H, Xia Z, Qin X, Wang X, Lu W, Luo Q, et al. The clinical efficacy of collagen dressing on chronic wounds: a meta-analysis of 11 randomized controlled trials. Front Surg 2022;9:978407. https://doi.org/10.3389/fsurg.2022.978407 574. Zhang F, Chen Z, Su F, Zhang T. Comparison of topical honey and povidone iodinebased dressings for wound healing: a systematic review and meta-analysis. J Wound Care 2021;30:S28–s36. https://doi.org/10.12968/jowc.2021.30.Sup4.S28 575. Yin XL, Hu L, Li T, Zou Y, Li HL. A meta-analysis on the efficacy of vacuum sealing drainage combined with autologous platelet-rich plasma in the treatment of grade 2 and grade 3 diabetic foot ulcers. Int Wound J 2022;20:1033–41. https://doi.org/10. 1111/iwj.13956 576. Lim K, Lim X, Hong Q, Yong E, Chandrasekar S, Tan GWL, et al. Use of home negative pressure wound therapy in peripheral artery disease and diabetic limb salvage. Int Wound J 2020;17:531–9. https://doi.org/10.1111/iwj.13307 577. Uddin A, Russell D, Game F, Santos D, Siddle HJ. The effectiveness of systemic antibiotics for osteomyelitis of the foot in adults with diabetes mellitus: a systematic review protocol. J Foot Ankle Res 2022;15:48. https://doi.org/10.1186/s13047-022-00554-3 578. O’Meara S, Nelson EA, Golder S, Dalton JE, Craig D, Iglesias C. Systematic review of methods to diagnose infection in foot ulcers in diabetes. Diabet Med 2006;23:341–7. https://doi.org/10.1111/j.1464-5491.2006.01830.x 579. Nelson A, Wright-Hughes A, Backhouse MR, Lipsky BA, Nixon J, Bhogal MS, et al. CODIFI (concordance in diabetic foot ulcer infection): a cross-sectional study of wound swab versus tissue sampling in infected diabetic foot ulcers in England. BMJ Open 2018;8:e019437. https://doi.org/10.1136/bmjopen-2017-019437 580. Gardner SE, Frantz RA. Wound bioburden and infection-related complications in diabetic foot ulcers. Biol Res Nurs 2008;10:44–53. https://doi.org/10.1177/ 1099800408319056 581. Selva Olid A, Solà I, Barajas-Nava LA, Gianneo OD, Bonfill Cosp X, Lipsky BA. Systemic antibiotics for treating diabetic foot infections. Cochrane Database Syst Rev 2015;9: CD009061. https://doi.org/10.1002/14651858.CD009061.pub2 582. Patton D, Avsar P, Sayeh A, Budri A, O’Connor T, Walsh S, et al. A meta-review of the impact of compression therapy on venous leg ulcer healing. Int Wound J 2023;20: 430–47. https://doi.org/10.1111/iwj.13891 583. Lazzarini PA, Armstrong DG, Crews RT, Gooday C, Jarl G, Kirketerp-Moller K, et al. Effectiveness of offloading interventions for people with diabetes-related foot ulcers: a systematic review and meta-analysis. Diabetes Metab Res Rev 2024;40:e3650. https:// doi.org/10.1002/dmrr.3650 584. Elraiyah T, Prutsky G, Domecq JP, Tsapas A, Nabhan M, Frykberg RG, et al. A systematic review and meta-analysis of off-loading methods for diabetic foot ulcers. J Vasc Surg 2016;63:59S–68S.e2. https://doi.org/10.1016/j.jvs.2015.10.006 585. Lumsden AB, Davies MG, Peden EK. Medical and endovascular management of critical limb ischemia. J Endovasc Ther 2009;16:Ii31–62. https://doi.org/10.1583/08-2657.1 586. Manzi M, Palena L, Cester G. Endovascular techniques for limb salvage in diabetics with crural and pedal disease. J Cardiovasc Surg 2011;52:485–92. 587. Dominguez A, III, Bahadorani J, Reeves R, Mahmud E, Patel M. Endovascular therapy for critical limb ischemia. Expert Rev Cardiovasc Ther 2015;13:429–44. https://doi.org/10. 1586/14779072.2015.1019472 588. Abu Dabrh AM, Steffen MW, Undavalli C, Asi N, Wang Z, Elamin MB, et al. The natural history of untreated severe or critical limb ischemia. J Vasc Surg 2015;62:1642–51.e3. https://doi.org/10.1016/j.jvs.2015.07.065 589. Adam DJ, Beard JD, Cleveland T, Bell J, Bradbury AW, Forbes JF, et al. Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised controlled trial. Lancet 2005;366:1925–34. https://doi.org/10.1016/s0140-6736(05)67704-5 590. Bradbury AW, Moakes CA, Popplewell M, Meecham L, Bate GR, Kelly L, et al. A vein bypass first versus a best endovascular treatment first revascularisation strategy for patients with chronic limb threatening ischaemia who required an infra-popliteal, with or without an additional more proximal infra-inguinal revascularisation procedure to restore limb perfusion (BASIL-2): an open-label, randomised, multicentre, phase 3 trial. Lancet 2023;401:1798–809. https://doi.org/10.1016/S0140-6736(23)00462-2 591. Popplewell MA, Davies H, Jarrett H, Bate G, Grant M, Patel S, et al. Bypass versus angio plasty in severe ischaemia of the leg—2 (BASIL-2) trial: study protocol for a randomised controlled trial. Trials 2016;17:11. https://doi.org/10.1186/s13063-015-1114-2 592. Patel K, Liu Y, Etaee F, Patel C, Monteleone P, Patel M, et al. Differences between patients with intermittent claudication and critical limb ischemia undergoing endovascular intervention: insights from the excellence in peripheral artery disease registry. Circ Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.140
Cardiovasc Interv 2021;14:e010635. https://doi.org/10.1161/CIRCINTERVENTIONS. 121.010635 593. Almasri J, Adusumalli J, Asi N, Lakis S, Alsawas M, Prokop LJ, et al. A systematic review and meta-analysis of revascularization outcomes of infrainguinal chronic limbthreatening ischemia. Eur J Vasc Endovasc Surg 2019;58:S110–s119. https://doi.org/10. 1016/j.ejvs.2019.04.013 594. Söder HK, Manninen HI, Jaakkola P, Matsi PJ, Räsänen HT, Kaukanen E, et al. Prospective trial of infrapopliteal artery balloon angioplasty for critical limb ischemia: angiographic and clinical results. J Vasc Interv Radiol 2000;11:1021–31. https://doi.org/ 10.1016/s1051-0443(07)61332-3 595. Balmer H, Mahler F, Do DD, Triller J, Baumgartner I. Balloon angioplasty in chronic critical limb ischemia: factors affecting clinical and angiographic outcome. J Endovasc Ther 2002;9:403–10. https://doi.org/10.1177/152660280200900403 596. Kudo T, Chandra FA, Kwun WH, Haas BT, Ahn SS. Changing pattern of surgical revascularization for critical limb ischemia over 12 years: endovascular vs. open bypass surgery. J Vasc Surg 2006;44:304–13. https://doi.org/10.1016/j.jvs.2006.03.040 597. Kim KG, Meshkin DH, Tirrell AR, Bekeny JC, Tefera EA, Fan KL, et al. A systematic review and meta-analysis of endovascular angiosomal revascularization in the setting of collateral vessels. J Vasc Surg 2021;74:1406–16.e3. https://doi.org/10.1016/j.jvs.2021. 04.026 598. Shishehbor MH, Powell RJ, Montero-Baker MF, Dua A, Martínez-Trabal JL, Bunte MC, et al. Transcatheter arterialization of deep veins in chronic limb-threatening ischemia. N Engl J Med 2023;388:1171–80. https://doi.org/10.1056/NEJMoa2212754 599. Salem M, Hosny MS, Francia F, Sallam M, Saratzis A, Saha P, et al. Management of extensive aorto-iliac disease: a systematic review and meta-analysis of 9319 patients. Cardiovasc Intervent Radiol 2021;44:1518–35. https://doi.org/10.1007/s00270-021- 02785-6 600. Bekken JA, Vroegindeweij D, Vos JA, de Vries J-PPM, Lardenoije JWHP, Petri B-J, et al. Editor’s choice—two year results of the randomised DISCOVER trial comparing covered versus bare metal stents in the common iliac artery. Eur J Vasc Endovasc Surg 2023; 65:359–68. https://doi.org/10.1016/j.ejvs.2022.11.008 601. Jongkind V, Akkersdijk GJ, Yeung KK, Wisselink W. A systematic review of endovascular treatment of extensive aortoiliac occlusive disease. J Vasc Surg 2010;52:1376–83. https://doi.org/10.1016/j.jvs.2010.04.080 602. Ye W, Liu CW, Ricco JB, Mani K, Zeng R, Jiang J. Early and late outcomes of percutaneous treatment of TransAtlantic inter-society consensus class C and D aorto-iliac lesions. J Vasc Surg 2011;53:1728–37. https://doi.org/10.1016/j.jvs.2011.02.005 603. Bosiers M, Deloose K, Callaert J, Maene L, Beelen R, Keirse K, et al. BRAVISSIMO: 12-month results from a large scale prospective trial. J Cardiovasc Surg 2013;54: 235–53. 604. Danczyk RC, Mitchell EL, Petersen BD, Edwards J, Liem TK, Landry GJ, et al. Outcomes of open operation for aortoiliac occlusive disease after failed endovascular therapy. Arch Surg 2012;147:841–5. https://doi.org/10.1001/archsurg.2012.1649 605. Fereydooni A, Zhou B, Xu Y, Deng Y, Dardik A, Ochoa Chaar CI. Rapid increase in hybrid surgery for the treatment of peripheral artery disease in the vascular quality initiative database. J Vasc Surg 2020;72:977–86.e1. https://doi.org/10.1016/j.jvs.2019.11. 041 606. Zeller T, Baumgartner I, Scheinert D, Brodmann M, Bosiers M, Micari A, et al. Drug-eluting balloon versus standard balloon angioplasty for infrapopliteal arterial revascularization in critical limb ischemia: 12-month results from the IN.PACT DEEP randomized trial. J Am Coll Cardiol 2014;64:1568–76. https://doi.org/10.1016/j.jacc. 2014.06.1198 607. Zeller T, Micari A, Scheinert D, Baumgartner I, Bosiers M, Vermassen FEG, et al. The IN.PACT DEEP clinical drug-coated balloon trial: 5-year outcomes. JACC Cardiovasc Interv 2020;13:431–43. https://doi.org/10.1016/j.jcin.2019.10.059 608. Brizzi V, Caradu C, Berard X, Sassoust G, Midy D, Ducasse E. Six-year multicenter experience of standard endovascular treatment of critical limb ischemia in the era of drug-eluting devices. J Cardiovasc Surg 2018;59:707–15. https://doi.org/10.23736/ S0021-9509.16.09737-8 609. Jude EB, Oyibo SO, Chalmers N, Boulton AJ. Peripheral arterial disease in diabetic and nondiabetic patients: a comparison of severity and outcome. Diabetes Care 2001;24: 1433–7. https://doi.org/10.2337/diacare.24.8.1433 610. Ozkan U, Oguzkurt L, Tercan F. Atherosclerotic risk factors and segmental distribution in symptomatic peripheral artery disease. J Vasc Interv Radiol 2009;20:437–41. https://doi.org/10.1016/j.jvir.2009.01.010 611. Todd KE, Jr, Ahanchi SS, Maurer CA, Kim JH, Chipman CR, Panneton JM. Atherectomy offers no benefits over balloon angioplasty in tibial interventions for critical limb ischemia. J Vasc Surg 2013;58:941–8. https://doi.org/10.1016/j.jvs.2013.04.024 612. Teichgraber U, Lehmann T, Thieme M, Wahl K-U, Stelzner C, Bormann A, et al. Drug-coated balloon angioplasty of infrapopliteal lesions in patients with critical limb ischaemia: 1-year results of the APOLLO trial. Cardiovasc Intervent Radiol 2019;42: 1380–90. https://doi.org/10.1007/s00270-019-02279-6 613. Yang X, Lu X, Ye K, Li X, Qin J, Jiang M. Systematic review and meta-analysis of balloon angioplasty versus primary stenting in the infrapopliteal disease. Vasc Endovascular Surg 2014;48:18–26. https://doi.org/10.1177/1538574413510626 614. Zhang J, Xu X, Kong J, Xu R, Fan X, Chen J, et al. Systematic review and meta-analysis of drug-eluting balloon and stent for infrapopliteal artery revascularization. Vasc Endovascular Surg 2017;51:72–83. https://doi.org/10.1177/1538574416689426 615. Matsuoka EK, Hasebe T, Ishii R, Miyazaki N, Soejima K, Iwasaki K. Comparative performance analysis of interventional devices for the treatment of ischemic disease in below-the-knee lesions: a systematic review and meta-analysis. Cardiovasc Interv Ther 2022;37:145–57. https://doi.org/10.1007/s12928-021-00758-7 616. Fong KY, Xin L, Ng J, Loh SEK, Ng JJ, Choong AMTL. A systematic review and meta-analysis of sirolimus-eluting stents for treatment of below-the-knee arterial disease. J Vasc Surg 2023;77:1264–73.e3. https://doi.org/10.1016/j.jvs.2022.09.022 617. Ubbink DT, Vermeulen H. Spinal cord stimulation for non-reconstructable chronic critical leg ischaemia. Cochrane Database Syst Rev 2013;2:CD004001. https://doi.org/ 10.1002/14651858.CD004001.pub3 618. Asimakidou E, Matis GK. Spinal cord stimulation in the treatment of peripheral vascular disease: a systematic review—revival of a promising therapeutic option? Br J Neurosurg 2022;36:555–63. https://doi.org/10.1080/02688697.2021.1884189 619. Nicoloff AD, Taylor LM, Jr, Sexton GJ, Schuff RA, Edwards JM, Yeager RA, et al. Relationship between site of initial symptoms and subsequent progression of disease in a prospective study of atherosclerosis progression in patients receiving long-term treatment for symptomatic peripheral arterial disease. J Vasc Surg 2002;35:38–46; discussion 46–37. 620. Bhatt DL, Steg PG, Ohman EM, Hirsch AT, Ikeda Y, Mas JL, et al. International prevalence, recognition, and treatment of cardiovascular risk factors in outpatients with atherothrombosis. JAMA 2006;295:180–9. https://doi.org/10.1001/jama.295.2.180 621. Wilson YG, Davies AH, Currie IC, Morgan M, McGrath C, Baird RN, et al. Vein graft stenosis: incidence and intervention. Eur J Vasc Endovasc Surg 1996;11:164–9. https:// doi.org/10.1016/s1078-5884(96)80046-3 622. Armstrong PA, Bandyk DF, Wilson JS, Shames ML, Johnson BL, Back MR. Optimizing infrainguinal arm vein bypass patency with duplex ultrasound surveillance and endovascular therapy. J Vasc Surg 2004;40:724–31; discussion 730–721. https://doi.org/10. 1016/j.jvs.2004.07.037 623. Pulli R, Dorigo W, Fargion A, Innocenti AA, Pratesi G, Marek J, et al. Early and longterm comparison of endovascular treatment of iliac artery occlusions and stenosis. J Vasc Surg 2011;53:92–8. https://doi.org/10.1016/j.jvs.2010.08.034 624. Lo RC, Darling J, Bensley RP, Giles KA, Dahlberg SE, Hamdan AD, et al. Outcomes following infrapopliteal angioplasty for critical limb ischemia. J Vasc Surg 2013;57: 1455–64; discussion 1463–1454. https://doi.org/10.1016/j.jvs.2012.10.109 625. Rodway AD, Hanna L, Harris J, Jarrett R, Allan C, Pazos Casal F, et al. Prognostic and predictive value of ultrasound-based estimated ankle brachial pressure index at early follow-up after endovascular revascularization of chronic limb-threatening ischaemia: a prospective, single-centre, service evaluation. EClinicalMedicine 2024;68:102410. https://doi.org/10.1016/j.eclinm.2023.102410 626. Poursina O, Elizondo-Adamchik H, Montero-Baker M, Pallister ZS, Mills JL, Chung J. Safety and efficacy of an endovascular-first approach to acute limb ischemia. J Vasc Surg 2021;73:1741–9. https://doi.org/10.1016/j.jvs.2020.10.002 627. Hawkins KE, Valentine RJ, Duke JM, Wang Q, Reed AB. Ankle-brachial index use in peripheral vascular interventions for claudication. J Vasc Surg 2022;76:196–201. https://doi.org/10.1016/j.jvs.2022.02.049 628. Armstrong EJ, Chen DC, Westin GG, Singh S, McCoach CE, Bang H, et al. Adherence to guideline-recommended therapy is associated with decreased major adverse cardiovascular events and major adverse limb events among patients with peripheral arterial disease. J Am Heart Assoc 2014;3:e000697. https://doi.org/10.1161/jaha.113. 000697 629. Araujo ST, Moreno DH, Cacione DG. Percutaneous thrombectomy or ultrasound-accelerated thrombolysis for initial management of acute limb ischaemia. Cochrane Database Syst Rev 2022;1:CD013486. https://doi.org/10.1002/14651858. CD013486.pub2 630. Kokkinidis DG, Arfaras-Melainis A, Giannopoulos S, Katsaros I, Jawaid O, Jonnalagadda AK, et al. Statin therapy for reduction of cardiovascular and limb-related events in critical limb ischemia: a systematic review and meta-analysis. Vasc Med 2020;25:106–17. https://doi.org/10.1177/1358863x19894055 631. Londero LS, Nørgaard B, Houlind K. Patient delay is the main cause of treatment delay in acute limb ischemia: an investigation of pre- and in-hospital time delay. World J Emerg Surg 2014;9:56. https://doi.org/10.1186/1749-7922-9-56 632. Duval S, Keo HH, Oldenburg NC, Baumgartner I, Jaff MR, Peacock JM, et al. The impact of prolonged lower limb ischemia on amputation, mortality, and functional status: the FRIENDS registry. Am Heart J 2014;168:577–87. https://doi.org/10.1016/j.ahj.2014.06. 013 633. Kulezic A, Macek M, Acosta S. Inadequacies of physical examination in patients with acute lower limb ischemia are associated with dreadful consequences. Ann Vasc Surg 2022;82:190–6. https://doi.org/10.1016/j.avsg.2021.10.067 634. Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review. Cardiovasc Surg 2002;10:620–30. https://doi.org/10.1016/s0967- 2109(02)00070-4
ESC Guidelines 3677
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.141
635. Jivegård L, Bergqvist D, Holm J. When is urgent revascularization unnecessary for acute lower limb ischaemia? Eur J Vasc Endovasc Surg 1995;9:448–53. https://doi.org/10.1016/ s1078-5884(05)80014-0 636. Crawford JD, Perrone KH, Jung E, Mitchell EL, Landry GJ, Moneta GL, et al. Arterial duplex for diagnosis of peripheral arterial emboli. J Vasc Surg 2016;64:1351–6. https://doi.org/10.1016/j.jvs.2016.04.005 637. Hemingway J, Emanuels D, Aarabi S, Quiroga E, Tran N, Starnes B, et al. Safety of transfer, type of procedure, and factors predictive of limb salvage in a modern series of acute limb ischemia. J Vasc Surg 2019;69:1174–9. https://doi.org/10.1016/j.jvs.2018. 08.174 638. Currie IS, Wakelin SJ, Lee AJ, Chalmers RT. Plasma creatine kinase indicates major amputation or limb preservation in acute lower limb ischemia. J Vasc Surg 2007;45:733–9. https://doi.org/10.1016/j.jvs.2006.12.050 639. Brow TD, Kakkar VV, Das SK. The significance of creatine kinase in cardiac patients with acute limb ischaemia. J Cardiovasc Surg 1999;40:637–44. 640. Adiseshiah M, Round JM, Jones DA. Reperfusion injury in skeletal muscle: a prospective study in patients with acute limb ischaemia and claudicants treated by revascularization. Br J Surg 2005;79:1026–9. https://doi.org/10.1002/bjs.1800791013 641. Rutherford RB, Baker JD, Ernst C, Johnston KW, Porter JM, Ahn S, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vasc Surg 1997;26:517–38. https://doi.org/10.1016/s0741-5214(97)70045-4 642. Ontario Health. Mechanical thrombectomy for acute and subacute blocked arteries and veins in the lower limbs: a health technology assessment. Ont Health Technol Assess Ser 2023;23:1–244. 643. Gong M, He X, Zhao B, Kong J, Gu J, Chen G, et al. Endovascular revascularization strategies using catheter-based thrombectomy versus conventional catheter-directed thrombolysis for acute limb ischemia. Thromb J 2021;19:96. https://doi.org/10.1186/ s12959-021-00349-9 644. Doelare SAN, Koedam TWA, Ebben HP, Tournoij E, Hoksbergen AWJ, Yeung KK, et al. Catheter directed thrombolysis for not immediately threatening acute limb ischaemia: systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2023;65: 537–45. https://doi.org/10.1016/j.ejvs.2022.12.030 645. Veenstra EB, van der Laan MJ, Zeebregts CJ, de Heide E-J, Kater M, Bokkers RPH. A systematic review and meta-analysis of endovascular and surgical revascularization techniques in acute limb ischemia. J Vasc Surg 2020;71:654–68.e3. https://doi.org/10. 1016/j.jvs.2019.05.031 646. Kolte D, Kennedy KF, Shishehbor MH, Mamdani ST, Stangenberg L, Hyder ON, et al. Endovascular versus surgical revascularization for acute limb ischemia: a propensityscore matched analysis. Circ Cardiovasc Interv 2020;13:e008150. https://doi.org/10. 1161/CIRCINTERVENTIONS.119.008150 647. Grip O, Wanhainen A, Michaelsson K, Lindhagen L, Bjorck M. Open or endovascular revascularization in the treatment of acute lower limb ischaemia. Br J Surg 2018;105: 1598–606. https://doi.org/10.1002/bjs.10954 648. Darwood R, Berridge DC, Kessel DO, Robertson I, Forster R. Surgery versus thrombolysis for initial management of acute limb ischaemia. Cochrane Database Syst Rev 2018; 8:CD002784. https://doi.org/10.1002/14651858.CD002784.pub3 649. Schrijver AM, van Leersum M, Fioole B, Reijnen MMPJ, Hoksbergen AWJ, Vahl AC, et al. Dutch randomized trial comparing standard catheter-directed thrombolysis and ultrasound-accelerated thrombolysis for arterial thromboembolic infrainguinal disease (DUET). J Endovasc Ther 2015;22:87–95. https://doi.org/10.1177/ 1526602814566578 650. Juneja A, Garuthara M, Talathi S, Rao A, Landis G, Etkin Y. Predictors of poor outcomes after lower extremity revascularization for acute limb ischemia. Vascular 2024;32:632–9. https://doi.org/10.1177/17085381231154290 651. Ouriel K, Veith FJ. Acute lower limb ischemia: determinants of outcome. Surgery 1998; 124:336–41; discussion 341–332. https://doi.org/10.1016/S0039-6060(98)70139-4 652. Sobel M, Verhaeghe R. Antithrombotic therapy for peripheral artery occlusive disease: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest 2008;133:815s–43s. https://doi.org/10.1378/chest.08-0686 653. Hess CN, Debus ES, Nehler MR, Anand SS, Patel MR, Szarek M, et al. Reduction in acute limb ischemia with rivaroxaban versus placebo in peripheral artery disease after lower extremity revascularization: insights from VOYAGER PAD. Circulation 2021; 144:1831–41. https://doi.org/10.1161/circulationaha.121.055146 654. Jivegård L, Holm J, Bergqvist D, Björck CG, Björkman H, Brunius U, et al. Acute lower limb ischemia: failure of anticoagulant treatment to improve one-month results of arterial thromboembolectomy. A prospective randomized multi-center study. Surgery 1991;109:610–6. 655. Jivegård L, Holm J, Scherstén T. Arterial thromboembolectomy—should anticoagulants be administered? Acta Chir Scand 1986;152:493–7. 656. Campbell WB, Ridler BM, Szymanska TH. Two-year follow-up after acute thromboembolic limb ischaemia: the importance of anticoagulation. Eur J Vasc Endovasc Surg 2000;19:169–73. https://doi.org/10.1053/ejvs.1999.0999 657. Benjamin EJ, Virani SS, Callaway CW, Chamberlain AM, Chang AR, Cheng S, et al. Heart disease and stroke statistics–2018 update: a report from the American Heart Association. Circulation 2018;137:e67–492. https://doi.org/10.1161/cir. 0000000000000558 658. Touboul PJ, Hennerici MG, Meairs S, Adams H, Amarenco P, Bornstein N, et al. Mannheim carotid intima-media thickness and plaque consensus (2004–2006–2011). An update on behalf of the advisory board of the 3rd, 4th and 5th watching the risk symposia, at the 13th, 15th and 20th European Stroke Conferences, Mannheim, Germany, 2004, Brussels, Belgium, 2006, and Hamburg, Germany, 2011. Cerebrovasc Dis 2012;34:290–6. https://doi.org/10.1159/000343145 659. Johri AM, Nambi V, Naqvi TZ, Feinstein SB, Kim ESH, Park MM, et al. Recommendations for the assessment of carotid arterial plaque by ultrasound for the characterization of atherosclerosis and evaluation of cardiovascular risk: from the American Society of Echocardiography. J Am Soc Echocardiogr 2020;33:917–33. https://doi.org/10.1016/j.echo.2020.04.021 660. Barnett HJM, Taylor DW, Haynes RB, Sackett DL, Peerless SJ, Ferguson GG, et al. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325:445–53. https://doi.org/10.1056/ nejm199108153250701 661. Gornik HL, Rundek T, Gardener H, Benenati JF, Dahiya N, Hamburg NM, et al. Optimization of duplex velocity criteria for diagnosis of internal carotid artery (ICA) stenosis: a report of the Intersocietal Accreditation Commission (IAC) Vascular Testing Division Carotid Diagnostic Criteria Committee. Vasc Med 2021;26:515–25. https://doi.org/10.1177/1358863X211011253 662. Grant EG, Benson CB, Moneta GL, Alexandrov AV, Baker JD, Bluth EI, et al. Carotid artery stenosis: grayscale and Doppler ultrasound diagnosis—Society of Radiologists in ultrasound consensus conference. Ultrasound Q 2003;19:190–8. https://doi.org/10. 1097/00013644-200312000-00005 663. Rustempasic N, Gengo M. Assesment of carotid stenosis with CT angiography and color Doppler ultrasonography. Med Arch 2019;73:321–5. https://doi.org/10.5455/ medarh.2019.73.321-325 664. Clezar CN, Flumignan CD, Cassola N, Nakano LCU, Trevisani VFM, Flumignan RLG. Pharmacological interventions for asymptomatic carotid stenosis. Cochrane Database Syst Rev 2023;8:CD013573. https://doi.org/10.1002/14651858.CD013573.pub2 665. Côté R, Battista RN, Abrahamowicz M, Langlois Y, Bourque F, Mackey A. Lack of effect of aspirin in asymptomatic patients with carotid bruits and substantial carotid narrowing. The asymptomatic cervical bruit study group. Ann Intern Med 1995;123:649–55. https://doi.org/10.7326/0003-4819-123-9-199511010-00002 666. Aboyans V, Bauersachs R, Mazzolai L, Brodmann M, Palomares JFR, Debus S, et al. Antithrombotic therapies in aortic and peripheral arterial diseases in 2021: a consensus document from the ESC working group on aorta and peripheral vascular diseases, the ESC working group on thrombosis, and the ESC working group on cardiovascular pharmacotherapy. Eur Heart J 2021;42:4013–24. https://doi.org/10.1093/eurheartj/ ehab390 667. Johnston SC, Easton JD, Farrant M, Barsan W, Conwit RA, Elm JJ, et al. Clopidogrel and aspirin in acute ischemic stroke and high-risk TIA. N Engl J Med 2018;379:215–25. https://doi.org/10.1056/NEJMoa1800410 668. Wang Y, Wang Y, Zhao X, Liu L, Wang D, Wang C, et al. Clopidogrel with aspirin in acute minor stroke or transient ischemic attack. N Engl J Med 2013;369:11–9. https:// doi.org/10.1056/NEJMoa1215340 669. Kennedy J, Hill MD, Ryckborst KJ, Eliasziw M, Demchuk AM, Buchan AM. Fast assessment of stroke and transient ischaemic attack to prevent early recurrence (FASTER): a randomised controlled pilot trial. Lancet Neurol 2007;6:961–9. https://doi.org/10.1016/ S1474-4422(07)70250-8 670. Murphy SJX, Naylor AR, Ricco JB, Sillesen H, Kakkos S, Halliday A, et al. Optimal antiplatelet therapy in moderate to severe asymptomatic and symptomatic carotid stenosis: a comprehensive review of the literature. Eur J Vasc Endovasc Surg 2019;57: 199–211. https://doi.org/10.1016/j.ejvs.2018.09.018 671. King A, Shipley M, Markus H, Investigators A. The effect of medical treatments on stroke risk in asymptomatic carotid stenosis. Stroke 2013;44:542–6. https://doi.org/ 10.1161/STROKEAHA.112.673608 672. Endarterectomy for asymptomatic carotid artery stenosis. Executive committee for the asymptomatic carotid atherosclerosis study. JAMA 1995;273:1421–8. 673. Halliday A, Mansfield A, Marro J, Peto C, Peto R, Potter J, et al. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet 2004;363:1491–502. https://doi.org/10.1016/s0140-6736(04)16146-1 674. Halliday A, Harrison M, Hayter E, Kong X, Mansfield A, Marro J, et al. 10-year stroke prevention after successful carotid endarterectomy for asymptomatic stenosis (ACST-1): a multicentre randomised trial. Lancet 2010;376:1074–84. https://doi.org/ 10.1016/s0140-6736(10)61197-x 675. Rothwell PM, Goldstein LB. Carotid endarterectomy for asymptomatic carotid stenosis: asymptomatic carotid surgery trial. Stroke 2004;35:2425–7. https://doi.org/10. 1161/01.STR.0000141706.50170.a7 676. Hadar N, Raman G, Moorthy D, O’Donnell TF, Thaler DE, Feldmann E, et al. Asymptomatic carotid artery stenosis treated with medical therapy alone: temporal trends and implications for risk assessment and the design of future studies. Cerebrovasc Dis 2014;38:163–73. https://doi.org/10.1159/000365206 677. Reiff T, Eckstein HH, Mansmann U, Jansen O, Fraedrich G, Mudra H, et al. Angioplasty in asymptomatic carotid artery stenosis vs. endarterectomy compared to best medical Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.142
treatment: one-year interim results of SPACE-2. Int J Stroke 2020;15:638–49. https:// doi.org/10.1177/1747493019833017 678. Naylor AR, Schroeder TV, Sillesen H. Clinical and imaging features associated with an increased risk of late stroke in patients with asymptomatic carotid disease. Eur J Vasc Endovasc Surg 2014;48:633–40. https://doi.org/10.1016/j.ejvs.2014.08.017 679. Paraskevas KI, Brown MM, Lal BK, Myrcha P, Lyden SP, Schneider PA, et al. Recent advances and controversial issues in the optimal management of asymptomatic carotid stenosis. J Vasc Surg 2024;79:695–703. https://doi.org/10.1016/j.jvs.2023.11.004 680. Naylor R, Rantner B, Ancetti S, de Borst GJ, De Carlo M, Halliday A, et al. Editor’s choice—European Society for Vascular Surgery (ESVS) 2023 clinical practice guidelines on the management of atherosclerotic carotid and vertebral artery disease. Eur J Vasc Endovasc Surg 2023;65:7–111. https://doi.org/10.1016/j.ejvs.2022.04.011 681. Kashyap VS, Schneider PA, Foteh M, Motaganahalli R, Shah R, Eckstein H-H, et al. Early outcomes in the ROADSTER 2 study of transcarotid artery revascularization in patients with significant carotid artery disease. Stroke 2020;51:2620–9. https://doi.org/ 10.1161/strokeaha.120.030550 682. Nicolaides AN, Kakkos SK, Griffin M, Sabetai M, Dhanjil S, Tegos T, et al. Severity of asymptomatic carotid stenosis and risk of ipsilateral hemispheric ischaemic events: results from the ACSRS study. Eur J Vasc Endovasc Surg 2005;30:275–84. https://doi.org/ 10.1016/j.ejvs.2005.04.031 683. Lovett JK, Coull AJ, Rothwell PM. Early risk of recurrence by subtype of ischemic stroke in population-based incidence studies. Neurology 2004;62:569–73. https://doi. org/10.1212/01.wnl.0000110311.09970.83 684. Kakkos SK, Sabetai M, Tegos T, Stevens J, Thomas D, Griffin M, et al. Silent embolic infarcts on computed tomography brain scans and risk of ipsilateral hemispheric events in patients with asymptomatic internal carotid artery stenosis. J Vasc Surg 2009;49: 902–9. https://doi.org/10.1016/j.jvs.2008.10.059 685. Kakkos SK, Nicolaides AN, Charalambous I, Thomas D, Giannopoulos A, Naylor AR, et al. Predictors and clinical significance of progression or regression of asymptomatic carotid stenosis. J Vasc Surg 2014;59:956–67.e1. https://doi.org/10.1016/j.jvs.2013.10. 073 686. Markus HS, King A, Shipley M, Topakian R, Cullinane M, Reihill S, et al. Asymptomatic embolisation for prediction of stroke in the Asymptomatic Carotid Emboli Study (ACES): a prospective observational study. Lancet Neurol 2010;9:663–71. https://doi. org/10.1016/s1474-4422(10)70120-4 687. Fields WS, Lemak NA, Frankowski RF, Hardy RJ. Controlled trial of aspirin in cerebral ischemia. Stroke 1977;8:301–14. https://doi.org/10.1161/01.str.8.3.301 688. King A, Serena J, Bornstein NM, Markus HS. Does impaired cerebrovascular reactivity predict stroke risk in asymptomatic carotid stenosis? A prospective substudy of the asymptomatic carotid emboli study. Stroke 2011;42:1550–5. https://doi.org/10.1161/ strokeaha.110.609057 689. Amarenco P, Albers GW, Denison H, Easton JD, Evans SR, Held P, et al. Efficacy and safety of ticagrelor versus aspirin in acute stroke or transient ischaemic attack of atherosclerotic origin: a subgroup analysis of SOCRATES, a randomised, double-blind, controlled trial. Lancet Neurol 2017;16:301–10. https://doi.org/10.1016/s1474- 4422(17)30038-8 690. Kakkos SK, Griffin MB, Nicolaides AN, Kyriacou E, Sabetai MM, Tegos T, et al. The size of juxtaluminal hypoechoic area in ultrasound images of asymptomatic carotid plaques predicts the occurrence of stroke. J Vasc Surg 2013;57:609–18.e1; discussion 617–608. https://doi.org/10.1016/j.jvs.2012.09.045 691. Gupta A, Kesavabhotla K, Baradaran H, Kamel H, Pandya A, Giambrone AE, et al. Plaque echolucency and stroke risk in asymptomatic carotid stenosis: a systematic review and meta-analysis. Stroke 2015;46:91–7. https://doi.org/10.1161/strokeaha.114. 006091 692. Palacio S, Hart RG, Pearce LA, Anderson DC, Sharma M, Birnbaum LA, et al. Effect of addition of clopidogrel to aspirin on stroke incidence: meta-analysis of randomized trials. Int J Stroke 2015;10:686–91. https://doi.org/10.1111/ijs.12050 693. Gupta A, Baradaran H, Schweitzer AD, Kamel H, Pandya A, Delgado D, et al. Carotid plaque MRI and stroke risk: a systematic review and meta-analysis. Stroke 2013;44: 3071–7. https://doi.org/10.1161/strokeaha.113.002551 694. Wong KS, Chen C, Fu J, Chang HM, Suwanwela NC, Huang YN, et al. Clopidogrel plus aspirin versus aspirin alone for reducing embolisation in patients with acute symptomatic cerebral or carotid artery stenosis (CLAIR study): a randomised, open-label, blinded-endpoint trial. Lancet Neurol 2010;9:489–97. https://doi.org/10.1016/s1474- 4422(10)70060-0 695. Karlöf E, Buckler A, Liljeqvist ML, Lengquist M, Kronqvist M, Toonsi MA, et al. Carotid plaque phenotyping by correlating plaque morphology from computed tomography angiography with transcriptional profiling. Eur J Vasc Endovasc Surg 2021;62:716–26. https://doi.org/10.1016/j.ejvs.2021.07.011 696. Silver FL, Mackey A, Clark WM, Brooks W, Timaran CH, Chiu D, et al. Safety of stenting and endarterectomy by symptomatic status in the Carotid Revascularization Endarterectomy Versus Stenting Trial (CREST). Stroke 2011;42:675–80. https://doi. org/10.1161/strokeaha.110.610212 697. Baker WH, Howard VJ, Howard G, Toole JF. Effect of contralateral occlusion on longterm efficacy of endarterectomy in the asymptomatic carotid atherosclerosis study (ACAS). ACAS Investigators. Stroke 2000;31:2330–4. https://doi.org/10.1161/01.str. 31.10.2330 698. Kamtchum-Tatuene J, Noubiap JJ, Wilman AH, Saqqur M, Shuaib A, Jickling GC. Prevalence of high-risk plaques and risk of stroke in patients with asymptomatic carotid stenosis: a meta-analysis. JAMA Neurol 2020;77:1524–35. https://doi.org/10. 1001/jamaneurol.2020.2658 699. Saratzis A, Naylor R. 30 day outcomes after carotid interventions: an updated meta-analysis of randomised controlled trials in asymptomatic patients. Eur J Vasc Endovasc Surg 2022;63:157–8. https://doi.org/10.1016/j.ejvs.2021.10.029 700. Amarenco P, Denison H, Evans SR, Himmelmann A, James S, Knutsson M, et al. Ticagrelor added to aspirin in acute nonsevere ischemic stroke or transient ischemic attack of atherosclerotic origin. Stroke 2020;51:3504–13. https://doi.org/10.1161/ strokeaha.120.032239 701. Halliday A, Bulbulia R, Bonati LH, Chester J, Cradduck-Bamford A, Peto R, et al. Second asymptomatic carotid surgery trial (ACST-2): a randomised comparison of carotid artery stenting versus carotid endarterectomy. Lancet 2021;398:1065–73. https://doi. org/10.1016/s0140-6736(21)01910-3 702. Rosenfield K, Matsumura JS, Chaturvedi S, Riles T, Ansel GM, Metzger DC, et al. Randomized trial of stent versus surgery for asymptomatic carotid stenosis. N Engl J Med 2016;374:1011–20. https://doi.org/10.1056/NEJMoa1515706 703. Brott TG, Howard G, Roubin GS, Meschia JF, Mackey A, Brooks W, et al. Long-term results of stenting versus endarterectomy for carotid-artery stenosis. N Engl J Med 2016;374:1021–31. https://doi.org/10.1056/NEJMoa1505215 704. Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351:1493–501. https://doi.org/10.1056/NEJMoa040127 705. Karpenko A, Bugurov S, Ignatenko P, Starodubtsev V, Popova I, Malinowski K, et al. Randomized controlled trial of conventional versus micronet-covered stent in carotid artery revascularization. JACC Cardiovasc Interv 2021;14:2377–87. https://doi.org/10. 1016/j.jcin.2021.08.005 706. Karpenko A, Bugurov S, Ignatenko P, Starodubtsev V, Popova I, Malinowski K, et al. Randomized controlled trial of conventional versus micronet-covered stent in carotid artery revascularization: 12-month outcomes. JACC Cardiovasc Interv 2023;16:878–80. https://doi.org/10.1016/j.jcin.2023.01.369 707. Columbo JA, Martinez-Camblor P, Stone DH, Goodney PP, O’Malley AJ. Procedural safety comparison between transcarotid artery revascularization, carotid endarterectomy, and carotid stenting: perioperative and 1-year rates of stroke or death. J Am Heart Assoc 2022;11:e024964. https://doi.org/10.1161/jaha.121.024964 708. de Borst GJ. Transcarotid artery revascularization. Br J Surg 2023;110:127–8. https:// doi.org/10.1093/bjs/znac421 709. Hawkins BM, Kennedy KF, Aronow HD, Nguyen LL, White CJ, Rosenfield K, et al. Hospital variation in carotid stenting outcomes. JACC Cardiovasc Interv 2015;8: 858–63. https://doi.org/10.1016/j.jcin.2015.01.026 710. Paraskevas KI, Kalmykov EL, Naylor AR. Stroke/death rates following carotid artery stenting and carotid endarterectomy in contemporary administrative dataset registries: a systematic review. Eur J Vasc Endovasc Surg 2016;51:3–12. https://doi.org/10. 1016/j.ejvs.2015.07.032 711. Brott TG, Hobson RW, II, Howard G, Roubin GS, Clark WM, Brooks W, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010; 363:11–23. https://doi.org/10.1056/NEJMoa0912321 712. Sacco RL, Diener HC, Yusuf S, Cotton D, Ôunpuu S, Lawton WA, et al. Aspirin and extended-release dipyridamole versus clopidogrel for recurrent stroke. N Engl J Med 2008;359:1238–51. https://doi.org/10.1056/NEJMoa0805002 713. Halkes PH, van Gijn J, Kappelle LJ, Koudstaal PJ, Algra A. Medium intensity oral anticoagulants versus aspirin after cerebral ischaemia of arterial origin (ESPRIT): a randomised controlled trial. Lancet Neurol 2007;6:115–24. https://doi.org/10.1016/s1474- 4422(06)70685-8 714. Markus HS, Droste DW, Kaps M, Larrue V, Lees KR, Siebler M, et al. Dual antiplatelet therapy with clopidogrel and aspirin in symptomatic carotid stenosis evaluated using Doppler embolic signal detection: the clopidogrel and aspirin for reduction of emboli in symptomatic carotid stenosis (CARESS) trial. Circulation 2005;111:2233–40. https:// doi.org/10.1161/01.Cir.0000163561.90680.1c 715. Johnston SC, Amarenco P, Denison H, Evans SR, Himmelmann A, James S, et al. Ticagrelor and aspirin or aspirin alone in acute ischemic stroke or TIA. N Engl J Med 2020;383:207–17. https://doi.org/10.1056/NEJMoa1916870 716. Wang Y, Pan Y, Li H, Amarenco P, Denison H, Evans SR, et al. Efficacy and safety of ticagrelor and aspirin in patients with moderate ischemic stroke: an exploratory analysis of the THALES randomized clinical trial. JAMA Neurol 2021;78:1091–8. https://doi. org/10.1001/jamaneurol.2021.2440 717. Messas E, Goudot G, Halliday A, Sitruk J, Mirault T, Khider L, et al. Management of carotid stenosis for primary and secondary prevention of stroke: state-of-the-art 2020: a critical review. Eur Heart J Suppl 2020;22:M35–42. https://doi.org/10.1093/eurheartj/ suaa162 718. Rothwell PM, Eliasziw M, Gutnikov SA, Fox AJ, Taylor DW, Mayberg MR, et al. Analysis of pooled data from the randomised controlled trials of endarterectomy for
ESC Guidelines 3679
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.143
symptomatic carotid stenosis. Lancet 2003;361:107–16. https://doi.org/10.1016/ s0140-6736(03)12228-3 719. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet 1998;351: 1379–87. https://doi.org/10.1016/S0140-6736(97)09292-1 720. Mayberg MR, Wilson SE, Yatsu F, Weiss DG, Messina L, Hershey LA, et al. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. Veterans affairs cooperative studies program 309 trialist group. JAMA 1991;266: 3289–94. 721. Naylor AR, Sillesen H, Schroeder TV. Clinical and imaging features associated with an increased risk of early and late stroke in patients with symptomatic carotid disease. Eur J Vasc Endovasc Surg 2015;49:513–23. https://doi.org/10.1016/j.ejvs.2015.01.011 722. Tsantilas P, Kuehnl A, König T, Breitkreuz T, Kallmayer M, Knappich C, et al. Short time interval between neurologic event and carotid surgery is not associated with an increased procedural risk. Stroke 2016;47:2783–90. https://doi.org/10.1161/strokeaha. 116.014058 723. Loftus IM, Paraskevas KI, Johal A, Waton S, Heikkila K, Naylor AR, et al. Editor’s choice —delays to surgery and procedural risks following carotid endarterectomy in the UK national vascular registry. Eur J Vasc Endovasc Surg 2016;52:438–43. https://doi.org/10. 1016/j.ejvs.2016.05.031 724. Strömberg S, Gelin J, Osterberg T, Bergström GML, Karlström L, Österberg K, et al. Very urgent carotid endarterectomy confers increased procedural risk. Stroke 2012; 43:1331–5. https://doi.org/10.1161/strokeaha.111.639344 725. Bush CK, Kurimella D, Cross LJ, Conner KR, Martin-Schild D, He J, et al. Endovascular treatment with stent-retriever devices for acute ischemic stroke: a meta-analysis of randomized controlled trials. PLoS One 2016;11:e0147287. https://doi.org/10.1371/ journal.pone.0147287 726. Savardekar AR, Narayan V, Patra DP, Spetzler RF, Sun H. Timing of carotid endarterectomy for symptomatic carotid stenosis: a snapshot of current trends and systematic review of literature on changing paradigm towards early surgery. Neurosurgery 2019; 85:E214–25. https://doi.org/10.1093/neuros/nyy557 727. Hill MD, Brooks W, Mackey A, Clark WM, Meschia JF, Morrish WF, et al. Stroke after carotid stenting and endarterectomy in the carotid revascularization endarterectomy versus stenting trial (CREST). Circulation 2012;126:3054–61. https://doi.org/10.1161/ circulationaha.112.120030 728. Blackshear JL, Cutlip DE, Roubin GS, Hill MD, Leimgruber PP, Begg RJ, et al. Myocardial infarction after carotid stenting and endarterectomy: results from the carotid revascularization endarterectomy versus stenting trial. Circulation 2011;123:2571–8. https:// doi.org/10.1161/circulationaha.110.008250 729. Howard G, Roubin GS, Jansen O, Hendrikse J, Halliday A, Fraedrich G, et al. Association between age and risk of stroke or death from carotid endarterectomy and carotid stenting: a meta-analysis of pooled patient data from four randomised trials. Lancet 2016;387:1305–11. https://doi.org/10.1016/s0140-6736(15)01309-4 730. Alamowitch S, Eliasziw M, Algra A, Meldrum H, Barnett HJ. Risk, causes, and prevention of ischaemic stroke in elderly patients with symptomatic internal-carotid-artery stenosis. Lancet 2001;357:1154–60. https://doi.org/10.1016/s0140-6736(00)04332-4 731. Bonati LH, Lyrer P, Ederle J, Featherstone R, Brown MM. Percutaneous transluminal balloon angioplasty and stenting for carotid artery stenosis. Cochrane Database Syst Rev 2012;9:CD000515. https://doi.org/10.1002/14651858.CD000515.pub4 732. Economopoulos KP, Sergentanis TN, Tsivgoulis G, Mariolis AD, Stefanadis C. Carotid artery stenting versus carotid endarterectomy: a comprehensive meta-analysis of short-term and long-term outcomes. Stroke 2011;42:687–92. https://doi.org/10. 1161/strokeaha.110.606079 733. Bonati LH, Dobson J, Featherstone RL, Ederle J, van der Worp HB, de Borst GJ, et al. Long-term outcomes after stenting versus endarterectomy for treatment of symptomatic carotid stenosis: the International Carotid Stenting Study (ICSS) randomised trial. Lancet 2015;385:529–38. https://doi.org/10.1016/s0140-6736(14)61184-3 734. Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ. Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery. Lancet 2004;363:915–24. https://doi.org/10.1016/s0140-6736(04)15785-1 735. Rantner B, Kollerits B, Roubin GS, Ringleb PA, Jansen O, Howard G, et al. Early endarterectomy carries a lower procedural risk than early stenting in patients with symptomatic stenosis of the internal carotid artery: results from 4 randomized controlled trials. Stroke 2017;48:1580–7. https://doi.org/10.1161/strokeaha.116.016233 736. Schermerhorn ML, Fokkema M, Goodney P, Dillavou ED, Jim J, Kenwood CT, et al. The impact of centers for medicare and medicaid services high-risk criteria on outcome after carotid endarterectomy and carotid artery stenting in the SVS vascular registry. J Vasc Surg 2013;57:1318–24. https://doi.org/10.1016/j.jvs.2012.10.107 737. Schermerhorn ML, Liang P, Eldrup-Jorgensen J, Cronenwett JL, Nolan BW, Kashyap VS, et al. Association of transcarotid artery revascularization vs transfemoral carotid artery stenting with stroke or death among patients with carotid artery stenosis. JAMA 2019;322:2313–22. https://doi.org/10.1001/jama.2019.18441 738. Pineau S, Fajardo A, Saqib NU, Tanaka A, Motaganahalli RL, Keyhani A, et al. Transcarotid revascularization timing and early postoperative outcomes in symptomatic patients. Vasc Endovascular Surg 2023;57:344–9. https://doi.org/10.1177/ 15385744221146678 739. Kieffer E, Praquin B, Chiche L, Koskas F, Bahnini A. Distal vertebral artery reconstruction: long-term outcome. J Vasc Surg 2002;36:549–54. https://doi.org/10.1067/mva. 2002.126092 740. Berguer R, Flynn LM, Kline RA, Caplan L. Surgical reconstruction of the extracranial vertebral artery: management and outcome. J Vasc Surg 2000;31:9–18. https://doi. org/10.1016/s0741-5214(00)70063-2 741. Markus HS, Harshfield EL, Compter A, Kuker W, Kappelle LJ, Clifton A, et al. Stenting for symptomatic vertebral artery stenosis: a preplanned pooled individual patient data analysis. Lancet Neurol 2019;18:666–73. https://doi.org/10.1016/s1474-4422(19) 30149-8 742. Hanel RA, Brasiliense LB, Spetzler RF. Microsurgical revascularization of proximal vertebral artery: a single-center, single-operator analysis. Neurosurgery 2009;64:1043–51; discussion 1051. https://doi.org/10.1227/01.Neu.0000347099.17437.64 743. Asiddao CB, Donegan JH, Whitesell RC, Kalbfleisch JH. Factors associated with perioperative complications during carotid endarterectomy. Anesth Analg 1982;61:631–7. 744. Obeid T, Arhuidese I, Gaidry A, Qazi U, Abularrage C, Goodney P, et al. Beta-blocker use is associated with lower stroke and death after carotid artery stenting. J Vasc Surg 2016;63:363–9. https://doi.org/10.1016/j.jvs.2015.08.108 745. Abou-Chebl A, Reginelli J, Bajzer CT, Yadav JS. Intensive treatment of hypertension decreases the risk of hyperperfusion and intracerebral hemorrhage following carotid artery stenting. Catheter Cardiovasc Interv 2007;69:690–6. https://doi.org/10.1002/ccd. 20693 746. Lindblad B, Persson NH, Takolander R, Bergqvist D. Does low-dose acetylsalicylic acid prevent stroke after carotid surgery? A double-blind, placebo-controlled randomized trial. Stroke 1993;24:1125–8. https://doi.org/10.1161/01.str.24.8.1125 747. Kretschmer G, Pratschner T, Prager M, Wenzi E, Polterauer P, Schemper M, et al. Antiplatelet treatment prolongs survival after carotid bifurcation endarterectomy. Analysis of the clinical series followed by a controlled trial. Ann Surg 1990;211: 317–22. https://doi.org/10.1097/00000658-199003000-00002 748. Dalainas I, Nano G, Bianchi P, Stegher S, Malacrida G, Tealdi DG. Dual antiplatelet regime versus acetyl-acetic acid for carotid artery stenting. Cardiovasc Intervent Radiol 2006;29:519–21. https://doi.org/10.1007/s00270-005-5288-y 749. AbuRahma AF, Avgerinos ED, Chang RW, Darling RC, Duncan AA, Forbes TL, et al. The Society for Vascular Surgery implementation document for management of extracranial cerebrovascular disease. J Vasc Surg 2022;75:26s–98s. https://doi.org/10.1016/j. jvs.2021.04.074 750. Naylor AR, Ricco JB, de Borst GJ, Debus S, de Haro J, Halliday A, et al. Editor’s choice— management of atherosclerotic carotid and vertebral artery disease: 2017 clinical practice guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg 2018;55:3–81. https://doi.org/10.1016/j.ejvs.2017.06.021 751. Ghamraoui AK, Chang H, Maldonado TS, Ricotta JJ, II. Clopidogrel versus ticagrelor for antiplatelet therapy in transcarotid artery revascularization in the Society for Vascular Surgery vascular quality initiative. J Vasc Surg 2022;75:1652–60. https://doi.org/10. 1016/j.jvs.2021.11.060 752. Marcaccio CL, Patel PB, Liang P, Rastogi V, Stangenberg L, Jim J, et al. Efficacy and safety of perioperative dual antiplatelet therapy with ticagrelor versus clopidogrel in carotid artery stenting. J Vasc Surg 2022;75:1293–303.e8. https://doi.org/10.1016/j.jvs.2021.09. 045 753. Ghamraoui AK, Ricotta JJ, II. Outcomes and strategy of tailored antiplatelet therapy with ticagrelor in patients undergoing transcarotid artery revascularization. J Vasc Surg 2021;73:132–41. https://doi.org/10.1016/j.jvs.2020.04.518 754. Zierler RE, Jordan WD, Lal BK, Mussa F, Leers S, Fulton J, et al. The Society for Vascular Surgery practice guidelines on follow-up after vascular surgery arterial procedures. J Vasc Surg 2018;68:256–84. https://doi.org/10.1016/j.jvs.2018.04.018 755. Cheun TJ, Jayakumar L, Sheehan MK, Sideman MJK, Pounds LL, Davies MG. Outcomes of upper extremity interventions for chronic critical ischemia. J Vasc Surg 2019;69: 120–8.e2. https://doi.org/10.1016/j.jvs.2018.04.056 756. Awad El-Karim G, Kennedy SA, Ferraresi R, Addas JAK, Oreopoulos GD, Jaberi A, et al. Percutaneous transluminal angioplasty for below-the-elbow critical hand ischemia: a systematic review. J Endovasc Ther 2022;29:468–77. https://doi.org/10.1177/ 15266028211050309 757. Raimbeau A, Pistorius MA, Goueffic Y, Connault J, Plissonneau-Duquene P, Maurel B, et al. Digital ischaemia aetiologies and mid-term follow-up: a cohort study of 323 patients. Medicine 2021;100:e25659. https://doi.org/10.1097/md.0000000000025659 758. Clark CE, Taylor RS, Shore AC, Ukoumunne OC, Campbell JL. Association of a difference in systolic blood pressure between arms with vascular disease and mortality: a systematic review and meta-analysis. Lancet 2012;379:905–14. https://doi.org/10. 1016/s0140-6736(11)61710-8 759. Aboyans V, Kamineni A, Allison MA, McDermott MM, Crouse JR, Ni H, et al. The epidemiology of subclavian stenosis and its association with markers of subclinical atherosclerosis: the multi-ethnic study of atherosclerosis (MESA). Atherosclerosis 2010;211: 266–70. https://doi.org/10.1016/j.atherosclerosis.2010.01.013 760. Labropoulos N, Nandivada P, Bekelis K. Prevalence and impact of the subclavian steal syndrome. Ann Surg 2010;252:166–70. https://doi.org/10.1097/SLA. 0b013e3181e3375a Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.144
761. Zhang J, Wang L, Chen Y, Wang S, Xing Y, Cui L. Color Doppler ultrasonography for the evaluation of subclavian artery stenosis. Front Neurol 2022;13:804039. https://doi. org/10.3389/fneur.2022.804039 762. Harper C, Cardullo PA, Weyman AK, Patterson RB. Transcranial Doppler ultrasonography of the basilar artery in patients with retrograde vertebral artery flow. J Vasc Surg 2008;48:859–64. https://doi.org/10.1016/j.jvs.2008.05.057 763. Chidambaram PK, Swaminathan RK, Ganesan P, Mayavan M. Segmental comparison of peripheral arteries by Doppler ultrasound and CT angiography. J Clin Diagn Res 2016; 10:TC12–16. https://doi.org/10.7860/JCDR/2016/17191.7242 764. Tsao TF, Cheng KL, Shen CY, Wu M-C, Huang H-H, Su C-H, et al. Diagnostic performance of combined contrast-enhanced magnetic resonance angiography and phasecontrast magnetic resonance imaging in suspected subclavian steal syndrome. Can Assoc Radiol J 2016;67:190–201. https://doi.org/10.1016/j.carj.2015.08.007 765. Klitfod L, Jensen LP. Treatment of chronic upper limb ischaemia is safe and results are good. Dan Med J 2014;61:A4859. 766. Duran M, Grotemeyer D, Danch MA, Grabitz K, Schelzig H, Sagban TA. Subclavian carotid transposition: immediate and long-term outcomes of 126 surgical reconstructions. Ann Vasc Surg 2015;29:397–403. https://doi.org/10.1016/j.avsg.2014.09.030 767. Daniel VT, Madenci AL, Nguyen LL, Eslami MH, Kalish JA, Farber A, et al. Contemporary comparison of supra-aortic trunk surgical reconstructions for occlusive disease. J Vasc Surg 2014;59:1577–82, 1582.e1–2. https://doi.org/10.1016/j.jvs. 2013.12.017 768. Burihan E, Soma F, Iared W. Angioplasty versus stenting for subclavian artery stenosis. Cochrane Database Syst Rev 2011;10:CD008461. https://doi.org/10.1002/14651858. CD008461.pub2 769. Hüttl K, Nemes B, Simonffy A, Entz L, Bérczi V. Angioplasty of the innominate artery in 89 patients: experience over 19 years. Cardiovasc Intervent Radiol 2002;25:109–14. https://doi.org/10.1007/s00270-001-0074-y 770. Modarai B, Ali T, Dourado R, Reidy JF, Taylor PR, Burnand KG. Comparison of extraanatomic bypass grafting with angioplasty for atherosclerotic disease of the supra-aortic trunks. Br J Surg 2004;91:1453–7. https://doi.org/10.1002/bjs.4751 771. Song L, Zhang J, Li J, Gu Y, Yu H, Chen B, et al. Endovascular stenting vs. extrathoracic surgical bypass for symptomatic subclavian steal syndrome. J Endovasc Ther 2012;19: 44–51. https://doi.org/10.1583/11-3692.1 772. Owens LV, Tinsley EA, Jr, Criado E, Burnham SJ, Keagy BA. Extrathoracic reconstruction of arterial occlusive disease involving the supraaortic trunks. J Vasc Surg 1995;22: 217–21; discussion 221–2. https://doi.org/10.1016/s0741-5214(95)70133-8 773. Huijben M, Meershoek AJA, de Borst GJ, Toorop RJ. Long-term outcome of axillo-axillary bypass in patients with subclavian or innominate artery stenosis. Ann Vasc Surg 2021;73:321–8. https://doi.org/10.1016/j.avsg.2020.10.029 774. Lee AD, Agarwal S, Sadhu D. A 7-year experience with thoracoscopic sympathectomy for critical upper limb ischemia. World J Surg 2006;30:1644–7. https://doi.org/10.1007/ s00268-005-0559-y 775. Schillinger M, Haumer M, Schillinger S, Mlekusch W, Ahmadi R, Minar E. Outcome of conservative versus interventional treatment of subclavian artery stenosis. J Endovasc Ther 2002;9:139–46. https://doi.org/10.1177/152660280200900201 776. Ahmed AT, Mohammed K, Chehab M, Brinjikji W, Hassan Murad M, Cloft H, et al. Comparing percutaneous transluminal angioplasty and stent placement for treatment of subclavian arterial occlusive disease: a systematic review and meta-analysis. Cardiovasc Intervent Radiol 2016;39:652–67. https://doi.org/10.1007/s00270-015- 1250-9 777. Che W, Dong H, Jiang X, Peng M, Zou Y, Song L, et al. Subclavian artery stenting for coronary-subclavian steal syndrome. Catheter Cardiovasc Interv 2017;89:601–8. https:// doi.org/10.1002/ccd.26902 778. Hamdan R, Guilleminot P, Leclercq T, Monin A. Coronary-subclavian steal syndrome causing myocardial infarction after arteriovenous fistula creation: a case report. ESC Heart Fail 2023;10:2084–9. https://doi.org/10.1002/ehf2.14341 779. Che WQ, Dong H, Jiang XJ, Peng M, Zou Y, Qian H, et al. Stenting for left subclavian artery stenosis in patients scheduled for left internal mammary artery-coronary artery bypass grafting. Catheter Cardiovasc Interv 2016;87:579–88. https://doi.org/10.1002/ ccd.26477 780. Muller AM, Bertram J, Bradaric C, Koppara T, Cassese S, Xhepa E, et al. Frequency of subclavian artery stenosis in patients with mammarian artery coronary bypass and suspected coronary artery disease progression. Clin Res Cardiol 2023;112:1204–11. https://doi.org/10.1007/s00392-022-02113-z 781. Angle JF, Matsumoto AH, McGraw JK, Spinosa DJ, Hagspiel KD, Leung DA, et al. Percutaneous angioplasty and stenting of left subclavian artery stenosis in patients with left internal mammary-coronary bypass grafts: clinical experience and long-term follow-up. Vasc Endovascular Surg 2003;37:89–97. https://doi.org/10.1177/ 153857440303700202 782. Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med 2001;344:431–42. https:// doi.org/10.1056/nejm200102083440607 783. Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG, et al. Prevalence of renovascular disease in the elderly: a population-based study. J Vasc Surg 2002;36: 443–51. https://doi.org/10.1067/mva.2002.127351 784. Aboyans V, Desormais I, Magne J, Morange G, Mohty D, Lacroix P. Renal artery stenosis in patients with peripheral artery disease: prevalence, risk factors and long-term prognosis. Eur J Vasc Endovasc Surg 2017;53:380–5. https://doi.org/10.1016/j.ejvs. 2016.10.029 785. Safian RD. Renal artery stenosis. Prog Cardiovasc Dis 2021;65:60–70. https://doi.org/10. 1016/j.pcad.2021.03.003 786. Messerli FH, Bangalore S, Makani H, Rimoldi SF, Allemann Y, White CJ, et al. Flash pulmonary oedema and bilateral renal artery stenosis: the pickering syndrome. Eur Heart J 2011;32:2231–5. https://doi.org/10.1093/eurheartj/ehr056 787. Zeller T, Bonvini RF, Sixt S. Color-coded duplex ultrasound for diagnosis of renal artery stenosis and as follow-up examination after revascularization. Catheter Cardiovasc Interv 2008;71:995–9. https://doi.org/10.1002/ccd.21525 788. Prince M, Tafur JD, White CJ. When and how should we revascularize patients with atherosclerotic renal artery stenosis? JACC Cardiovasc Interv 2019;12:505–17. https:// doi.org/10.1016/j.jcin.2018.10.023 789. AbuRahma AF, Yacoub M. Renal imaging: duplex ultrasound, computed tomography angiography, magnetic resonance angiography, and angiography. Semin Vasc Surg 2013;26:134–43. https://doi.org/10.1053/j.semvascsurg.2014.06.001 790. Staub D, Canevascini R, Huegli RW, Aschwanden M, Thalhammer C, Imfeld S, et al. Best duplex-sonographic criteria for the assessment of renal artery stenosis—correlation with intra-arterial pressure gradient. Ultraschall Med 2007;28:45–51. https://doi. org/10.1055/s-2007-962881 791. Williams GJ, Macaskill P, Chan SF, Karplus TE, Yung W, Hodson EM, et al. Comparative accuracy of renal duplex sonographic parameters in the diagnosis of renal artery stenosis: paired and unpaired analysis. AJR Am J Roentgenol 2007;188:798–811. https://doi. org/10.2214/ajr.06.0355 792. Parikh SA, Shishehbor MH, Gray BH, White CJ, Jaff MR. SCAI expert consensus statement for renal artery stenting appropriate use. Catheter Cardiovasc Interv 2014;84: 1163–71. https://doi.org/10.1002/ccd.25559 793. Caps MT, Perissinotto C, Zierler RE, Polissar NL, Bergelin RO, Tullis MJ, et al. Prospective study of atherosclerotic disease progression in the renal artery. Circulation 1998;98:2866–72. https://doi.org/10.1161/01.cir.98.25.2866 794. Amighi J, Schlager O, Haumer M, Dick P, Mlekusch W, Loewe C, et al. Renal artery stenosis predicts adverse cardiovascular and renal outcome in patients with peripheral artery disease. Eur J Clin Invest 2009;39:784–92. https://doi.org/10.1111/j.1365-2362. 2009.02180.x 795. Fatica RA, Port FK, Young EW. Incidence trends and mortality in end-stage renal disease attributed to renovascular disease in the United States. Am J Kidney Dis 2001;37: 1184–90. https://doi.org/10.1053/ajkd.2001.24521 796. Ritchie J, Green D, Alderson HV, Chrysochou C, Vassallo D, Sinha S, et al. Associations of antiplatelet therapy and beta blockade with patient outcomes in atherosclerotic renovascular disease. J Am Soc Hypertens 2016;10:149–58.e3. https://doi.org/10.1016/j. jash.2015.12.002 797. Raman G, Adam GP, Halladay CW, Langberg VN, Azodo IA, Balk EM. Comparative effectiveness of management strategies for renal artery stenosis: an updated systematic review. Ann Intern Med 2016;165:635–49. https://doi.org/10.7326/M16-1053 798. Bhalla V, Textor SC, Beckman JA, Casanegra AI, Cooper CJ, Kim ESH, et al. Revascularization for renovascular disease: a scientific statement from the American Heart Association. Hypertension 2022;79:e128–43. https://doi.org/10.1161/hyp. 0000000000000217 799. Piaggio D, Bracale U, Pecchia L, Di Taranto MD, Sodo M, Bracale UM. Endovascular treatment versus medical therapy for hypertensive patients with renal artery stenosis: an updated systematic review. Ann Vasc Surg 2019;61:445–54. https://doi.org/10.1016/ j.avsg.2019.04.050 800. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009;361:1953–62. https:// doi.org/10.1056/NEJMoa0905368 801. Bax L, Woittiez AJ, Kouwenberg HJ, Mali WP, Buskens E, Beek FJ, et al. Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function: a randomized trial. Ann Intern Med 2009;150:840–8, w150–1. https://doi.org/10.7326/0003- 4819-150-12-200906160-00119 802. Webster J, Marshall F, Abdalla M, Dominiczak A, Edwards R, Isles CG, et al. Randomised comparison of percutaneous angioplasty vs continued medical therapy for hypertensive patients with atheromatous renal artery stenosis. Scottish and Newcastle Renal Artery Stenosis Collaborative Group. J Hum Hypertens 1998;12: 329–35. https://doi.org/10.1038/sj.jhh.1000599 803. van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FHM, Deinum J, Postma CT, et al. The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group. N Engl J Med 2000;342:1007–14. https://doi.org/10.1056/nejm200004063421403 804. Plouin PF, Chatellier G, Darné B, Raynaud A. Blood pressure outcome of angioplasty in atherosclerotic renal artery stenosis: a randomized trial. Essai Multicentrique Medicaments vs Angioplastie (EMMA) Study Group. Hypertension 1998;31:823–9. https://doi.org/10.1161/01.hyp.31.3.823
ESC Guidelines 3681
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.145
805. Abela R, Ivanova S, Lidder S, Morris R, Hamilton G. An analysis comparing open surgical and endovascular treatment of atherosclerotic renal artery stenosis. Eur J Vasc Endovasc Surg 2009;38:666–75. https://doi.org/10.1016/j.ejvs.2009.08.002 806. Balzer KM, Pfeiffer T, Rossbach S, Voiculescu A, Mödder U, Godehardt E, et al. Prospective randomized trial of operative vs interventional treatment for renal artery ostial occlusive disease (RAOOD). J Vasc Surg 2009;49:667–75; discussion 674–665. https://doi.org/10.1016/j.jvs.2008.10.006 807. Mohler ER, III, Gornik HL, Gerhard-Herman M, Misra S, Olin JW, Zierler RE. ACCF/ ACR/AIUM/ASE/ASN/ICAVL/SCAI/SCCT/SIR/SVM/SVS/SVU [corrected] 2012 appropriate use criteria for peripheral vascular ultrasound and physiological testing part I: arterial ultrasound and physiological testing: a report of the American College of Cardiology Foundation appropriate use criteria task force, American College of Radiology, American Institute of Ultrasound in Medicine, American Society of Echocardiography, American Society of Nephrology, Intersocietal Commission for the Accreditation of Vascular Laboratories, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, Society for Interventional Radiology, Society for Vascular Medicine, Society for Vascular Surgery, [corrected] and Society for Vascular Ultrasound. [corrected]. J Am Coll Cardiol 2012;60:242–76. https://doi.org/10.1016/j.jacc.2012.02.009 808. Davies MG, Saad WA, Bismuth JX, Peden EK, Naoum JJ, Lumsden AB. Outcomes of endoluminal reintervention for restenosis after percutaneous renal angioplasty and stenting. J Vasc Surg 2009;49:946–52. https://doi.org/10.1016/j.jvs.2008.11.039 809. Hicks CW, Clark TWI, Cooper CJ, de Bhailís ÁM, De Carlo M, Green D, et al. Atherosclerotic renovascular disease: A KDIGO (kidney disease: improving global outcomes) controversies conference. Am J Kidney Dis 2022;79:289–301. https://doi.org/ 10.1053/j.ajkd.2021.06.025 810. Johansen KL, Garimella PS, Hicks CW, Kalra PA, Kelly DM, Martens S, et al. Central and peripheral arterial diseases in chronic kidney disease: conclusions from a kidney disease: improving global outcomes (KDIGO) controversies conference. Kidney Int 2021;100:35–48. https://doi.org/10.1016/j.kint.2021.04.029 811. Pappaccogli M, Robberechts T, Lengele JP, Van der Niepen P, Sarafidis P, Rabbia F, et al. Endovascular versus medical management of atherosclerotic renovascular disease: update and emerging concepts. Hypertension 2023;80:1150–61. https://doi.org/10.1161/ HYPERTENSIONAHA.122.17965 812. Tian Y, Yuan B, Zhang N, Huang Z. Outcomes following the endovascular treatment of renal artery stenosis caused by fibromuscular dysplasia: a systematic review and meta-analysis. Ann Vasc Surg 2022;78:362–72. https://doi.org/10.1016/j.avsg.2021.06. 042 813. Persu A, Giavarini A, Touzé E, Januszewicz A, Sapoval M, Azizi M, et al. European consensus on the diagnosis and management of fibromuscular dysplasia. J Hypertens 2014; 32:1367–78. https://doi.org/10.1097/hjh.0000000000000213 814. Zeller T, Krankenberg H, Erglis A, Blessing E, Fuss T, Scheinert D, et al. A randomized, multi-center, prospective study comparing best medical treatment versus best medical treatment plus renal artery stenting in patients with hemodynamically relevant atherosclerotic renal artery stenosis (RADAR)—one-year results of a pre-maturely terminated study. Trials 2017;18:380. https://doi.org/10.1186/s13063-017-2126-x 815. Tamme K, Reintam Blaser A, Laisaar KT, Mändul M, Kals J, Forbes A, et al. Incidence and outcomes of acute mesenteric ischaemia: a systematic review and meta-analysis. BMJ Open 2022;12:e062846. https://doi.org/10.1136/bmjopen-2022-062846 816. Acosta S. Epidemiology of mesenteric vascular disease: clinical implications. Semin Vasc Surg 2010;23:4–8. https://doi.org/10.1053/j.semvascsurg.2009.12.001 817. Acosta S, Ogren M, Sternby NH, Bergqvist D, Björck M. Incidence of acute thromboembolic occlusion of the superior mesenteric artery—a population-based study. Eur J Vasc Endovasc Surg 2004;27:145–50. https://doi.org/10.1016/j.ejvs.2003.11.003 818. Carver TW, Vora RS, Taneja A. Mesenteric ischemia. Crit Care Clin 2016;32:155–71. https://doi.org/10.1016/j.ccc.2015.11.001 819. Klass AA. Embolectomy in acute mesenteric occlusion. Ann Surg 1951;134:913–7. https://doi.org/10.1097/00000658-195111000-00016 820. Acosta S, Björck M. Acute thrombo-embolic occlusion of the superior mesenteric artery: a prospective study in a well defined population. Eur J Vasc Endovasc Surg 2003;26: 179–83. https://doi.org/10.1053/ejvs.2002.1893 821. Kärkkäinen JM, Acosta S. Acute mesenteric ischemia (part I)—incidence, etiologies, and how to improve early diagnosis. Best Pract Res Clin Gastroenterol 2017;31: 15–25. https://doi.org/10.1016/j.bpg.2016.10.018 822. Kärkkäinen JM. Acute mesenteric ischemia: a challenge for the acute care surgeon. Scand J Surg 2021;110:150–8. https://doi.org/10.1177/14574969211007590 823. Powell A, Armstrong P. Plasma biomarkers for early diagnosis of acute intestinal ischemia. Semin Vasc Surg 2014;27:170–5. https://doi.org/10.1053/j.semvascsurg.2015.01. 008 824. Block T, Nilsson TK, Björck M, Acosta S. Diagnostic accuracy of plasma biomarkers for intestinal ischaemia. Scand J Clin Lab Invest 2008;68:242–8. https://doi.org/10.1080/ 00365510701646264 825. Kougias P, Lau D, El Sayed HF, Zhou W, Huynh TT, Lin PH. Determinants of mortality and treatment outcome following surgical interventions for acute mesenteric ischemia. J Vasc Surg 2007;46:467–74. https://doi.org/10.1016/j.jvs.2007.04.045 826. Lehtimäki TT, Kärkkäinen JM, Saari P, Manninen H, Paajanen H, Vanninen R. Detecting acute mesenteric ischemia in CT of the acute abdomen is dependent on clinical suspicion: review of 95 consecutive patients. Eur J Radiol 2015;84:2444–53. https://doi.org/ 10.1016/j.ejrad.2015.09.006 827. Kirkpatrick ID, Kroeker MA, Greenberg HM. Biphasic CT with mesenteric CT angiography in the evaluation of acute mesenteric ischemia: initial experience. Radiology 2003; 229:91–8. https://doi.org/10.1148/radiol.2291020991 828. Oliva IB, Davarpanah AH, Rybicki FJ, Desjardins B, Flamm SD, Francois CJ, et al. ACR appropriateness Criteria ® imaging of mesenteric ischemia. Abdom Imaging 2013;38: 714–9. https://doi.org/10.1007/s00261-012-9975-2 829. Salsano G, Salsano A, Sportelli E, Petrocelli F, Dahmane M, Spinella G, et al. What is the best revascularization strategy for acute occlusive arterial mesenteric ischemia: systematic review and meta-analysis. Cardiovasc Intervent Radiol 2018;41:27–36. https:// doi.org/10.1007/s00270-017-1749-3 830. El Farargy M, Abdel Hadi A, Abou Eisha M, Bashaeb K, Antoniou GA. Systematic review and meta-analysis of endovascular treatment for acute mesenteric ischaemia. Vascular 2017;25:430–8. https://doi.org/10.1177/1708538116689353 831. Kärkkäinen JM, Acosta S. Acute mesenteric ischemia (part II)—vascular and endovascular surgical approaches. Best Pract Res Clin Gastroenterol 2017;31:27–38. https://doi. org/10.1016/j.bpg.2016.11.003 832. Wyers MC, Powell RJ, Nolan BW, Cronenwett JL. Retrograde mesenteric stenting during laparotomy for acute occlusive mesenteric ischemia. J Vasc Surg 2007;45: 269–75. https://doi.org/10.1016/j.jvs.2006.10.047 833. Tilsed JV, Casamassima A, Kurihara H, Mariani D, Martinez I, Pereira J, et al. ESTES guidelines: acute mesenteric ischaemia. Eur J Trauma Emerg Surg 2016;42:253–70. https://doi.org/10.1007/s00068-016-0634-0 834. Tallarita T, Oderich GS, Gloviczki P, Duncan AA, Kalra M, Cha S, et al. Patient survival after open and endovascular mesenteric revascularization for chronic mesenteric ischemia. J Vasc Surg 2013;57:747–55; discussion 754–745. https://doi.org/10.1016/j. jvs.2012.09.047 835. Alahdab F, Arwani R, Pasha AK, Razouki ZA, Prokop LJ, Huber TS, et al. A systematic review and meta-analysis of endovascular versus open surgical revascularization for chronic mesenteric ischemia. J Vasc Surg 2018;67:1598–605. https://doi.org/10.1016/ j.jvs.2017.12.046 836. Mensink PB, Moons LM, Kuipers EJ. Chronic gastrointestinal ischaemia: shifting paradigms. Gut 2011;60:722–37. https://doi.org/10.1136/gut.2009.199695 837. Roobottom CA, Dubbins PA. Significant disease of the celiac and superior mesenteric arteries in asymptomatic patients: predictive value of Doppler sonography. AJR Am J Roentgenol 1993;161:985–8. https://doi.org/10.2214/ajr.161.5.8273642 838. Høyer C, Christensen MH, Sandermann J, Leusink R, Abrahamsen J. Chronic mesenteric ischaemia: the importance of the individual mesenteric artery. Clin Physiol Funct Imaging 2022;42:15–22. https://doi.org/10.1111/cpf.12730 839. Mensink PB, van Petersen AS, Geelkerken RH, Otte JA, Huisman AB, Kolkman JJ, et al. Clinical significance of splanchnic artery stenosis. Br J Surg 2006;93:1377–82. https:// doi.org/10.1002/bjs.5481 840. van Noord D, Mensink PB, de Knegt RJ, Ouwendijk M, Francke J, van Vuuren AJ, et al. Serum markers and intestinal mucosal injury in chronic gastrointestinal ischemia. Dig Dis Sci 2011;56:506–12. https://doi.org/10.1007/s10620-010-1303-5 841. Mensink PB, Hol L, Borghuis-Koertshuis N, Geelkerken RH, Huisman AB, Doelman CJA, et al. Transient postprandial ischemia is associated with increased intestinal fatty acid binding protein in patients with chronic gastrointestinal ischemia. Eur J Gastroenterol Hepatol 2009;21:278–82. https://doi.org/10.1097/MEG. 0b013e32832183a7 842. van Noord D, Kolkman JJ. Functional testing in the diagnosis of chronic mesenteric ischemia. Best Pract Res Clin Gastroenterol 2017;31:59–68. https://doi.org/10.1016/j.bpg. 2016.12.002 843. van Petersen AS, Meerwaldt R, Kolkman JJ, Huisman AB, van der Palen J, van Bockel JH, et al. The influence of respiration on criteria for transabdominal duplex examination of the splanchnic arteries in patients with suspected chronic splanchnic ischemia. J Vasc Surg 2013;57:1603–11, 1611.e1–10. https://doi.org/10.1016/j.jvs.2012.11.120 844. Zwolak RM, Fillinger MF, Walsh DB, LaBombard FA, Musson A, Darling CE, et al. Mesenteric and celiac duplex scanning: a validation study. J Vasc Surg 1998;27: 1078–88; discussion 1088. https://doi.org/10.1016/s0741-5214(98)60010-0 845. Schaefer PJ, Pfarr J, Trentmann J, Wulff A, Langer C, Siggelkow M, et al. Comparison of noninvasive imaging modalities for stenosis grading in mesenteric arteries. Rofo 2013; 185:628–34. https://doi.org/10.1055/s-0033-1335212 846. Cademartiri F, Palumbo A, Maffei E, Martini C, Malagò R, Belgrano M, et al. Noninvasive evaluation of the celiac trunk and superior mesenteric artery with multislice CT in patients with chronic mesenteric ischaemia. Radiol Med 2008;113:1135–42. https://doi. org/10.1007/s11547-008-0330-1 847. Pecoraro F, Rancic Z, Lachat M, Mayer D, Amann-Vesti B, Pfammatter T, et al. Chronic mesenteric ischemia: critical review and guidelines for management. Ann Vasc Surg 2013;27:113–22. https://doi.org/10.1016/j.avsg.2012.05.012 848. Gupta PK, Horan SM, Turaga KK, Miller WJ, Pipinos II. Chronic mesenteric ischemia: endovascular versus open revascularization. J Endovasc Ther 2010;17:540–9. https:// doi.org/10.1583/09-2935.1 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.146
849. Huber TS, Björck M, Chandra A, Clouse WD, Dalsing MC, Oderich GS, et al. Chronic mesenteric ischemia: clinical practice guidelines from the society for vascular surgery. J Vasc Surg 2021;73:87s–115s. https://doi.org/10.1016/j.jvs.2020.10.029 850. Fernández-Friera L, Fuster V, López-Melgar B, Oliva B, Sánchez-González J, Macías A, et al. Vascular inflammation in subclinical atherosclerosis detected by hybrid PET/MRI. J Am Coll Cardiol 2019;73:1371–82. https://doi.org/10.1016/j.jacc.2018.12.075 851. Meissner I, Whisnant JP, Khandheria BK, Spittell PC, O’Fallon WM, Pascoe RD, et al. Prevalence of potential risk factors for stroke assessed by transesophageal echocardiography and carotid ultrasonography: the SPARC study. Stroke prevention: assessment of risk in a community. Mayo Clin Proc 1999;74:862–9. https://doi.org/10.4065/ 74.9.862 852. Russo C, Jin Z, Rundek T, Homma S, Sacco RL, Di Tullio MR. Atherosclerotic disease of the proximal aorta and the risk of vascular events in a population-based cohort: the Aortic Plaques and Risk of Ischemic Stroke (APRIS) study. Stroke 2009;40:2313–8. https://doi.org/10.1161/strokeaha.109.548313 853. Oyama N, Gona P, Salton CJ, Chuang ML, Jhaveri RR, Blease SJ, et al. Differential impact of age, sex, and hypertension on aortic atherosclerosis: the Framingham heart study. Arterioscler Thromb Vasc Biol 2008;28:155–9. https://doi.org/10.1161/atvbaha.107. 153544 854. Montgomery DH, Ververis JJ, McGorisk G, Frohwein S, Martin RP, Taylor WR. Natural history of severe atheromatous disease of the thoracic aorta: a transesophageal echocardiographic study. J Am Coll Cardiol 1996;27:95–101. https://doi.org/10.1016/0735- 1097(95)00431-9 855. Amarenco P, Cohen A, Hommel M, Moulin T, Leys D, Bousser M-G. Atherosclerotic disease of the aortic arch as a risk factor for recurrent ischemic stroke. N Engl J Med 1996;334:1216–21. https://doi.org/10.1056/nejm199605093341902 856. Fujimoto S, Yasaka M, Otsubo R, Oe H, Nagatsuka K, Minematsu K. Aortic arch atherosclerotic lesions and the recurrence of ischemic stroke. Stroke 2004;35:1426–9. https://doi.org/10.1161/01.STR.0000127788.32550.d4 857. Koren MJ, Bryant B, Hilton TC. Atherosclerotic disease of the aortic arch and the risk of ischemic stroke. N Engl J Med 1995;332:1237–8. author reply 1237-1238. https:// doi.org/10.1056/NEJM199505043321815 858. Meissner I, Khandheria BK, Sheps SG, Schwartz GL, Wiebers DO, Whisnant JP, et al. Atherosclerosis of the aorta: risk factor, risk marker, or innocent bystander? A prospective population-based transesophageal echocardiography study. J Am Coll Cardiol 2004;44:1018–24. https://doi.org/10.1016/j.jacc.2004.05.075 859. Mitusch R, Doherty C, Wucherpfennig H, Memmesheimer C, Tepe C, Stierle U, et al. Vascular events during follow-up in patients with aortic arch atherosclerosis. Stroke 1997;28:36–9. https://doi.org/10.1161/01.str.28.1.36 860. Tunick PA, Rosenzweig BP, Katz ES, Freedberg RS, Perez JL, Kronzon I. High risk for vascular events in patients with protruding aortic atheromas: a prospective study. J Am Coll Cardiol 1994;23:1085–90. https://doi.org/10.1016/0735-1097(94)90595-9 861. Di Tullio MR, Russo C, Jin Z, Sacco RL, Mohr JP, Homma S. Aortic arch plaques and risk of recurrent stroke and death. Circulation 2009;119:2376–82. https://doi.org/10.1161/ circulationaha.108.811935 862. Tunick PA, Nayar AC, Goodkin GM, Mirchandani S, Francescone S, Rosenzweig BP, et al. Effect of treatment on the incidence of stroke and other emboli in 519 patients with severe thoracic aortic plaque. Am J Cardiol 2002;90:1320–5. https://doi.org/10. 1016/s0002-9149(02)02870-9 863. Diener HC, Bogousslavsky J, Brass LM, Cimminiello C, Csiba L, Kaste M, et al. Aspirin and clopidogrel compared with clopidogrel alone after recent ischaemic stroke or transient ischaemic attack in high-risk patients (MATCH): randomised, double-blind, placebo-controlled trial. Lancet 2004;364:331–7. https://doi.org/10.1016/s0140- 6736(04)16721-4 864. Bowdish ME, Weaver FA, Liebman HA, Rowe VL, Hood DB. Anticoagulation is an effective treatment for aortic mural thrombi. J Vasc Surg 2002;36:713–9. 865. Kleindorfer DO, Towfighi A, Chaturvedi S, Cockroft KM, Gutierrez J, Lombardi-Hill D, et al. 2021 Guideline for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline from the American Heart Association/ American Stroke Association. Stroke 2021;52:e364–467. https://doi.org/10.1161/ str.0000000000000375 866. Amarenco P, Davis S, Jones EF, Cohen AA, Heiss W-D, Kaste M, et al. Clopidogrel plus aspirin versus warfarin in patients with stroke and aortic arch plaques. Stroke 2014;45: 1248–57. https://doi.org/10.1161/strokeaha.113.004251 867. Benavente OR, Hart RG, McClure LA, Szychowski JM, Coffey CS, Pearce LA. Effects of clopidogrel added to aspirin in patients with recent lacunar stroke. N Engl J Med 2012; 367:817–25. https://doi.org/10.1056/NEJMoa1204133 868. Amarenco P, Kim JS, Labreuche J, Charles H, Abtan J, Béjot Y, et al. A comparison of two LDL cholesterol targets after ischemic stroke. N Engl J Med 2020;382:9. https:// doi.org/10.1056/NEJMoa1910355 869. Devereux RB, de Simone G, Arnett DK, Best LG, Boerwinkle E, Howard BV, et al. Normal limits in relation to age, body size and gender of two-dimensional echocardiographic aortic root dimensions in persons ≥15 years of age. Am J Cardiol 2012;110: 1189–94. https://doi.org/10.1016/j.amjcard.2012.05.063 870. van Kimmenade RR, Kempers M, de Boer MJ, Loeys BL, Timmermans J. A clinical appraisal of different Z-score equations for aortic root assessment in the diagnostic evaluation of Marfan syndrome. Genet Med 2013;15:528–32. https://doi.org/10. 1038/gim.2012.172 871. Davies RR, Gallo A, Coady MA, Tellides G, Botta DM, Burke B, et al. Novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg 2006;81:169–77. https://doi.org/10.1016/j.athoracsur.2005.06.026 872. Hannawa KK, Eliason JL, Upchurch GR, Jr. Gender differences in abdominal aortic aneurysms. Vascular 2009;17:30–9. https://doi.org/10.2310/6670.2008.00092 873. Boczar KE, Cheung K, Boodhwani M, Beauchesne L, Dennie C, Nagpal S, et al. Sex differences in thoracic aortic aneurysm growth. Hypertension 2019;73:190–6. https://doi. org/10.1161/hypertensionaha.118.11851 874. Hultgren R, Larsson E, Wahlgren CM, Swedenborg J. Female and elderly abdominal aortic aneurysm patients more commonly have concurrent thoracic aortic aneurysm. Ann Vasc Surg 2012;26:918–23. https://doi.org/10.1016/j.avsg.2012.01.023 875. Chaer RA, Vasoncelos R, Marone LK, Al-Khoury G, Rhee RY, Cho JS, et al. Synchronous and metachronous thoracic aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg 2012;56:1261–5. https://doi.org/10.1016/j.jvs.2012.04.056 876. Olsen PS, Schroeder T, Agerskov K, Agerskov K, Røder O, Sørensen S, et al. Surgery for abdominal aortic aneurysms. A survey of 656 patients. J Cardiovasc Surg 1991;32: 636–42. 877. Tuveson V, Löfdahl HE, Hultgren R. Patients with abdominal aortic aneurysm have a high prevalence of popliteal artery aneurysms. Vasc Med 2016;21:369–75. https:// doi.org/10.1177/1358863x16648404 878. Brunkwall J, Hauksson H, Bengtsson H, Bergqvist D, Takolander R, Bergentz S-E. Solitary aneurysms of the iliac arterial system: an estimate of their frequency of occurrence. J Vasc Surg 1989;10:381–4. https://doi.org/10.1067/mva.1989.13733 879. Bickerstaff LK, Pairolero PC, Hollier LH, Melton LJ, Van Peenen HJ, Cherry KJ, et al. Thoracic aortic aneurysms: a population-based study. Surgery 1982;92:1103–8. 880. Coady MA, Rizzo JA, Goldstein LJ, Elefteriades JA. Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin 1999;17:615–35; vii. https://doi.org/10.1016/s0733-8651(05)70105-3 881. Diwan A, Sarkar R, Stanley JC, Zelenock GB, Wakefield TW. Incidence of femoral and popliteal artery aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg 2000;31:863–9. https://doi.org/10.1067/mva.2000.105955 882. Brown LC, Thompson SG, Greenhalgh RM, Powell JT. Incidence of cardiovascular events and death after open or endovascular repair of abdominal aortic aneurysm in the randomized EVAR trial 1. Br J Surg 2011;98:935–42. https://doi.org/10.1002/bjs. 7485 883. Hammo S, Grannas D, Wahlgren CM. High risk of early and late cardiovascular events after endovascular aortic aneurysm repair. Ann Vasc Surg 2022;86:320–7. https://doi. org/10.1016/j.avsg.2022.04.028 884. Kuzmik GA, Sang AX, Elefteriades JA. Natural history of thoracic aortic aneurysms. J Vasc Surg 2012;56:565–71. https://doi.org/10.1016/j.jvs.2012.04.053 885. Olsson C, Thelin S, Ståhle E, Ekbom A, Granath F. Thoracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002. Circulation 2006;114:2611–8. https://doi.org/10.1161/circulationaha.106.630400 886. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, et al. 2010 ACCF/ AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation 2010; 121:e266–369. https://doi.org/10.1161/CIR.0b013e3181d4739e 887. Goldfinger JZ, Halperin JL, Marin ML, Stewart AS, Eagle KA, Fuster V. Thoracic aortic aneurysm and dissection. J Am Coll Cardiol 2014;64:1725–39. https://doi.org/10.1016/j. jacc.2014.08.025 888. Caruana M, Baars MJ, Bashiardes E, Benke K, Björck E, Codreanu A, et al. HTAD patient pathway: strategy for diagnostic work-up of patients and families with (suspected) heritable thoracic aortic diseases (HTAD). A statement from the HTAD working group of VASCERN. Eur J Med Genet 2023;66:104673. https://doi.org/10.1016/j. ejmg.2022.104673 889. Patel HJ, Deeb GM. Ascending and arch aorta: pathology, natural history, and treatment. Circulation 2008;118:188–95. https://doi.org/10.1161/circulationaha.107. 690933 890. Boodhwani M, de Kerchove L, Glineur D, Poncelet A, Rubay J, Astarci P, et al. Repair-oriented classification of aortic insufficiency: impact on surgical techniques and clinical outcomes. J Thorac Cardiovasc Surg 2009;137:286–94. https://doi.org/10. 1016/j.jtcvs.2008.08.054 891. Ganapathi AM, Ranney DN, Peterson MD, Lindsay ME, Patel HJ, Pyeritz RE, et al. Location of aortic enlargement and risk of type A dissection at smaller diameters. J Am Coll Cardiol 2022;79:1890–7. https://doi.org/10.1016/j.jacc.2022.02.053 892. Kalogerakos PD, Zafar MA, Li Y, Mukherjee SK, Ziganshin BA, Rizzo JA, et al. Root dilatation is more malignant than ascending aortic dilation. J Am Heart Assoc 2021;10: e020645. https://doi.org/10.1161/jaha.120.020645
ESC Guidelines 3683
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.147
893. Della Corte A, Bancone C, Buonocore M, Dialetto G, Covino FE, Manduca S, et al. Pattern of ascending aortic dimensions predicts the growth rate of the aorta in patients with bicuspid aortic valve. JACC Cardiovasc Imaging 2013;6:1301–10. https:// doi.org/10.1016/j.jcmg.2013.07.009 894. Kim JB, Spotnitz M, Lindsay ME, MacGillivray TE, Isselbacher EM, Sundt TM. Risk of aortic dissection in the moderately dilated ascending aorta. J Am Coll Cardiol 2016;68: 1209–19. https://doi.org/10.1016/j.jacc.2016.06.025 895. Saeyeldin A, Zafar MA, Velasquez CA, Ip K, Gryaznov A, Brownstein AJ, et al. Natural history of aortic root aneurysms in Marfan syndrome. Ann Cardiothorac Surg 2017;6: 625–32. https://doi.org/10.21037/acs.2017.11.10 896. Cheung K, Boodhwani M, Chan KL, Beauchesne L, Dick A, Coutinho T. Thoracic aortic aneurysm growth: role of sex and aneurysm etiology. J Am Heart Assoc 2017;6: e003792. https://doi.org/10.1161/jaha.116.003792 897. Nataf P, Lansac E. Dilation of the thoracic aorta: medical and surgical management. Heart 2006;92:1345–52. https://doi.org/10.1136/hrt.2005.074781 898. Yiu RS, Cheng SW. Natural history and risk factors for rupture of thoracic aortic arch aneurysms. J Vasc Surg 2016;63:1189–94. https://doi.org/10.1016/j.jvs.2015.12.043 899. Coady MA, Rizzo JA, Hammond GL, Mandapati D, Darr U, Kopf GS, et al. What is the appropriate size criterion for resection of thoracic aortic aneurysms? J Thorac Cardiovasc Surg 1997;113:476–91; discussion 489–491. https://doi.org/10.1016/ s0022-5223(97)70360-x 900. Safi HJ, Winnerkvist A, Miller CC, III, Iliopoulos DC, Reardon MJ, Espada R, et al. Effect of extended cross-clamp time during thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 1998;66:1204–8. https://doi.org/10.1016/s0003-4975(98)00781-4 901. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation 2005;111: 816–28. https://doi.org/10.1161/01.Cir.0000154569.08857.7a 902. Zafar MA, Chen JF, Wu J, Li Y, Papanikolaou D, Abdelbaky M, et al. Natural history of descending thoracic and thoracoabdominal aortic aneurysms. J Thorac Cardiovasc Surg 2021;161:498–511.e1. https://doi.org/10.1016/j.jtcvs.2019.10.125 903. Oladokun D, Patterson BO, Sobocinski J, Karthikesalingam A, Loftus I, Thompson MM, et al. Systematic review of the growth rates and influencing factors in thoracic aortic aneurysms. Eur J Vasc Endovasc Surg 2016;51:674–81. https://doi.org/10.1016/j.ejvs. 2016.01.017 904. Davies RR, Goldstein LJ, Coady MA, Tittle SL, Rizzo JA, Kopf GS, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002;73:17–28; discussion 27–18. https://doi.org/10.1016/s0003-4975(01) 03236-2 905. Verloes A, Sakalihasan N, Koulischer L, Limet R. Aneurysms of the abdominal aorta: familial and genetic aspects in three hundred thirteen pedigrees. J Vasc Surg 1995; 21:646–55. https://doi.org/10.1016/s0741-5214(95)70196-6 906. Thompson SG, Brown LC, Sweeting MJ, Bown MJ, Kim LG, Glover MJ, et al. Systematic review and meta-analysis of the growth and rupture rates of small abdominal aortic aneurysms: implications for surveillance intervals and their cost-effectiveness. Health Technol Assess 2013;17:1–118. https://doi.org/10.3310/hta17410 907. Sakalihasan N, Defraigne JO, Kerstenne MA, Cheramy-Bien J-P, Smelser DT, Tromp G, et al. Family members of patients with abdominal aortic aneurysms are at increased risk for aneurysms: analysis of 618 probands and their families from the Liege AAA family study. Ann Vasc Surg 2014;28:787–97. https://doi.org/10.1016/j.avsg.2013.11.005 908. Brown LC, Powell JT. Risk factors for aneurysm rupture in patients kept under ultrasound surveillance. UK small aneurysm trial participants. Ann Surg 1999;230:289–96; discussion 296–287. https://doi.org/10.1097/00000658-199909000-00002 909. Mani K, Wanhainen A. Accurate and reproducible diameter measurement is essential in surveillance and treatment of thoracic aortic aneurysms. Eur J Vasc Endovasc Surg 2014;47:27. https://doi.org/10.1016/j.ejvs.2013.10.004 910. Isselbacher EM, Preventza O, Hamilton Black J, III, Augoustides JG, Beck AW, Bolen MA, et al. 2022 ACC/AHA guideline for the diagnosis and management of aortic disease: a report of the American Heart Association/American College of Cardiology joint committee on clinical practice guidelines. Circulation 2022;146:e334-482. https://doi.org/10.1161/cir.0000000000001106 911. Booher AM, Eagle KA. Diagnosis and management issues in thoracic aortic aneurysm. Am Heart J 2011;162:38–46.e1. https://doi.org/10.1016/j.ahj.2011.04.010 912. Wang TKM, Desai MY. Thoracic aortic aneurysm: optimal surveillance and treatment. Cleve Clin J Med 2020;87:557–68. https://doi.org/10.3949/ccjm.87a.19140-1 913. Roberts DA. Magnetic resonance imaging of thoracic aortic aneurysm and dissection. Semin Roentgenol 2001;36:295–308. https://doi.org/10.1053/sroe.2001.26938 914. Rajiah P. CT and MRI in the evaluation of thoracic aortic diseases. Int J Vasc Med 2013; 2013:797189. https://doi.org/10.1155/2013/797189 915. Lin FY, Devereux RB, Roman MJ, Meng J, Jow VM, Jacobs A, et al. Assessment of the thoracic aorta by multidetector computed tomography: age- and sex-specific reference values in adults without evident cardiovascular disease. J Cardiovasc Comput Tomogr 2008;2:298–308. https://doi.org/10.1016/j.jcct.2008.08.002 916. McPhee JT, Hill JS, Eslami MH. The impact of gender on presentation, therapy, and mortality of abdominal aortic aneurysm in the United States, 2001–2004. J Vasc Surg 2007;45:891–9. https://doi.org/10.1016/j.jvs.2007.01.043 917. Forsdahl SH, Singh K, Solberg S, Jacobsen BK. Risk factors for abdominal aortic aneurysms: a 7-year prospective study: the Tromsø study, 1994–2001. Circulation 2009;119: 2202–8. https://doi.org/10.1161/circulationaha.108.817619 918. Jahangir E, Lipworth L, Edwards TL, Kabagambe EK, Mumma MT, Mensah GA, et al. Smoking, sex, risk factors and abdominal aortic aneurysms: a prospective study of 18 782 persons aged above 65 years in the southern community cohort study. J Epidemiol Community Health 2015;69:481–8. https://doi.org/10.1136/jech-2014- 204920 919. Strachan DP. Predictors of death from aortic aneurysm among middle-aged men: the Whitehall study. Br J Surg 2005;78:401–4. https://doi.org/10.1002/bjs.1800780407 920. Wanhainen A, Bergqvist D, Boman K, Nilsson TK, Rutegård J, Björck M. Risk factors associated with abdominal aortic aneurysm: a population-based study with historical and current data. J Vasc Surg 2005;41:390–6. https://doi.org/10.1016/j.jvs.2005.01.002 921. Kent KC, Zwolak RM, Egorova NN, Riles TS, Manganaro A, Moskowitz AJ, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg 2010;52:539–48. https://doi.org/10.1016/j.jvs.2010.05.090 922. Raffort J, Lareyre F, Clément M, Hassen-Khodja R, Chinetti G, Mallat Z. Diabetes and aortic aneurysm: current state of the art. Cardiovasc Res 2018;114:1702–13. https:// doi.org/10.1093/cvr/cvy174 923. Avdic T, Franzén S, Zarrouk M, Acosta S, Nilsson P, Gottsäter A, et al. Reduced longterm risk of aortic aneurysm and aortic dissection among individuals with type 2 diabetes mellitus: a nationwide observational study. J Am Heart Assoc 2018;7:e007618. https://doi.org/10.1161/jaha.117.007618 924. Nordness MJ, Baxter BT, Matsumura J, Terrin M, Zhang K, Ye F, et al. The effect of diabetes on abdominal aortic aneurysm growth over 2 years. J Vasc Surg 2022;75: 1211–22.e1. https://doi.org/10.1016/j.jvs.2021.10.019 925. Yusuf K, Murat B, Unal A, Ulku K, Taylan K, Ozerdem O, et al. Inflammatory abdominal aortic aneurysm: predictors of long-term outcome in a case-control study. Surgery 2007;141:83–9. https://doi.org/10.1016/j.surg.2006.04.007 926. Oliver-Williams C, Sweeting MJ, Turton G, Parkin D, Cooper D, Rodd C, et al. Lessons learned about prevalence and growth rates of abdominal aortic aneurysms from a 25-year ultrasound population screening programme. Br J Surg 2018;105:68–74. https://doi.org/10.1002/bjs.10715 927. Golledge J, Tsao PS, Dalman RL, Norman PE. Circulating markers of abdominal aortic aneurysm presence and progression. Circulation 2008;118:2382–92. https://doi.org/10. 1161/circulationaha.108.802074 928. Vermeulen JJM, Meijer M, de Vries FBG, Reijnen MMPJ, Holewijn S, Thijssen DHJ, et al. A systematic review summarizing local vascular characteristics of aneurysm wall to predict for progression and rupture risk of abdominal aortic aneurysms. J Vasc Surg 2023;77:288–98.e2. https://doi.org/10.1016/j.jvs.2022.07.008 929. Brady AR, Thompson SG, Fowkes FG, Greenhalgh RM, Powell JT. Abdominal aortic aneurysm expansion: risk factors and time intervals for surveillance. Circulation 2004; 110:16–21. https://doi.org/10.1161/01.Cir.0000133279.07468.9f 930. Malayala SV, Raza A, Vanaparthy R. Gender-based differences in abdominal aortic aneurysm rupture: a retrospective study. J Clin Med Res 2020;12:794–802. https://doi. org/10.14740/jocmr4376 931. Skibba AA, Evans JR, Hopkins SP, Yoon HR, Katras T, Kalbfleisch JH, et al. Reconsidering gender relative to risk of rupture in the contemporary management of abdominal aortic aneurysms. J Vasc Surg 2015;62:1429–36. https://doi.org/10. 1016/j.jvs.2015.07.079 932. Catalano O, Siani A. Ruptured abdominal aortic aneurysm: categorization of sonographic findings and report of 3 new signs. J Ultrasound Med 2005;24:1077–83. https://doi.org/10.7863/jum.2005.24.8.1077 933. Schermerhorn ML, Bensley RP, Giles KA, Hurks R, O’Malley AJ, Cotterill P, et al. Changes in abdominal aortic aneurysm rupture and short-term mortality, 1995-2008: a retrospective observational study. Ann Surg 2012;256:651–8. https:// doi.org/10.1097/SLA.0b013e31826b4f91 934. Rakita D, Newatia A, Hines JJ, Siegel DN, Friedman B. Spectrum of CT findings in rupture and impending rupture of abdominal aortic aneurysms. Radiographics 2007;27: 497–507. https://doi.org/10.1148/rg.272065026 935. Schwartz SA, Taljanovic MS, Smyth S, O’Brien MJ, Rogers LF. CT findings of rupture, impending rupture, and contained rupture of abdominal aortic aneurysms. AJR Am J Roentgenol 2007;188:W57–62. https://doi.org/10.2214/ajr.05.1554 936. Tomee SM, Bulder RMA, Meijer CA, van Berkum I, Hinnen J-W, Schoones JW, et al. Excess mortality for abdominal aortic aneurysms and the potential of strict implementation of cardiovascular risk management: a multifaceted study integrating meta-analysis, national registry, and PHAST and TEDY trial data. Eur J Vasc Endovasc Surg 2023;65:348–57. https://doi.org/10.1016/j.ejvs.2022.11.019 937. Freiberg MS, Arnold AM, Newman AB, Edwards MS, Kraemer KL, Kuller LH. Abdominal aortic aneurysms, increasing infrarenal aortic diameter, and risk of total mortality and incident cardiovascular disease events: 10-year follow-up data from the cardiovascular health study. Circulation 2008;117:1010–7. https://doi.org/10. 1161/circulationaha.107.720219 938. Bown MJ, Sweeting MJ, Brown LC, Powell JT, Thompson SG. Surveillance intervals for small abdominal aortic aneurysms: a meta-analysis. JAMA 2013;309:806–13. https://doi. org/10.1001/jama.2013.950 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.148
939. Dugas A, Therasse E, Kauffmann C, Tang A, Elkouri S, Nozza A, et al. Reproducibility of abdominal aortic aneurysm diameter measurement and growth evaluation on axial and multiplanar computed tomography reformations. Cardiovasc Intervent Radiol 2012;35: 779–87. https://doi.org/10.1007/s00270-011-0259-y 940. Kontopodis N, Metaxa E, Gionis M, Papaharilaou Y, Ioannou CV. Discrepancies in determination of abdominal aortic aneurysms maximum diameter and growth rate, using axial and orhtogonal computed tomography measurements. Eur J Radiol 2013;82: 1398–403. https://doi.org/10.1016/j.ejrad.2013.04.031 941. Foo FJ, Hammond CJ, Goldstone AR, Abuhamdiah M, Rashid ST, West RM, et al. Agreement between computed tomography and ultrasound on abdominal aortic aneurysms and implications on clinical decisions. Eur J Vasc Endovasc Surg 2011;42: 608–14. https://doi.org/10.1016/j.ejvs.2011.07.003 942. Zhu C, Tian B, Leach JR, Liu Q, Lu J, Chen L, et al. Non-contrast 3D black blood MRI for abdominal aortic aneurysm surveillance: comparison with CT angiography. Eur Radiol 2017;27:1787–94. https://doi.org/10.1007/s00330-016-4559-0 943. Sakalihasan N, Michel JB, Katsargyris A, Kuivaniemi H, Defraigne J-O, Nchimi A, et al. Abdominal aortic aneurysms. Nat Rev Dis Primers 2018;4:34. https://doi.org/10.1038/ s41572-018-0030-7 944. Wemmelund H, Jørgensen TM, Høgh A, Behr-Rasmussen C, Johnsen SP, Lindholt JS, et al. Low-dose aspirin and rupture of abdominal aortic aneurysm. J Vasc Surg 2017;65: 616–5.e4. https://doi.org/10.1016/j.jvs.2016.04.061 945. Wanhainen A, Mani K, Kullberg J, Svensjö S, Bersztel A, Karlsson L, et al. The effect of ticagrelor on growth of small abdominal aortic aneurysms–a randomized controlled trial. Cardiovasc Res 2020;116:450–6. https://doi.org/10.1093/cvr/cvz133 946. Golledge J, Thanigaimani S, Powell JT, Tsao PS. Pathogenesis and management of abdominal aortic aneurysm. Eur Heart J 2023;44:2682–97. https://doi.org/10.1093/ eurheartj/ehad386 947. Sweeting MJ, Thompson SG, Brown LC, Powell JT, Collaborators R. Meta-analysis of individual patient data to examine factors affecting growth and rupture of small abdominal aortic aneurysms. Br J Surg 2012;99:655–65. https://doi.org/10.1002/bjs.8707 948. Golledge J, Moxon J, Pinchbeck J, Anderson G, Rowbotham S, Jenkins J, et al. Association between metformin prescription and growth rates of abdominal aortic aneurysms. Br J Surg 2017;104:1486–93. https://doi.org/10.1002/bjs.10587 949. Thanigaimani S, Singh TP, Unosson J, Phie J, Moxon J, Wanhainen A, et al. Editor’s choice—association between metformin prescription and abdominal aortic aneurysm growth and clinical events: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2021;62:747–56. https://doi.org/10.1016/j.ejvs.2021.06.013 950. Wong KHF, Zlatanovic P, Bosanquet DC, Saratzis A, Kakkos SK, Aboyans V, et al. Antithrombotic therapy for aortic aneurysms: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2022;64:544–56. https://doi.org/10.1016/j.ejvs.2022.07.008 951. Newton ER, Akerman AW, Strassle PD, Kibbe MR. Association of fluoroquinolone use with short-term risk of development of aortic aneurysm. JAMA Surg 2021;156:264–72. https://doi.org/10.1001/jamasurg.2020.6165 952. Wee I, Chin B, Syn N, Lee KS, Ng JJ, Choong AMTL. The association between fluoroquinolones and aortic dissection and aortic aneurysms: a systematic review and meta-analysis. Sci Rep 2021;11:11073. https://doi.org/10.1038/s41598-021-90692-8 953. Pasternak B, Inghammar M, Svanström H. Fluoroquinolone use and risk of aortic aneurysm and dissection: nationwide cohort study. BMJ 2018;360:k678. https://doi. org/10.1136/bmj.k678 954. Garg M, Venugopalan V, Vouri SM, Diaby V, Iovine NM, Park H, et al. Oral fluoroquinolones and risk of aortic aneurysm or dissection: a nationwide population-based propensity score-matched cohort study. Pharmacotherapy 2023;43:883–93. https://doi. org/10.1002/phar.2841 955. Fatima K, Uzair SU, Salman A, Jawed A, Husain MA, Shah MG, et al. Fluoroquinolones and the risk of aortic aneurysm or aortic dissection: an updated systematic review and meta-analysis including 53,651,283 patients. Minerva Cardiol Angiol 2023;71:485–93. https://doi.org/10.23736/S2724-5683.22.06124-5 956. LeMaire SA, Zhang L, Luo W, Ren P, Azares AR, Wang Y, et al. Effect of ciprofloxacin on susceptibility to aortic dissection and rupture in mice. JAMA Surg 2018;153: e181804. https://doi.org/10.1001/jamasurg.2018.1804 957. Brown JP, Wing K, Leyrat C, Evans SJ, Mansfield KE, Wong AYS, et al. Association between fluoroquinolone use and hospitalization with aortic aneurysm or aortic dissection. JAMA Cardiol 2023;8:865. https://doi.org/10.1001/jamacardio.2023.2418 958. Gopalakrishnan C, Bykov K, Fischer MA, Connolly JG, Gagne JJ, Fralick M. Association of fluoroquinolones with the risk of aortic aneurysm or aortic dissection. JAMA Intern Med 2020;180:1596–605. https://doi.org/10.1001/jamainternmed.2020.4199 959. Lee CC, Lee MT, Chen YS, Lee S-H, Chen Y-S, Chen S-C, et al. Risk of aortic dissection and aortic aneurysm in patients taking oral fluoroquinolone. JAMA Intern Med 2015; 175:1839–47. https://doi.org/10.1001/jamainternmed.2015.5389 960. Huh K, Kang M, Jung J. Lack of association between fluoroquinolone and aortic aneurysm or dissection. Eur Heart J 2023;44:4476–84. https://doi.org/10.1093/eurheartj/ ehad627 961. Klotz S, Stock S, Sievers HH, Diwoky M, Petersen M, Stierle U, et al. Survival and reoperation pattern after 20 years of experience with aortic valve-sparing root replacement in patients with tricuspid and bicuspid valves. J Thorac Cardiovasc Surg 2018;155: 1403–11.e1. https://doi.org/10.1016/j.jtcvs.2017.12.039 962. Lee H, Cho YH, Sung K, Kim WS, Park K-H, Jeong DS, et al. Clinical outcomes of root reimplantation and Bentall procedure: propensity score matching analysis. Ann Thorac Surg 2018;106:539–47. https://doi.org/10.1016/j.athoracsur.2018.02.057 963. Mastrobuoni S, de Kerchove L, Navarra E, Watremez C, Vancraeynest D, Rubay J, et al. Long-term experience with valve-sparing reimplantation technique for the treatment of aortic aneurysm and aortic regurgitation. J Thorac Cardiovasc Surg 2019;158:14–23. https://doi.org/10.1016/j.jtcvs.2018.10.155 964. Leontyev S, Schamberger L, Davierwala PM, Von Aspern K, Etz C, Lehmann S, et al. Early and late results after David vs Bentall procedure: a propensity matched analysis. Ann Thorac Surg 2020;110:120–6. https://doi.org/10.1016/j.athoracsur.2019.10.020 965. Elbatarny M, Tam DY, Edelman JJ, Rocha RV, Chu MWA, Peterson MD, et al. Valve-sparing root replacement versus composite valve grafting in aortic root dilation: a meta-analysis. Ann Thorac Surg 2020;110:296–306. https://doi.org/10.1016/j. athoracsur.2019.11.054 966. Leyh RG, Fischer S, Kallenbach K, Kofidis T, Pethig K, Harringer W, et al. High failure rate after valve-sparing aortic root replacement using the “remodeling technique” in acute type A aortic dissection. Circulation 2002;106:I229–33. 967. Schäfers H, Fries R, Langer F, Nikoloudakis N, Graeter T, Grundmann U. Valve-preserving replacement of the ascending aorta: remodeling versus reimplantation. J Thorac Cardiovasc Surg 1998;116:990–6. https://doi.org/10.1016/s0022- 5223(98)70051-0 968. Rahnavardi M, Yan TD, Bannon PG, Wilson MK. Aortic valve-sparing operations in aortic root aneurysms: remodeling or reimplantation? Interact Cardiovasc Thorac Surg 2011;13:189–97. https://doi.org/10.1510/icvts.2011.267401 969. Vahanian A, Beyersdorf F, Praz F, Milojevic M, Baldus S, Bauersachs J, et al. 2021 ESC/ EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2022;43: 561–632. https://doi.org/10.1093/eurheartj/ehab395 970. Mok CK, Boey J, Wang R, Chan TK, Cheung KL, Lee PK, et al. Warfarin versus dipyridamole-aspirin and pentoxifylline-aspirin for the prevention of prosthetic heart valve thromboembolism: a prospective randomized clinical trial. Circulation 1985;72: 1059–63. https://doi.org/10.1161/01.cir.72.5.1059 971. Cannegieter SC, Rosendaal FR, Briët E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation 1994;89:635–41. https:// doi.org/10.1161/01.cir.89.2.635 972. Brennan JM, Edwards FH, Zhao Y, O’Brien S, Booth ME, Dokholyan RS, et al. Early anticoagulation of bioprosthetic aortic valves in older patients: results from the Society of Thoracic Surgeons Adult Cardiac Surgery National Database. J Am Coll Cardiol 2012; 60:971–7. https://doi.org/10.1016/j.jacc.2012.05.029 973. Rafiq S, Steinbrüchel DA, Lilleør NB, Møller CH, Lund JT, Thiis JJ, et al. Antithrombotic therapy after bioprosthetic aortic valve implantation: warfarin versus aspirin, a randomized controlled trial. Thromb Res 2017;150:104–10. https://doi.org/10.1016/j. thromres.2016.11.021 974. Czerny M, Rylski B, Della Corte A, Krüger T. Decision-making to perform elective surgery for patients with proximal thoracic aortic pathology: a European perspective. J Thorac Cardiovasc Surg 2022;163:2025–30. https://doi.org/10.1016/j.jtcvs.2021.01.141 975. Vorp DA, Schiro BJ, Ehrlich MP, Juvonen TS, Ergin MA, Griffith BP. Effect of aneurysm on the tensile strength and biomechanical behavior of the ascending thoracic aorta. Ann Thorac Surg 2003;75:1210–4. https://doi.org/10.1016/s0003-4975(02)04711-2 976. Della Corte A, Lo Presti F, Saade W, Rubino AS, Palmieri L, Patanè F, et al. Acute type A aortic dissection in bicuspid versus tricuspid aortic valve patients: focus on geometrical features of the aorta. Eur J Cardiothorac Surg 2023;63:ezac576. https://doi.org/10. 1093/ejcts/ezac576 977. Mullan CW, Mori M, Bin Mahmood SU, Yousef S, Mangi AA, Elefteriades JA, et al. Incidence and characteristics of hospitalization for proximal aortic surgery for acute syndromes and for aneurysms in the USA from 2005 to 2014. Eur J Cardiothorac Surg 2020;58:583–9. https://doi.org/10.1093/ejcts/ezaa067 978. Williams JB, Peterson ED, Zhao Y, O’Brien SM, Andersen ND, Miller DC, et al. Contemporary results for proximal aortic replacement in North America. J Am Coll Cardiol 2012;60:1156–62. https://doi.org/10.1016/j.jacc.2012.06.023 979. Wallen T, Habertheuer A, Bavaria JE, Hughes GC, Badhwar V, Jacobs JP, et al. Elective aortic root replacement in North America: analysis of STS adult cardiac surgery database. Ann Thorac Surg 2019;107:1307–12. https://doi.org/10.1016/j.athoracsur.2018. 12.039 980. Mori M, Shioda K, Wang X, Mangi AA, Yun JJ, Darr U, et al. Perioperative risk profiles and volume-outcome relationships in proximal thoracic aortic surgery. Ann Thorac Surg 2018;106:1095–104. https://doi.org/10.1016/j.athoracsur.2018.05.081 981. Wojnarski CM, Svensson LG, Roselli EE, Idrees JJ, Lowry AM, Ehrlinger J, et al. Aortic dissection in patients with bicuspid aortic valve-associated aneurysms. Ann Thorac Surg 2015;100:1666–73; discussion 1673–74. https://doi.org/10.1016/j.athoracsur.2015.04. 126 982. Wu J, Zafar MA, Liu Y, Chen JF, Li Y, Ziganshin BA, et al. Fate of the unoperated ascending thoracic aortic aneurysm: three-decade experience from the Aortic Institute at Yale University. Eur Heart J 2023;44:4579–88. https://doi.org/10.1093/ eurheartj/ehad148
ESC Guidelines 3685
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.149
983. Ziganshin BA, Zafar MA, Elefteriades JA. Descending threshold for ascending aortic aneurysmectomy: is it time for a “left-shift” in guidelines? J Thorac Cardiovasc Surg 2019; 157:37–42. https://doi.org/10.1016/j.jtcvs.2018.07.114 984. Rylski B, Branchetti E, Bavaria JE, Vallabhajosyula P, Szeto WY, Milewski RK, et al. Modeling of predissection aortic size in acute type A dissection: more than 90% fail to meet the guidelines for elective ascending replacement. J Thorac Cardiovasc Surg 2014;148:944–8.e1. https://doi.org/10.1016/j.jtcvs.2014.05.050 985. Mansour AM, Peterss S, Zafar MA, Rizzo JA, Fang H, Charilaou P, et al. Prevention of aortic dissection suggests a diameter shift to a lower aortic size threshold for intervention. Cardiology 2018;139:139–46. https://doi.org/10.1159/000481930 986. Masri A, Kalahasti V, Alkharabsheh S, Svensson LG, Sabik JF, Roselli EE, et al. Characteristics and long-term outcomes of contemporary patients with bicuspid aortic valves. J Thorac Cardiovasc Surg 2016;151:1650–9.e1. https://doi.org/10.1016/j.jtcvs. 2015.12.019 987. Winkler A, Puiu P, Krombholz-Reindl P, Vötsch A, Steindl J, Neuner M, et al. Impact of concomitant replacement of the ascending aorta in patients undergoing aortic valve replacement on operative morbidity and mortality. Eur J Cardiothorac Surg 2022;61: 587–93. https://doi.org/10.1093/ejcts/ezab420 988. Peterss S, Charilaou P, Dumfarth J, Li Y, Bhandari R, Tranquilli M, et al. Aortic valve disease with ascending aortic aneurysm: impact of concomitant root-sparing (supracoronary) aortic replacement in nonsyndromic patients. J Thorac Cardiovasc Surg 2016;152:791–8.e1. https://doi.org/10.1016/j.jtcvs.2016.05.020 989. Lim JY, Jung SH, Kim JB, Kim DK, Chung CH, Song H, et al. Concomitant replacement of the dilated ascending aorta during aortic valve replacement; does it increase the perioperative morbidity and mortality risks? J Card Surg 2013;28:285–90. https://doi. org/10.1111/jocs.12111 990. Idrees JJ, Roselli EE, Lowry AM, Reside JM, Javadikasgari H, Johnson DJ, et al. Outcomes after elective proximal aortic replacement: a matched comparison of isolated versus multicomponent operations. Ann Thorac Surg 2016;101:2185–92. https://doi.org/10. 1016/j.athoracsur.2015.12.026 991. Idrees JJ, Roselli EE, Blackstone EH, Lowry AM, Soltesz EG, Johnston DR, et al. Risk of adding prophylactic aorta replacement to a cardiac operation. J Thorac Cardiovasc Surg 2020;159:1669–78.e10. https://doi.org/10.1016/j.jtcvs.2019.05.001 992. Grabenwöger M, Alfonso F, Bachet J, Bonser R, Czerny M, Eggebrecht H, et al. Thoracic Endovascular Aortic Repair (TEVAR) for the treatment of aortic diseases: a position statement from the European Association for Cardio-Thoracic Surgery (EACTS) and the European Society of Cardiology (ESC), in collaboration with the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2012;33:1558–63. https://doi.org/10.1093/eurheartj/ehs074 993. Eggebrecht H, Thompson M, Rousseau H, Czerny M, Lönn L, Mehta RH, et al. Retrograde ascending aortic dissection during or after thoracic aortic stent graft placement: insight from the European registry on endovascular aortic repair complications. Circulation 2009;120:S276–281. https://doi.org/10.1161/circulationaha.108.835926 994. Zerwes S, Leissner G, Gosslau Y, Jakob R, Bruijnen H-K, Oertl F, et al. Clinical outcomes in hybrid repair procedures for pathologies involving the aortic arch. Vascular 2015;23:9–16. https://doi.org/10.1177/1708538114525608 995. Czerny M, Weigang E, Sodeck G, Schmidli J, Antona C, Gelpi G, et al. Targeting landing zone 0 by total arch rerouting and TEVAR: midterm results of a transcontinental registry. Ann Thorac Surg 2012;94:84–9. https://doi.org/10.1016/j.athoracsur.2012.03.024 996. Chiesa R, Melissano G, Tshomba Y, Civilini E, Marone EM, Bertoglio L, et al. Ten years of endovascular aortic arch repair. J Endovasc Ther 2010;17:1–11. https://doi.org/10. 1583/09-2884.1 997. Shrestha M, Bachet J, Bavaria J, Carrel TP, De Paulis R, Di Bartolomeo R, et al. Current status and recommendations for use of the frozen elephant trunk technique: a position paper by the vascular domain of EACTS. Eur J Cardiothorac Surg 2015;47:759–69. https://doi.org/10.1093/ejcts/ezv085 998. Czerny M, Schmidli J, Adler S, van den Berg JC, Bertoglio L, Carrel T, et al. Current options and recommendations for the treatment of thoracic aortic pathologies involving the aortic arch: an expert consensus document of the European Association for Cardio-Thoracic Surgery (EACTS) and the European Society for Vascular Surgery (ESVS). Eur J Cardiothorac Surg 2019;55:133–62. https://doi.org/10.1093/ejcts/ezy313 999. Abjigitova D, Veen KM, van Tussenbroek G, Mokhles MM, Bekkers JA, Takkenberg JJM, et al. Cerebral protection in aortic arch surgery: systematic review and meta-analysis. Interact Cardiovasc Thorac Surg 2022;35:ivac270. https://doi.org/10.1093/icvts/ivac128 1000. Malaisrie SC, Duncan BF, Mehta CK, Badiwala MV, Rinewalt D, Kruse J, et al. The addition of hemiarch replacement to aortic root surgery does not affect safety. J Thorac Cardiovasc Surg 2015;150:118–24.e2. https://doi.org/10.1016/j.jtcvs.2015.03.020 1001. Borger MA, Fedak PWM, Stephens EH, Gleason TG, Girdauskas E, Ikonomidis JS, et al. The American Association for Thoracic Surgery consensus guidelines on bicuspid aortic valve-related aortopathy: full online-only version. J Thorac Cardiovasc Surg 2018;156:e41–74. https://doi.org/10.1016/j.jtcvs.2018.02.115 1002. Kim JB, Kim K, Lindsay ME, MacGillivray T, Isselbacher EM, Cambria RP, et al. Risk of rupture or dissection in descending thoracic aortic aneurysm. Circulation 2015;132: 1620–9. https://doi.org/10.1161/circulationaha.114.015177 1003. Chen JF, Zafar MA, Wu J, Li Y, Rizzo JA, Papanikolaou D, et al. Increased virulence of descending thoracic and thoracoabdominal aortic aneurysms in women. Ann Thorac Surg 2021;112:45–52. https://doi.org/10.1016/j.athoracsur.2020.08.026 1004. Lobato AC, Puech-Leão P. Predictive factors for rupture of thoracoabdominal aortic aneurysm. J Vasc Surg 1998;27:446–53. https://doi.org/10.1016/s0741-5214(98) 70319-2 1005. Harris DG, Olson SL, Panthofer AM, Matsumura JS, DiMusto PD. A frailty-based risk score predicts morbidity and mortality after elective endovascular repair of descending thoracic aortic aneurysms. Ann Vasc Surg 2020;67:90–9. https://doi.org/10.1016/j. avsg.2019.10.090 1006. Goodney PP, Travis L, Lucas FL, Fillinger MF, Goodman DC, Cronenwett JL, et al. Survival after open versus endovascular thoracic aortic aneurysm repair in an observational study of the Medicare population. Circulation 2011;124:2661–9. https://doi. org/10.1161/circulationaha.111.033944 1007. Grausgruber W, Scharfen E. Problems of the fight against zoonoses in Austria. Wien Tierarztl Monatsschr 1968;55:625–36. 1008. Chiu P, Goldstone AB, Schaffer JM, Lingala B, Miller DC, Mitchell RS, et al. Endovascular versus open repair of intact descending thoracic aortic aneurysms. J Am Coll Cardiol 2019;73:643–51. https://doi.org/10.1016/j.jacc.2018.10.086 1009. Fairman RM, Criado F, Farber M, Kwolek C, Mehta M, White R, et al. Pivotal results of the medtronic vascular talent thoracic stent graft system: the VALOR trial. J Vasc Surg 2008;48:546–54.e2. https://doi.org/10.1016/j.jvs.2008.03.061 1010. Matsumura JS, Cambria RP, Dake MD, Moore RD, Svensson LG, Snyder S. International controlled clinical trial of thoracic endovascular aneurysm repair with the Zenith TX2 endovascular graft: 1-year results. J Vasc Surg 2008;47:247–57; discussion 257. https://doi.org/10.1016/j.jvs.2007.10.032 1011. Coselli JS, Bozinovski J, LeMaire SA. Open surgical repair of 2286 thoracoabdominal aortic aneurysms. Ann Thorac Surg 2007;83:S862–4; discussion S890–862. https://doi. org/10.1016/j.athoracsur.2006.10.088 1012. Coselli JS, Green SY, Price MD, Hash JA, Ouyang Y, Volguina IV, et al. Results of open surgical repair in patients with Marfan syndrome and distal aortic dissection. Ann Thorac Surg 2016;101:2193–201. https://doi.org/10.1016/j.athoracsur.2015.11.008 1013. Tong MZ, Eagleton MJ, Roselli EE, Blackstone EH, Xiang F, Ibrahim M, et al. Outcomes of open versus endovascular repair of descending thoracic and thoracoabdominal aortic aneurysms. Ann Thorac Surg 2022;113:1144–52. https://doi.org/10.1016/j. athoracsur.2021.04.100 1014. Goldstein LJ, Davies RR, Rizzo JA, Davila JJ, Cooperberg MR, Shaw RK, et al. Stroke in surgery of the thoracic aorta: incidence, impact, etiology, and prevention. J Thorac Cardiovasc Surg 2001;122:935–45. https://doi.org/10.1067/mtc.2001.117276 1015. Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357– 68; discussion 368–70. 1016. Schermerhorn ML, Giles KA, Hamdan AD, Dalhberg SE, Hagberg R, Pomposelli F. Population-based outcomes of open descending thoracic aortic aneurysm repair. J Vasc Surg 2008;48:821–7. https://doi.org/10.1016/j.jvs.2008.05.022 1017. Yamauchi T, Takano H, Nishimura M, Matsumiya G, Sawa Y. Paraplegia and paraparesis after descending thoracic aortic aneurysm repair: a risk factor analysis. Ann Thorac Cardiovasc Surg 2006;12:179–83. 1018. Patel VI, Mukhopadhyay S, Ergul E, Aranson N, Conrad MF, LaMuraglia GM, et al. Impact of hospital volume and type on outcomes of open and endovascular repair of descending thoracic aneurysms in the United States Medicare population. J Vasc Surg 2013;58:346–54. https://doi.org/10.1016/j.jvs.2013.01.035 1019. Cheng D, Martin J, Shennib H, Dunning J, Muneretto C, Schueler S, et al. Endovascular aortic repair versus open surgical repair for descending thoracic aortic disease a systematic review and meta-analysis of comparative studies. J Am Coll Cardiol 2010;55: 986–1001. https://doi.org/10.1016/j.jacc.2009.11.047 1020. Harky A, Kai Chan JS, Ming Wong CH, Bashir M. Open versus endovascular repair of descending thoracic aortic aneurysm disease: a systematic review and meta-analysis. Ann Vasc Surg 2019;54:304–15.e5. https://doi.org/10.1016/j.avsg.2018.05.043 1021. Ranney DN, Cox ML, Yerokun BA, Benrashid E, McCann RL, Hughes GC. Long-term results of endovascular repair for descending thoracic aortic aneurysms. J Vasc Surg 2018;67:363–8. https://doi.org/10.1016/j.jvs.2017.06.094 1022. Biancari F, Mariscalco G, Mariani S, Saari P, Satta J, Juvonen T. Endovascular treatment of degenerative aneurysms involving only the descending thoracic aorta: systematic review and meta-analysis. J Endovasc Ther 2016;23:387–92. https://doi.org/10.1177/ 1526602815626560 1023. Mousa AY, Morcos R, Broce M, Bates MC, AbuRahma AF. New preoperative spinal cord ischemia risk stratification model for patients undergoing thoracic endovascular aortic repair. Vasc Endovascular Surg 2020;54:487–96. https://doi.org/10.1177/ 1538574420929135 1024. Walsh SR, Tang TY, Sadat U, Naik J, Gaunt ME, Boyle JR, et al. Endovascular stenting versus open surgery for thoracic aortic disease: systematic review and meta-analysis of perioperative results. J Vasc Surg 2008;47:1094–8.e3. https://doi.org/10.1016/j.jvs. 2007.09.062 1025. Kotelis D, Geisbüsch P, Hinz U, Hyhlik-Dürr A, von Tengg-Kobligk H, Allenberg JR, et al. Short and midterm results after left subclavian artery coverage during Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.150
endovascular repair of the thoracic aorta. J Vasc Surg 2009;50:1285–92. https://doi. org/10.1016/j.jvs.2009.07.106 1026. Cooper DG, Walsh SR, Sadat U, Noorani A, Hayes PD, Boyle JR, et al. Neurological complications after left subclavian artery coverage during thoracic endovascular aortic repair: a systematic review and meta-analysis. J Vasc Surg 2009;49:1594–601. https://doi.org/10.1016/j.jvs.2008.12.075 1027. Buth J, Harris PL, Hobo R, van Eps R, Cuypers P, Duijm L, et al. Neurologic complications associated with endovascular repair of thoracic aortic pathology: incidence and risk factors. a study from the European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry. J Vasc Surg 2007;46:1103–10; discussion 1110–1. https://doi.org/10.1016/j.jvs.2007.08.020 1028. Teixeira PG, Woo K, Beck AW, Scali ST, Weaver FA. Association of left subclavian artery coverage without revascularization and spinal cord ischemia in patients undergoing thoracic endovascular aortic repair: a Vascular Quality Initiative® analysis. Vascular 2017;25:587–97. https://doi.org/10.1177/1708538116681910 1029. Chen X, Wang J, Premaratne S, Zhao J, Zhang WW. Meta-analysis of the outcomes of revascularization after intentional coverage of the left subclavian artery for thoracic endovascular aortic repair. J Vasc Surg 2019;70:1330–40. https://doi.org/10.1016/j.jvs. 2019.03.022 1030. Banno H, Ikeda S, Kawai Y, Meshii K, Takahashi N, Sugimoto M, et al. Early and midterm outcomes of celiac artery coverage during thoracic endovascular aortic repair. J Vasc Surg 2020;72:1552–7. https://doi.org/10.1016/j.jvs.2020.02.025 1031. Argyriou C, Spiliopoulos S, Katsanos K, Papatheodorou N, Lazarides MK, Georgiadis GS. Safety and efficacy of intentional celiac artery coverage in endovascular management of thoracoabdominal aortic diseases: a systematic review and meta-analysis. J Endovasc Ther 2022;29:646–58. https://doi.org/10.1177/15266028211059451 1032. Hanna L, Lam K, Agbeko AE, Amoako JK, Ashrafian H, Sounderajah V, et al. Coverage of the coeliac artery during thoracic endovascular aortic repair: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2022;63:828–37. https://doi.org/10.1016/j. ejvs.2022.02.026 1033. Cambria RA, Gloviczki P, Stanson AW, Cherry KJ, Bower TC, Hallett JW, et al. Outcome and expansion rate of 57 thoracoabdominal aortic aneurysms managed nonoperatively. Am J Surg 1995;170:213–7. https://doi.org/10.1016/s0002-9610(99) 80289-x 1034. Elefteriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann Thorac Surg 2002;74:S1877–80; discussion S1892–8. https://doi.org/10.1016/s0003-4975(02)04147-4 1035. Girardi LN, Ohmes LB, Lau C, Di Franco A, Gambardella I, Elsayed M, et al. Open repair of descending thoracic and thoracoabdominal aortic aneurysms in patients with preoperative renal failure. Eur J Cardiothorac Surg 2017;51:971–7. https://doi. org/10.1093/ejcts/ezx007 1036. LeMaire SA, Miller CC, III, Conklin LD, Schmittling ZC, Köksoy C, Coselli JS, et al. A new predictive model for adverse outcomes after elective thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 2001;71:1233–8. https://doi.org/10.1016/s0003- 4975(00)02678-3 1037. Suzuki S, Davis CA, III, Miller CC, III, Huynh TT, Estrera AL, Porat EE, et al. Cardiac function predicts mortality following thoracoabdominal and descending thoracic aortic aneurysm repair. Eur J Cardiothorac Surg 2003;24:119–24; discussion 124. https:// doi.org/10.1016/s1010-7940(03)00170-2 1038. Mohebali J, Carvalho S, Lancaster RT, Ergul EA, Conrad MF, Clouse WD, et al. Use of extracorporeal bypass is associated with improved outcomes in open thoracic and thoracoabdominal aortic aneurysm repair. J Vasc Surg 2018;68:941–7. https://doi. org/10.1016/j.jvs.2017.12.072 1039. Coselli JS, LeMaire SA, Preventza O, de la Cruz KI, Cooley DA, Price MD, et al. Outcomes of 3309 thoracoabdominal aortic aneurysm repairs. J Thorac Cardiovasc Surg 2016;151:1323–38. https://doi.org/10.1016/j.jtcvs.2015.12.050 1040. Drinkwater SL, Goebells A, Haydar A, Bourke P, Brown L, Hamady M, et al.. The incidence of spinal cord ischaemia following thoracic and thoracoabdominal aortic endovascular intervention. Eur J Vasc Endovasc Surg 2010;40:729–35. https://doi.org/10. 1016/j.ejvs.2010.08.013 1041. Bicknell CD, Riga CV, Wolfe JH. Prevention of paraplegia during thoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg 2009;37:654–60. https://doi.org/ 10.1016/j.ejvs.2009.02.008 1042. Von Aspern K, Luehr M, Mohr FW, Etz CD. Spinal cord protection in open- and endovascular thoracoabdominal aortic aneurysm repair: critical review of current concepts and future perspectives. J Cardiovasc Surg (Torino) 2015;56:745–9. 1043. Hsu CC, Kwan GN, van Driel ML, Rophael JA. Distal aortic perfusion during thoracoabdominal aneurysm repair for prevention of paraplegia. Cochrane Database Syst Rev 2012;3:CD008197. https://doi.org/10.1002/14651858.CD008197.pub2 1044. Bischoff MS, Di Luozzo G, Griepp EB, Griepp RB. Spinal cord preservation in thoracoabdominal aneurysm repair. Perspect Vasc Surg Endovasc Ther 2011;23:214–22. https://doi.org/10.1177/1531003511400622 1045. Cowan JA, Jr, Dimick JB, Henke PK, Huber TS, Stanley JC, Upchurch GR. Surgical treatment of intact thoracoabdominal aortic aneurysms in the United States: hospital and surgeon volume-related outcomes. J Vasc Surg 2003;37:1169–74. https://doi.org/ 10.1016/s0741-5214(03)00085-5 1046. Rigberg DA, McGory ML, Zingmond DS, Maggard MA, Agustin M, Lawrence PF, et al. Thirty-day mortality statistics underestimate the risk of repair of thoracoabdominal aortic aneurysms: a statewide experience. J Vasc Surg 2006;43:217–22; discussion 223. https://doi.org/10.1016/j.jvs.2005.10.070 1047. Pomy BJ, Rosenfeld ES, Lala S, Lee KB, Sparks AD, Amdur RL, et al. Fenestrated endovascular aneurysm repair affords fewer renal complications than open surgical repair for juxtarenal abdominal aortic aneurysms in patients with chronic renal insufficiency. Ann Vasc Surg 2021;75:349–57. https://doi.org/10.1016/j.avsg.2021.03. 026 1048. Varkevisser RRB, O’Donnell TFX, Swerdlow NJ, Liang P, Li C, Ultee KHJ, et al. Fenestrated endovascular aneurysm repair is associated with lower perioperative morbidity and mortality compared with open repair for complex abdominal aortic aneurysms. J Vasc Surg 2019;69:1670–8. https://doi.org/10.1016/j.jvs.2018.08.192 1049. Gallitto E, Faggioli G, Melissano G, Fargion A, Isernia G, Lenti M, et al. Preoperative and postoperative predictors of clinical outcome of fenestrated and branched endovascular repair for complex abdominal and thoracoabdominal aortic aneurysms in an Italian multicenter registry. J Vasc Surg 2021;74:1795–806.e6. https://doi.org/10.1016/ j.jvs.2021.04.072 1050. Silverberg D, Bar-Dayan A, Hater H, Khaitovich B, Halak M. Short-term outcomes of inner branches for endovascular repair of complex abdominal and thoracoabdominal aortic aneurysms. Vascular 2021;29:644–51. https://doi.org/10.1177/ 1708538120977279 1051. Hu Z, Li Y, Peng R, Liu J, Jia X, Liu X, et al. Multibranched stent-grafts for the treatment of thoracoabdominal aortic aneurysms: a systematic review and meta-analysis. J Endovasc Ther 2016;23:626–33. https://doi.org/10.1177/1526602816647723 1052. Simonte G, Isernia G, Gatta E, Neri E, Parlani G, Candeloro L, et al. Inner branched complex aortic repair outcomes from a national multicenter registry using the E-xtra design platform. J Vasc Surg 2023;77:338–46. https://doi.org/10.1016/j.jvs.2022.08. 034 1053. Gallitto E, Faggioli G, Pini R, Logiacco A, Mascoli C, Fenelli C, et al. Proximal aortic coverage and clinical results of the endovascular repair of juxta-/para-renal and type IV thoracoabdominal aneurysm with custom-made fenestrated endografts. Ann Vasc Surg 2021;73:397–406. https://doi.org/10.1016/j.avsg.2020.12.008 1054. Sultan S, Concannon J, Veerasingam D, Tawfick W, McHugh P, Jordan F, et al. Endovascular versus conventional open surgical repair for thoracoabdominal aortic aneurysms. Cochrane Database Syst Rev 2022;4:CD012926. https://doi.org/10.1002/ 14651858.CD012926.pub2 1055. Kölbel T, Spanos K, Jama K, Behrendt CA, Panuccio G, Eleshra A, et al. Early outcomes of the t-Branch off-the-shelf multi-branched stent graft in 542 patients for elective and urgent aortic pathologies: a retrospective observational study. J Vasc Surg 2021;74:1817–24. https://doi.org/10.1016/j.jvs.2021.05.041 1056. Oderich GS, Ribeiro M, Hofer J, Wigham J, Cha S, Chini J, et al. Prospective, nonrandomized study to evaluate endovascular repair of pararenal and thoracoabdominal aortic aneurysms using fenestrated-branched endografts based on supraceliac sealing zones. J Vasc Surg 2017;65:1249–59.e10. https://doi.org/10.1016/j.jvs.2016.09.038 1057. Oderich GS, Tenorio ER, Mendes BC, Lima GBB, Marcondes GB, Saqib N, et al. Midterm outcomes of a prospective, nonrandomized study to evaluate endovascular repair of complex aortic aneurysms using fenestrated-branched endografts. Ann Surg 2021;274:491–9. https://doi.org/10.1097/sla.0000000000004982 1058. Konstantinou N, Antonopoulos CN, Jerkku T, Banafsche R, Kölbel T, Fiorucci B, et al. Systematic review and meta-analysis of published studies on endovascular repair of thoracoabdominal aortic aneurysms with the t-Branch off-the-shelf multibranched endograft. J Vasc Surg 2020;72:716–25.e1. https://doi.org/10.1016/j.jvs.2020.01.049 1059. Ellahi A, Shaikh FN, Kashif H, Khan H, Ali E, Nasim B, et al. Effectiveness of endovascular repair versus open surgery for the treatment of thoracoabdominal aneurysm: a systematic review and meta analysis. Ann Med Surg 2022;81:104477. https://doi.org/ 10.1016/j.amsu.2022.104477 1060. Hongku K, Sonesson B, Bjorses K, Holst J, Resch T, Dias NV, et al. Mid-term Outcomes of Endovascular Repair of Ruptured Thoraco-abdominal Aortic Aneurysms with Off the Shelf Branched Stent Grafts. Eur J Vasc Endovasc Surg 2018;55:377–84. https://doi.org/10.1016/j.ejvs.2017.11.021 1061. Youssef M, Deglise S, Szopinski P, Jost-Philipp S, Jomha A, Vahl CF, et al. A multicenter experience with a new fenestrated-branched device for endovascular repair of thoracoabdominal aortic aneurysms. J Endovasc Ther 2018;25:209–19. https://doi.org/10. 1177/1526602817752147 1062. Ouzounian M, Tadros RO, Svensson LG, Lyden SP, Oderich GS, Coselli JS Thoracoabdominal aortic disease and repair: JACC focus seminar, part 3. J Am Coll Cardiol 2022;80:845–56. https://doi.org/10.1016/j.jacc.2021.05.056 1063. Hofmann Bowman MA, Eagle KA, Milewicz DM. Update on clinical trials of losartan with and without β-blockers to block aneurysm growth in patients with Marfan syndrome: a review. JAMA Cardiol 2019;4:702–7. https://doi.org/10.1001/jamacardio. 2019.1176 1064. Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. The UK Small Aneurysm Trial Participants. Lancet 1998;352:1649–55.
ESC Guidelines 3687
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.151
1065. Powell JT, Brady AR, Brown LC, Fowkes FG, Greenhalgh RM, Ruckley CV, et al. Long-term outcomes of immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med 2002;346:1445–52. https://doi.org/10. 1056/NEJMoa013527 1066. Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN, Acher CW, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med 2002;346:1437–44. https://doi.org/10.1056/NEJMoa012573 1067. Shirasu T, Takagi H, Yasuhara J, Kuno T, Kent KC, Clouse WD. Smaller size is more suitable for pharmacotherapy among undersized abdominal aortic aneurysm: a systematic review and meta-analysis. Vasc Med 2022;27:261–8. https://doi.org/10. 1177/1358863x211061603 1068. Ouriel K, Clair DG, Kent KC, Zarins CK. Endovascular repair compared with surveillance for patients with small abdominal aortic aneurysms. J Vasc Surg 2010;51:1081–7. https://doi.org/10.1016/j.jvs.2009.10.113 1069. Golledge J, Parr A, Boult M, Maddern G, Fitridge R. The outcome of endovascular repair of small abdominal aortic aneurysms. Ann Surg 2007;245:326–33. https://doi.org/ 10.1097/01.sla.0000253965.95368.52 1070. Filardo G, Powell JT, Martinez MA, Ballard DJ. Surgery for small asymptomatic abdominal aortic aneurysms. Cochrane Database Syst Rev 2015;2:CD001835. https:// doi.org/10.1002/14651858.CD001835.pub4 1071. Cao P, De Rango P, Verzini F, Parlani G, Romano L, Cieri E. Comparison of surveillance versus aortic endografting for small aneurysm repair (CAESAR): results from a randomised trial. Eur J Vasc Endovasc Surg 2011;41:13–25. https://doi.org/10.1016/j. ejvs.2010.08.026 1072. Lo RC, Lu B, Fokkema MT, Conrad M, Patel VI, Fillinger M, et al. Relative importance of aneurysm diameter and body size for predicting abdominal aortic aneurysm rupture in men and women. J Vasc Surg 2014;59:1209–16. https://doi.org/10.1016/j.jvs. 2013.10.104 1073. Bath MF, Gokani VJ, Sidloff DA, Jones LR, Choke E, Sayers RD, et al. Systematic review of cardiovascular disease and cardiovascular death in patients with a small abdominal aortic aneurysm. Br J Surg 2015;102:866–72. https://doi.org/10.1002/bjs.9837 1074. Kristensen SD, Knuuti J. New ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management. Eur Heart J 2014;35:2344–5. https://doi.org/10. 1093/eurheartj/ehu285 1075. Devereaux PJ, Chan MT, Alonso-Coello P, Walsh M, Berwanger O, Villar JC, et al. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery. JAMA 2012;307:2295–304. https://doi.org/10. 1001/jama.2012.5502 1076. EVAR trial participants. Endovascular aneurysm repair versus open repair in patients with abdominal aortic aneurysm (EVAR trial 1): randomised controlled trial. Lancet 2005;365:2179–86. https://doi.org/10.1016/s0140-6736(05)66627-5 1077. Lederle FA, Freischlag JA, Kyriakides TC, Padberg FT, Jr, Matsumura JS, Kohler TR, et al. Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial. JAMA 2009;302:1535–42. https://doi.org/10.1001/jama.2009.1426 1078. Becquemin JP, Pillet JC, Lescalie F, Sapoval M, Goueffic Y, Lermusiaux P, et al. A randomized controlled trial of endovascular aneurysm repair versus open surgery for abdominal aortic aneurysms in low- to moderate-risk patients. J Vasc Surg 2011;53: 1167–73.e1. https://doi.org/10.1016/j.jvs.2010.10.124 1079. Antoniou GA, Antoniou SA, Torella F. Editor’s choice—endovascular vs. open repair for abdominal aortic aneurysm: systematic review and meta-analysis of updated perioperative and long term data of randomised controlled trials. Eur J Vasc Endovasc Surg 2020;59:385–97. https://doi.org/10.1016/j.ejvs.2019.11.030 1080. Halvorsen S, Mehilli J, Cassese S, Hall TS, Abdelhamid M, Barbato E, et al. 2022 ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery. Eur Heart J 2022;43:3826–924. https://doi.org/10.1093/ eurheartj/ehac270 1081. McFalls EO, Ward HB, Moritz TE, Goldman S, Krupski WC, Littooy F, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004;351:2795–804. https://doi.org/10.1056/NEJMoa041905 1082. Saida T, Mori K, Sato F, Shindo M, Takahashi H, Takahashi N, et al. Prospective intraindividual comparison of unenhanced magnetic resonance imaging vs contrast-enhanced computed tomography for the planning of endovascular abdominal aortic aneurysm repair. J Vasc Surg 2012;55:679–87. https://doi.org/10.1016/j.jvs. 2011.09.091 1083. Parker MV, O’Donnell SD, Chang AS, Johnson CA, Gillespie DL, Goff JM, et al. What imaging studies are necessary for abdominal aortic endograft sizing? A prospective blinded study using conventional computed tomography, aortography, and threedimensional computed tomography. J Vasc Surg 2005;41:199–205. https://doi.org/ 10.1016/j.jvs.2004.12.010 1084. Schanzer A, Greenberg RK, Hevelone N, Robinson WP, Eslami MH, Goldberg RJ, et al. Predictors of abdominal aortic aneurysm sac enlargement after endovascular repair. Circulation 2011;123:2848–55. https://doi.org/10.1161/circulationaha.110. 014902 1085. Protto S, Hahl T, Koskinen KJA, Järvenpää V, Uurto I, Väärämäki S, et al. Endovascular repair of abdominal aortic aneurysms is a valid alternative to open repair also in patients treated outside of instructions for use criteria. Cardiovasc Intervent Radiol 2022;45:1765–73. https://doi.org/10.1007/s00270-022-03297-7 1086. Charbonneau P, Hongku K, Herman CR, Habib M, Girsowicz E, Doonan RJ, et al. Long-term survival after endovascular and open repair in patients with anatomy outside instructions for use criteria for endovascular aneurysm repair. J Vasc Surg 2019; 70:1823–30. https://doi.org/10.1016/j.jvs.2019.01.081 1087. O’Donnell TFX, McElroy IE, Boitano LT, Mohebali J, Lamuraglia GM, Kwolek CJ, et al. Comparison of treatment options for aortic necks outside standard endovascular aneurysm repair instructions for use. J Vasc Surg 2021;74:1548–57. https://doi.org/10. 1016/j.jvs.2021.04.052 1088. Antoniou GA, Juszczak MT, Nasr H, Narlawar R, Antoniou SA, Matsagkas M, et al. Prognosis review and time-to-event data meta-analysis of endovascular aneurysm repair outside versus within instructions for use of aortic endograft devices. J Vasc Surg 2020;71:1415–31.e15. https://doi.org/10.1016/j.jvs.2019.08.247 1089. Chaikof EL, Blankensteijn JD, Harris PL, White GH, Zarins CK, Bernhard VM, et al. Reporting standards for endovascular aortic aneurysm repair. J Vasc Surg 2002;35: 1048–60. https://doi.org/10.1067/mva.2002.123763 1090. Falster MO, Garland SK, Jorm LR, Beiles CB, Freeman AJ, Sedrakyan A, et al. Editor’s choice—comparison of outcomes for major contemporary endograft devices used for endovascular repair of intact abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2023;65:272–80. https://doi.org/10.1016/j.ejvs.2022.11.005 1091. van Laarhoven C, Jorritsma NKN, Balderston J, Brinjikji W, Björck M, van Herwaarden JA, et al. Systematic review of the co-prevalence of arterial aneurysms within the vasculature. Eur J Vasc Endovasc Surg 2021;61:473–83. https://doi.org/10. 1016/j.ejvs.2020.10.002 1092. Hohneck A, Keese M, Ruemenapf G, Amendt K, Muertz H, Janda K, et al. Prevalence of abdominal aortic aneurysm and associated lower extremity artery aneurysm in men hospitalized for suspected or known cardiopulmonary disease. BMC Cardiovasc Disord 2019;19:284. https://doi.org/10.1186/s12872-019-1265-2 1093. D’Oria M, Scali S, Mao J, Szeberin Z, Thomson I, Beiles B, et al. Association between hospital volume and failure to rescue after open or endovascular repair of intact abdominal aortic aneurysms in the vascunet and international consortium of vascular registries. Ann Surg 2021;274:e452–9. https://doi.org/10.1097/sla. 0000000000005044 1094. Scali ST, Columbo JA, Suckow BD, D’Oria M, Neal D, Goodney PP, et al. Center volume is associated with diminished failure to rescue and improved outcomes following elective open abdominal aortic aneurysm repair. J Vasc Surg 2022;76:400–8.e2. https://doi.org/10.1016/j.jvs.2021.12.076 1095. Eid MA, Barnes JA, Mehta K, Wanken Z, Columbo J, Kang R, et al. Factors associated with preference of choice of aortic aneurysm repair in the PReference for Open Versus Endovascular repair of AAA (PROVE-AAA) study. J Vasc Surg 2022;76: 1556–64. https://doi.org/10.1016/j.jvs.2022.06.018 1096. Wanhainen A, Verzini F, Van Herzeele I, Allaire E, Bown M, Cohnert T, et al. Editor’s choice—European Society for Vascular Surgery (ESVS) 2019 clinical practice guidelines on the management of abdominal aorto-iliac artery aneurysms. Eur J Vasc Endovasc Surg 2019;57:8–93. https://doi.org/10.1016/j.ejvs.2018.09.020 1097. Reise JA, Sheldon H, Earnshaw J, Naylor AR, Dick F, Powell JT, et al. Patient preference for surgical method of abdominal aortic aneurysm repair: postal survey. Eur J Vasc Endovasc Surg 2010;39:55–61. https://doi.org/10.1016/j.ejvs.2009.08.008 1098. EVAR trial participants. Endovascular aneurysm repair and outcome in patients unfit for open repair of abdominal aortic aneurysm (EVAR trial 2): randomised controlled trial. Lancet 2005;365:2187–92. https://doi.org/10.1016/s0140-6736(05)66628-7 1099. Greenhalgh RM, Brown LC, Powell JT, Thompson SG, Epstein D. Endovascular repair of aortic aneurysm in patients physically ineligible for open repair. N Engl J Med 2010; 362:1872–80. https://doi.org/10.1056/NEJMoa0911056 1100. Patel R, Sweeting MJ, Powell JT, Greenhalgh RM. Endovascular versus open repair of abdominal aortic aneurysm in 15-years’ follow-up of the UK endovascular aneurysm repair trial 1 (EVAR trial 1): a randomised controlled trial. Lancet 2016;388:2366–74. https://doi.org/10.1016/s0140-6736(16)31135-7 1101. Lederle FA, Kyriakides TC, Stroupe KT, Freischlag JA, Padberg FT, Matsumura JS, et al. Open versus endovascular repair of abdominal aortic aneurysm. N Engl J Med 2019; 380:2126–35. https://doi.org/10.1056/NEJMoa1715955 1102. Lederle FA, Freischlag JA, Kyriakides TC, Matsumura JS, Padberg FT, Kohler TR, et al. Long-term comparison of endovascular and open repair of abdominal aortic aneurysm. N Engl J Med 2012;367:1988–97. https://doi.org/10.1056/NEJMoa1207481 1103. Schermerhorn ML, Buck DB, O’Malley AJ, Curran T, McCallum JC, Darling J, et al. Long-term outcomes of abdominal aortic aneurysm in the Medicare population. N Engl J Med 2015;373:328–38. https://doi.org/10.1056/NEJMoa1405778 1104. Nana P, Dakis K, Brodis A, Spanos K, Kouvelos G, Eckstein H-H, et al. A systematic review and meta-analysis on early mortality after abdominal aortic aneurysm repair in females in urgent and elective settings. J Vasc Surg 2022;75:1082–8.e6. https://doi.org/ 10.1016/j.jvs.2021.10.040 1105. Böckler D, Power AH, Bouwman LH, van Sterkenburg S, Bosiers M, Peeters P, et al. Improvements in patient outcomes with next generation endovascular aortic repair devices in the ENGAGE global registry and the EVAR-1 clinical trial. J Cardiovasc Surg 2020;61:604–9. https://doi.org/10.23736/s0021-9509.19.11021-x Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.152
1106. Teijink JAW, Power AH, Böckler D, Peeters P, van Sterkenburg S, Bouwman LH, et al. Editor’s choice—five year outcomes of the endurant stent graft for endovascular abdominal aortic aneurysm repair in the ENGAGE registry. Eur J Vasc Endovasc Surg 2019;58:175–81. https://doi.org/10.1016/j.ejvs.2019.01.008 1107. Oliveira-Pinto J, Oliveira NFG, Bastos-Gonçalves FM, Hoeks S, Rijn MJV, Raa ST, et al. Long-term results after standard endovascular aneurysm repair with the endurant and excluder stent grafts. J Vasc Surg 2020;71:64–74. https://doi.org/10.1016/j.jvs. 2019.03.039 1108. Deery SE, Shean KE, Pothof AB, O'Donnell TFX, Dalebout BA, Darling JD, et al. Three-Year Results of the Endurant Stent Graft System Post Approval Study. Ann Vasc Surg 2018;50:202–8. https://doi.org/10.1016/j.avsg.2017.12.017 1109. Prinssen M, Verhoeven EL, Buth J, Cuypers PWM, van Sambeek MRHM, Balm R, et al. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med 2004;351:1607–18. https://doi.org/10.1056/ NEJMoa042002 1110. Dakour-Aridi H, Paracha NZ, Locham S, Nejim B, Malas MB. Assessment of failure to rescue after abdominal aortic aneurysm repair using the National Surgical Quality Improvement Program procedure-targeted data set. J Vasc Surg 2018;68: 1335–44.e1. https://doi.org/10.1016/j.jvs.2018.01.059 1111. Scali ST, Giles KA, Kubilis P, Beck AW, Crippen CJ, Hughes SJ, et al. Impact of hospital volume on patient safety indicators and failure to rescue following open aortic aneurysm repair. J Vasc Surg 2020;71:1135–46.e4. https://doi.org/10.1016/j.jvs.2019.06.194 1112. Ma B, Wang YN, Chen KY, Zhang Y, Pan H, Yang K. Transperitoneal versus retroperitoneal approach for elective open abdominal aortic aneurysm repair. Cochrane Database Syst Rev 2016;2:CD010373. https://doi.org/10.1002/14651858. CD010373.pub2 1113. Camazine M, Bath J, Singh P, Kruse RL, Vogel TR. Characteristics associated with failure to rescue after open abdominal aortic aneurysm repair. J Surg Res 2023;283: 683–9. https://doi.org/10.1016/j.jss.2022.11.018 1114. Blair R, Harkin D, Johnston D, Lim A, McFetridge L, Mitchell H. Open surgery for abdominal aortic aneurysm: 980 consecutive patient outcomes from a high-volume centre in the United Kingdom. Vasc Endovascular Surg 2023;57:463–70. https://doi. org/10.1177/15385744221149585 1115. Hoornweg LL, Storm-Versloot MN, Ubbink DT, Koelemay MJW, Legemate DA, Balm R, et al. Meta analysis on mortality of ruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2008;35:558–70. https://doi.org/10.1016/j.ejvs.2007.11.019 1116. Kontopodis N, Galanakis N, Antoniou SA, Tsetis D, Ioannou CV, Veith FJ, et al. Meta-analysis and meta-regression analysis of outcomes of endovascular and open repair for ruptured abdominal aortic aneurysm. Eur J Vasc Endovasc Surg 2020;59: 399–410. https://doi.org/10.1016/j.ejvs.2019.12.023 1117. Wang LJ, Locham S, Al-Nouri O, Eagleton MJ, Clouse WD, Malas MB. Endovascular repair of ruptured abdominal aortic aneurysm is superior to open repair: propensitymatched analysis in the vascular quality initiative. J Vasc Surg 2020;72:498–507. https:// doi.org/10.1016/j.jvs.2019.11.063 1118. Tan TW, Eslami M, Rybin D, Doros G, Zhang WW, Farber A. Outcomes of endovascular and open surgical repair of ruptured abdominal aortic aneurysms in elderly patients. J Vasc Surg 2017;66:64–70. https://doi.org/10.1016/j.jvs.2016.10.119 1119. Dewulf M, Muysoms F, Vierendeels T, Huyghe M, Miserez M, Ruppert M, et al. Prevention of incisional hernias by prophylactic mesh-augmented reinforcement of midline laparotomies for abdominal aortic aneurysm treatment: five-year follow-up of a randomized controlled trial. Ann Surg 2022;276:e217–22. https://doi.org/10. 1097/sla.0000000000005545 1120. Honig S, Diener H, Kölbel T, Reinpold W, Zapf A, Bibiza-Freiwald E, et al. Abdominal incision defect following AAA-surgery (AIDA): 2-year results of prophylactic onlaymesh augmentation in a multicentre, double-blind, randomised controlled trial. Updates Surg 2022;74:1105–16. https://doi.org/10.1007/s13304-021-01125-0 1121. Indrakusuma R, Jalalzadeh H, van der Meij JE, Balm R, Koelemay MJW. Prophylactic mesh reinforcement versus sutured closure to prevent incisional hernias after open abdominal aortic aneurysm repair via midline laparotomy: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2018;56:120–8. https://doi.org/10.1016/j. ejvs.2018.03.021 1122. van Keulen JW, de Vries JP, Dekker H, Gonçalves FB, Moll FL, Verhagen HJ, et al. One-year multicenter results of 100 abdominal aortic aneurysm patients treated with the endurant stent graft. J Vasc Surg 2011;54:609–15. https://doi.org/10.1016/j. jvs.2011.02.053 1123. Piazza M, Squizzato F, Suominen V, Grego F, Trimarchi S, Antonello M, et al. Early and long-term outcomes of endovascular aortic repair in young and low surgical risk patients in the global registry for endovascular aortic treatment. J Endovasc Ther 2022; 29:248–57. https://doi.org/10.1177/15266028211045703 1124. Paravastu SC, Jayarajasingam R, Cottam R, Palfreyman SJ, Michaels JA, Thomas SM. Endovascular repair of abdominal aortic aneurysm. Cochrane Database Syst Rev 2014;1:CD004178. https://doi.org/10.1002/14651858.CD004178.pub2 1125. Dosluoglu HH, Lall P, Blochle R, Harris LM, Dryjski ML. Ambulatory percutaneous endovascular abdominal aortic aneurysm repair. J Vasc Surg 2014;59:58–64. https:// doi.org/10.1016/j.jvs.2013.06.076 1126. Geragotellis A, Cox K, Yip HCA, Jubouri M, Williams IM, Bailey DM, et al. Renal outcomes of suprarenal vs. infrarenal endograft fixation in endovascular abdominal aortic aneurysm repair: a narrative review. Cardiovasc Diagn Ther 2022;12:531–44. https:// doi.org/10.21037/cdt-22-196 1127. Verhoeven EL, Katsargyris A, Bachoo P, Larzon T, Fisher R, Ettles D, et al. Real-world performance of the new C3 gore excluder stent-graft: 1-year results from the European C3 module of the global registry for endovascular aortic treatment (GREAT). Eur J Vasc Endovasc Surg 2014;48:131–7. https://doi.org/10.1016/j.ejvs. 2014.04.009 1128. Torsello G, Scheinert D, Brunkwall JS, Chiesa R, Coppi G, Pratesi C. Safety and effectiveness of the INCRAFT AAA stent graft for endovascular repair of abdominal aortic aneurysms. J Vasc Surg 2015;61:1–8. https://doi.org/10.1016/j.jvs.2014.06.007 1129. Kontopodis N, Galanakis N, Tzartzalou I, Tavlas E, Georgakarakos E, Dimopoulos I, et al. An update on the improvement of patient eligibility with the use of new generation endografts for the treatment of abdominal aortic aneurysms. Expert Rev Med Devices 2020;17:1231–8. https://doi.org/10.1080/17434440.2020.1841629 1130. Kontopodis N, Papadopoulos G, Galanakis N, Tsetis D, Ioannou CV. Improvement of patient eligibility with the use of new generation endografts for the treatment of abdominal aortic aneurysms. A comparison study among currently used endografts and literature review. Expert Rev Med Devices 2017;14:245–50. https://doi.org/10.1080/ 17434440.2017.1281738 1131. Zlatanovic P, Mascia D, Ancetti S, Yeung KK, Graumans MJ, Jongkind V, et al. Short term and long term clinical outcomes of endovascular versus open repair for juxtarenal and pararenal abdominal aortic aneurysms using propensity score matching: results from juxta- and pararenal aortic aneurysm multicentre European study (JAMES). Eur J Vasc Endovasc Surg 2023;65:828–36. https://doi.org/10.1016/j.ejvs.2023.02.070 1132. Hajibandeh S, Hajibandeh S, Antoniou SA, Child E, Torella F, Antoniou GA. Percutaneous access for endovascular aortic aneurysm repair: a systematic review and meta-analysis. Vascular 2016;24:638–48. https://doi.org/10.1177/ 1708538116639201 1133. Antoniou GA, Antoniou SA. Editor’s choice—percutaneous access does not confer superior clinical outcomes over cutdown access for endovascular aneurysm repair: meta-analysis and trial sequential analysis of randomised controlled trials. Eur J Vasc Endovasc Surg 2021;61:383–94. https://doi.org/10.1016/j.ejvs.2020.11.008 1134. Cao Z, Wu W, Zhao K, Yang Yu, Jiang C, Zhu R. Safety and efficacy of totally percutaneous access compared with open femoral exposure for endovascular aneurysm repair: a meta-analysis. J Endovasc Ther 2017;24:246–53. https://doi.org/10.1177/ 1526602816689679 1135. Wang Q, Wu J, Ma Y, Zhu Y, Song X, Xie S, et al. Totally percutaneous versus surgical cut-down femoral artery access for elective bifurcated abdominal endovascular aneurysm repair. Cochrane Database Syst Rev 2023;1:CD010185. https://doi.org/10. 1002/14651858.CD010185.pub4 1136. Antoniou GA, Georgiadis GS, Antoniou SA, Neequaye S, Brennan JA, Torella F, et al. Late rupture of abdominal aortic aneurysm after previous endovascular repair: a systematic review and meta-analysis. J Endovasc Ther 2015;22:734–44. https://doi.org/10. 1177/1526602815601405 1137. Fransen GA, Vallabhaneni SR, Sr, van Marrewijk CJ, Laheij RJF, Harris PL, Buth J. Rupture of infra-renal aortic aneurysm after endovascular repair: a series from EUROSTAR registry. Eur J Vasc Endovasc Surg 2003;26:487–93. https://doi.org/10. 1016/s1078-5884(03)00350-2 1138. Marcaccio CL, Patel PB, de Guerre L, Wade JE, Rastogi V, Anjorin A, et al. Disparities in 5-year outcomes and imaging surveillance following elective endovascular repair of abdominal aortic aneurysm by sex, race, and ethnicity. J Vasc Surg 2022;76: 1205–15.e4. https://doi.org/10.1016/j.jvs.2022.03.886 1139. Schlösser FJ, Gusberg RJ, Dardik A, Lin PH, Verhagen HJM, Moll FL, et al. Aneurysm rupture after EVAR: can the ultimate failure be predicted? Eur J Vasc Endovasc Surg 2009;37:15–22. https://doi.org/10.1016/j.ejvs.2008.10.011 1140. Stather PW, Sidloff D, Dattani N, Choke E, Bown MJ, Sayers RD. Systematic review and meta-analysis of the early and late outcomes of open and endovascular repair of abdominal aortic aneurysm. Br J Surg 2013;100:863–72. https://doi.org/10.1002/bjs. 9101 1141. Swart M, McCarthy R. Shared decision making for elective abdominal aortic aneurysm surgery. Clin Med (Lond) 2019;19:473–7. https://doi.org/10.7861/clinmed.2019-0352 1142. Stubenrouch FE, Peters LJ, de Mik SML, Klemm PL, Peppelenbosch AG, Schreurs SCWM, et al. Improving shared decision making in vascular surgery: a stepped wedge cluster randomised trial. Eur J Vasc Endovasc Surg 2022;64:73–81. https://doi.org/10. 1016/j.ejvs.2022.04.016 1143. Machin M, Van Herzeele I, Ubbink D, Powell JT. Shared decision making in and management of intact abdominal aortic aneurysm: a scoping review of the literature. Eur J Vasc Endovasc Surg 2023;65:839–49. https://doi.org/10.1016/j.ejvs.2023.01.036 1144. Karthaus EG, Tong TML, Vahl A, Hamming JF. Saccular abdominal aortic aneurysms: patient characteristics, clinical presentation, treatment, and outcomes in the Netherlands. Ann Surg 2019;270:852–8. https://doi.org/10.1097/sla. 0000000000003529
ESC Guidelines 3689
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.153
1145. O’Donnell TF, McElroy IE, Mohebali J, Boitano LT, Lamuraglia GM, Kwolek CJ, et al. Late type 1A endoleaks: associated factors, prognosis and management strategies. Ann Vasc Surg 2022;80:273–82. https://doi.org/10.1016/j.avsg.2021.08.057 1146. De Rango P, Verzini F, Parlani G, Cieri E, Simonte G, Farchioni L, et al. Safety of chronic anticoagulation therapy after endovascular abdominal aneurysm repair (EVAR). Eur J Vasc Endovasc Surg 2014;47:296–303. https://doi.org/10.1016/j.ejvs.2013.12.009 1147. Rokosh RS, Wu WW, Dalman RL, Chaikof EL. Society for Vascular Surgery implementation of clinical practice guidelines for patients with an abdominal aortic aneurysm. Endoleak management. J Vasc Surg 2021;74:1792–4. https://doi.org/10.1016/j.jvs. 2021.04.042 1148. Jordan WD, Jr, Mehta M, Varnagy D, Moore WM, Arko FR, Joye J, et al. Results of the ANCHOR prospective, multicenter registry of EndoAnchors for type Ia endoleaks and endograft migration in patients with challenging anatomy. J Vasc Surg 2014;60: 885–92.e2. https://doi.org/10.1016/j.jvs.2014.04.063 1149. Sidloff DA, Stather PW, Choke E, Bown MJ, Sayers RD. Type II endoleak after endovascular aneurysm repair. Br J Surg 2013;100:1262–70. https://doi.org/10.1002/bjs. 9181 1150. Daye D, Walker TG. Complications of endovascular aneurysm repair of the thoracic and abdominal aorta: evaluation and management. Cardiovasc Diagn Ther 2018;8: S138–56. https://doi.org/10.21037/cdt.2017.09.17 1151. Latson LA, Jr, DeAnda A, Jr, Ko JP. Imaging of the postsurgical thoracic aorta: a state-of-the-art review. J Thorac Imaging 2017;32:1–25. https://doi.org/10.1097/rti. 0000000000000246 1152. Prescott-Focht JA, Martinez-Jimenez S, Hurwitz LM, Hoang JK, Christensen JD, Ghoshhajra BB, et al. Ascending thoracic aorta: postoperative imaging evaluation. Radiographics 2013;33:73–85. https://doi.org/10.1148/rg.331125090 1153. Riambau V, Böckler D, Brunkwall J, Cao P, Chiesa R, Coppi G, et al. Editor’s choice— management of descending thoracic aorta diseases: clinical practice guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg 2017;53:4–52. https://doi.org/10.1016/j.ejvs.2016.06.005 1154. Quevedo HC, Santiago-Trinidad R, Castellanos J, Atianzar K, Anwar A, Abi Rafeh N. Systematic review of interventions to repair ascending aortic pseudoaneurysms. Ochsner J 2014;14:576–85. 1155. Mesana TG, Caus T, Gaubert J, Collart F, Ayari R, Bartoli J-M, et al. Late complications after prosthetic replacement of the ascending aorta: what did we learn from routine magnetic resonance imaging follow-up? Eur J Cardiothorac Surg 2000;18:313–20. https://doi.org/10.1016/s1010-7940(00)00512-1 1156. Bianco V, Kilic A, Gleason TG, Arnaoutakis GJ, Sultan I. Management of thoracic aortic graft infections. J Card Surg 2018;33:658–65. https://doi.org/10.1111/jocs.13792 1157. Liisberg M, Baudier F, Akgül C, Lindholt JS. Long-term thoracic endovascular repair follow-up from 1999 to 2019: a single-center experience. Ann Vasc Surg 2022;86: 399–407. https://doi.org/10.1016/j.avsg.2022.04.013 1158. Nakhaei P, Bashir M, Jubouri M, Banar S, Ilkhani S, Borzeshi EZ, et al. Aortic remodeling, distal stent-graft induced new entry and endoleak following frozen elephant trunk: a systematic review and meta-analysis. J Card Surg 2022;37:3848–62. https:// doi.org/10.1111/jocs.16918 1159. Iribarne A, Keenan J, Benrashid E, Wang H, Meza JM, Ganapathi A, et al. Imaging surveillance after proximal aortic operations: is it necessary? Ann Thorac Surg 2017;103: 734–41. https://doi.org/10.1016/j.athoracsur.2016.06.085 1160. Hensley SE, Upchurch GR, Jr. Repair of abdominal aortic aneurysms: JACC focus seminar, part 1. J Am Coll Cardiol 2022;80:821–31. https://doi.org/10.1016/j.jacc. 2022.04.066 1161. Bastos Gonçalves F, Baderkhan H, Verhagen HJ, Wanhainen A, Björck M, Stolker RJ, et al. Early sac shrinkage predicts a low risk of late complications after endovascular aortic aneurysm repair. Br J Surg 2014;101:802–10. https://doi.org/10.1002/bjs.9516 1162. Troutman DA, Chaudry M, Dougherty MJ, Calligaro KD. Endovascular aortic aneurysm repair surveillance may not be necessary for the first 3 years after an initially normal duplex postoperative study. J Vasc Surg 2014;60:558–62. https://doi.org/10.1016/ j.jvs.2014.03.278 1163. Jean-Baptiste E, Feugier P, Cruzel C, Sarlon-Bartoli G, Reix T, Steinmetz E, et al. Computed tomography-aortography versus color-duplex ultrasound for surveillance of endovascular abdominal aortic aneurysm repair: a prospective multicenter diagnostic-accuracy study (the ESSEA trial). Circ Cardiovasc Imaging 2020;13: e009886. https://doi.org/10.1161/circimaging.119.009886 1164. Johnsen L, Hisdal J, Jonung T, Braaten A, Pedersen G. Contrast-enhanced ultrasound detects type II endoleaks during follow-up for endovascular aneurysm repair. J Vasc Surg 2020;72:1952–9. https://doi.org/10.1016/j.jvs.2020.02.020 1165. George J, Tadros RO, Rao A, Png CYM, Han DK, Ilonzo N, et al. Duplex ultrasound can successfully identify endoleaks and renovisceral stent patency in patients undergoing complex endovascular aneurysm repair. Vasc Endovascular Surg 2021;55:234–8. https://doi.org/10.1177/1538574420980605 1166. Smith L, Thomas N, Arnold A, Bell R, Zayed H, Tyrrell M, et al. Editor’s choice—a comparison of computed tomography angiography and colour duplex ultrasound surveillance post infrarenal endovascular aortic aneurysm repair: financial implications and impact of different international surveillance guidelines. Eur J Vasc Endovasc Surg 2021;62:193–201. https://doi.org/10.1016/j.ejvs.2021.04.005 1167. Iscan HZ, Unal EU, Akkaya B, Daglı M, Karahan M, Civelek I, et al. Color Doppler ultrasound for surveillance following EVAR as the primary tool. J Card Surg 2021; 36:111–7. https://doi.org/10.1111/jocs.15194 1168. Antoniou GA, Kontopodis N, Rogers SK, Golledge J, Forbes TL, Torella F, et al. Editor’s choice—meta-analysis of compliance with endovascular aneurysm repair surveillance: the EVAR surveillance paradox. Eur J Vasc Endovasc Surg 2023;65: 244–54. https://doi.org/10.1016/j.ejvs.2022.10.033 1169. Baderkhan H, Haller O, Wanhainen A, Björck M, Mani K. Follow-up after endovascular aortic aneurysm repair can be stratified based on first postoperative imaging. Br J Surg 2018;105:709–18. https://doi.org/10.1002/bjs.10766 1170. Png CY, Tadros RO, Faries PL, Torres MR, Kim SY, Lookstein R, et al. The effect of age on post-EVAR outcomes. Ann Vasc Surg 2016;35:156–62. https://doi.org/10. 1016/j.avsg.2016.01.022 1171. Xiong X, Wu Z, Qin X, Huang Q, Wang X, Qin J, et al. Meta-analysis suggests statins reduce mortality after abdominal aortic aneurysm repair. J Vasc Surg 2022;75: 356–62.e4. https://doi.org/10.1016/j.jvs.2021.06.033 1172. Schrimpf C, Teebken OE, Wilhelmi M. Thoracic endovascular aortic repair after iatrogenic aortic dissection and false lumen stent grafting. Ann Thorac Surg 2015;99: 1447–9. https://doi.org/10.1016/j.athoracsur.2014.05.101 1173. Sampson UK, Norman PE, Fowkes FG, Aboyans V, Song Y, Harrell FE, Jr, et al. Global and regional burden of aortic dissection and aneurysms: mortality trends in 21 world regions, 1990 to 2010. Glob Heart 2014;9:171–80.e110. https://doi.org/10.1016/j. gheart.2013.12.010 1174. Clough RE, Nienaber CA. Management of acute aortic syndrome. Nat Rev Cardiol 2015;12:103–14. https://doi.org/10.1038/nrcardio.2014.203 1175. Evangelista A, Isselbacher EM, Bossone E, Gleason TG, Eusanio MD, Sechtem U, et al. Insights from the international registry of acute aortic dissection: a 20-year experience of collaborative clinical research. Circulation 2018;137:1846–60. https://doi. org/10.1161/circulationaha.117.031264 1176. Booher AM, Isselbacher EM, Nienaber CA, Trimarchi S, Evangelista A, Montgomery DG, et al. The IRAD classification system for characterizing survival after aortic dissection. Am J Med 2013;126:730.e19–24. https://doi.org/10.1016/j.amjmed.2013.01. 020 1177. Howard C, Ponnapalli A, Shaikh S, Idhrees M, Bashir M. Non-A non-B aortic dissection: a literature review. J Card Surg 2021;36:1806–13. https://doi.org/10.1111/jocs. 15349 1178. Urbanski PP, Wagner M. Acute non-A-non-B aortic dissection: surgical or conservative approach? Eur J Cardiothorac Surg 2016;49:1249–54. https://doi.org/10.1093/ ejcts/ezv301 1179. Carino D, Singh M, Molardi A, Agostinelli A, Goldoni M, Pacini D, et al. Non-A non-B aortic dissection: a systematic review and meta-analysis. Eur J Cardiothorac Surg 2019; 55:653–9. https://doi.org/10.1093/ejcts/ezy337 1180. Sievers HH, Rylski B, Czerny M, Baier ALM, Kreibich M, Siepe M, et al. Aortic dissection reconsidered: type, entry site, malperfusion classification adding clarity and enabling outcome prediction. Interact Cardiovasc Thorac Surg 2020;30:451–7. https:// doi.org/10.1093/icvts/ivz281 1181. Aboyans V, Boukhris M. Dissecting the epidemiology of aortic dissection. Eur Heart J Acute Cardiovasc Care 2021;10:710–1. https://doi.org/10.1093/ehjacc/zuab065 1182. Pape LA, Awais M, Woznicki EM, Suzuki T, Trimarchi S, Evangelista A, et al. Presentation, diagnosis, and outcomes of acute aortic dissection: 17-year trends from the international registry of acute aortic dissection. J Am Coll Cardiol 2015;66: 350–8. https://doi.org/10.1016/j.jacc.2015.05.029 1183. Januzzi JL, Isselbacher EM, Fattori R, Cooper JV, Smith DE, Fang J, et al. Characterizing the young patient with aortic dissection: results from the international registry of aortic dissection (IRAD). J Am Coll Cardiol 2004;43:665–9. https://doi.org/10.1016/j.jacc. 2003.08.054 1184. Dalen JE, Alpert JS, Goldberg RJ, Weinstein RS. The epidemic of the 20(th) century: coronary heart disease. Am J Med 2014;127:807–12. https://doi.org/10.1016/j. amjmed.2014.04.015 1185. Bossone E, Pyeritz RE, O’Gara P, Harris KM, Braverman AC, Pape L, et al. Acute aortic dissection in blacks: insights from the international registry of acute aortic dissection. Am J Med 2013;126:909–15. https://doi.org/10.1016/j.amjmed.2013.04.020 1186. Rylski B, Hoffmann I, Beyersdorf F, Suedkamp M, Siepe M, Nitsch B, et al. Iatrogenic acute aortic dissection type A: insight from the German registry for acute aortic dissection type A (GERAADA). Eur J Cardiothorac Surg 2013;44:353–9; discussion 359. https://doi.org/10.1093/ejcts/ezt055 1187. Núñez-Gil IJ, Bautista D, Cerrato E, Salinas P, Varbella F, Omedè P, et al. Incidence, management, and immediate- and long-term outcomes after iatrogenic aortic dissection during diagnostic or interventional coronary procedures. Circulation 2015;131: 2114–9. https://doi.org/10.1161/circulationaha.115.015334 1188. Carbone A, Ranieri B, Castaldo R, Franzese M, Rega S, Cittadini A, et al. Sex differences in type A acute aortic dissection: a systematic review and meta-analysis. Eur J Prev Cardiol 2023;30:1074–89. https://doi.org/10.1093/eurjpc/zwad009 1189. Nienaber CA, Fattori R, Mehta RH, Richartz BM, Evangelista A, Petzsch M, et al. Gender-related differences in acute aortic dissection. Circulation 2004;109: 3014–21. https://doi.org/10.1161/01.Cir.0000130644.78677.2c Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.154
1190. Manalo-Estrella P, Barker AE. Histopathologic findings in human aortic media associated with pregnancy. Arch Pathol 1967;83:336–41. 1191. Lempel JK, Frazier AA, Jeudy J, Kligerman SJ, Schultz R, Ninalowo HA, et al. Aortic arch dissection: a controversy of classification. Radiology 2014;271:848–55. https:// doi.org/10.1148/radiol.14131457 1192. Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA. Acute aortic dissection and intramural hematoma: a systematic review. JAMA 2016;316:754–63. https://doi.org/10.1001/jama.2016.10026 1193. Tsai TT, Trimarchi S, Nienaber CA. Acute aortic dissection: perspectives from the international registry of acute aortic dissection (IRAD). Eur J Vasc Endovasc Surg 2009;37:149–59. https://doi.org/10.1016/j.ejvs.2008.11.032 1194. Neri E, Toscano T, Papalia U, Frati G, Massetti M, Capannini G, et al. Proximal aortic dissection with coronary malperfusion: presentation, management, and outcome. J Thorac Cardiovasc Surg 2001;121:552–60. https://doi.org/10.1067/mtc.2001.112534 1195. Trimarchi S, Tsai T, Eagle KA, Isselbacher EM, Froehlich J, et al. Acute abdominal aortic dissection: insight from the International Registry of Acute Aortic Dissection (IRAD). J Vasc Surg 2007;46:913–9. https://doi.org/10.1016/j.jvs.2007.07.030 1196. Gorla R, Erbel R, Kahlert P, Tsagakis K, Jakob H, Mahabadi A-A, et al. Accuracy of a diagnostic strategy combining aortic dissection detection risk score and D-dimer levels in patients with suspected acute aortic syndrome. Eur Heart J Acute Cardiovasc Care 2017;6:371–8. https://doi.org/10.1177/2048872615594497 1197. Strayer RJ, Shearer PL, Hermann LK. Screening, evaluation, and early management of acute aortic dissection in the ED. Curr Cardiol Rev 2012;8:152–7. https://doi.org/10. 2174/157340312801784970 1198. Nazerian P, Mueller C, Soeiro AM, Leidel BA, Salvadeo SAT, Giachino F, et al. Diagnostic accuracy of the aortic dissection detection risk score plus D-dimer for acute aortic syndromes: the ADvISED prospective multicenter study. Circulation 2018;137:250–8. https://doi.org/10.1161/circulationaha.117.029457 1199. Bima P, Pivetta E, Nazerian P, Toyofuku M, Gorla R, Bossone E, et al. Systematic review of aortic dissection detection risk score plus d-dimer for diagnostic rule-out of suspected acute aortic syndromes. Acad Emerg Med 2020;27:1013–27. https://doi. org/10.1111/acem.13969 1200. Rogers AM, Hermann LK, Booher AM, Nienaber CA, Williams DM, Kazerooni EA, et al. Sensitivity of the aortic dissection detection risk score, a novel guideline-based tool for identification of acute aortic dissection at initial presentation: results from the international registry of acute aortic dissection. Circulation 2011;123:2213–8. https:// doi.org/10.1161/CIRCULATIONAHA.110.988568 1201. Suzuki T, Distante A, Zizza A, Trimarchi S, Villani M, Salerno Uriarte JA, et al. Diagnosis of acute aortic dissection by D-dimer: the international registry of acute aortic dissection substudy on biomarkers (IRAD-bio) experience. Circulation 2009; 119:2702–7. https://doi.org/10.1161/circulationaha.108.833004 1202. Baliga RR, Nienaber CA, Bossone E, Oh JK, Isselbacher EM, Sechtem U, et al. The role of imaging in aortic dissection and related syndromes. JACC Cardiovasc Imaging 2014;7: 406–24. https://doi.org/10.1016/j.jcmg.2013.10.015 1203. Nazerian P, Mueller C, Vanni S, Soeiro AM, Leidel BA, Cerini G, et al. Integration of transthoracic focused cardiac ultrasound in the diagnostic algorithm for suspected acute aortic syndromes. Eur Heart J 2019;40:1952–60. https://doi.org/10.1093/ eurheartj/ehz207 1204. Shiga T, Wajima Z, Apfel CC, Inoue T, Ohe Y. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection: systematic review and meta-analysis. Arch Intern Med 2006;166:1350–6. https://doi.org/10.1001/archinte.166.13.1350 1205. Nienaber CA, Clough RE. Management of acute aortic dissection. Lancet 2015;385: 800–11. https://doi.org/10.1016/s0140-6736(14)61005-9 1206. Byrne RA, Rossello X, Coughlan JJ, Barbato E, Berry C, Chieffo A, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J 2023; 44:3720–826. https://doi.org/10.1093/eurheartj/ehad191 1207. Rogers IS, Banerji D, Siegel EL, Truong QA, Ghoshhajra BB, Irlbeck T, et al. Usefulness of comprehensive cardiothoracic computed tomography in the evaluation of acute undifferentiated chest discomfort in the emergency department (CAPTURE). Am J Cardiol 2011;107:643–50. https://doi.org/10.1016/j.amjcard.2010.10.039 1208. Evangelista A, Maldonado G, Gruosso D, Gutiérrez L, Granato C, Villalva N, et al. The current role of echocardiography in acute aortic syndrome. Echo Res Pract 2019;6: R53–r63. https://doi.org/10.1530/erp-18-0058 1209. Vignon P, Guéret P, Vedrinne JM, Lagrange P, Cornu E, Abrieu O, et al. Role of transesophageal echocardiography in the diagnosis and management of traumatic aortic disruption. Circulation 1995;92:2959–68. https://doi.org/10.1161/01.cir.92.10.2959 1210. Moral S, Avegliano G, Cuéllar H, Ballesteros E, Rodríguez-Palomares J, Teixidó G, et al. Usefulness of transesophageal echocardiography in the evaluation of celiac trunk and superior mesenteric artery involvement in acute aortic dissection. J Am Soc Echocardiogr 2021;34:327–35. https://doi.org/10.1016/j.echo.2020.12.019 1211. Nienaber CA, Clough RE, Sakalihasan N, Suzuki T, Gibbs R, Mussa F, et al. Aortic dissection. Nat Rev Dis Primers 2016;2:16053. https://doi.org/10.1038/nrdp.2016.53 1212. Vilacosta I, San Román JA, di Bartolomeo R, Eagle K, Estrera AL, Ferrera C, et al. Acute aortic syndrome revisited: JACC state-of-the-art review. J Am Coll Cardiol 2021;78:2106–25. https://doi.org/10.1016/j.jacc.2021.09.022 1213. Tadros RO, Tang GHL, Barnes HJ, Mousavi I, Kovacic JC, Faries P, et al. Optimal treatment of uncomplicated type B aortic dissection: JACC review topic of the week. J Am Coll Cardiol 2019;74:1494–504. https://doi.org/10.1016/j.jacc.2019.07.063 1214. Kodama K, Nishigami K, Sakamoto T, Sawamura T, Hirayama T, Misumi H, et al. Tight heart rate control reduces secondary adverse events in patients with type B acute aortic dissection. Circulation 2008;118:S167–70. https://doi.org/10.1161/ circulationaha.107.755801 1215. Estrera AL, Miller CC, III, Safi HJ, Goodrick JS, Keyhani A, Porat EE, et al. Outcomes of medical management of acute type B aortic dissection. Circulation 2006;114: I384–389. https://doi.org/10.1161/circulationaha.105.001479 1216. Nejim B, Mathlouthi A, Naazie I, Malas MB. The effect of intravenous and oral betablocker use in patients with type B thoracic aortic dissection. Ann Vasc Surg 2022;80: 170–9. https://doi.org/10.1016/j.avsg.2021.07.056 1217. Hameed I, Cifu AS, Vallabhajosyula P. Management of thoracic aortic dissection. JAMA 2023;329:756–7. https://doi.org/10.1001/jama.2023.0265 1218. Fukui T. Management of acute aortic dissection and thoracic aortic rupture. J Intensive Care 2018;6:15. https://doi.org/10.1186/s40560-018-0287-7 1219. Suzuki T, Mehta RH, Ince H, Nagai R, Sakomura Y, Weber F, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the international registry of aortic dissection (IRAD). Circulation 2003;108:Ii312–7. https://doi. org/10.1161/01.cir.0000087386.07204.09 1220. Mehta RH, Suzuki T, Hagan PG, Bossone E, Gilon D, Llovet A, et al. Predicting death in patients with acute type a aortic dissection. Circulation 2002;105:200–6. https://doi. org/10.1161/hc0202.102246 1221. Mészáros I, Mórocz J, Szlávi J, Schmidt J, Tornóci L, Nagy L, et al. Epidemiology and clinicopathology of aortic dissection. Chest 2000;117:1271–8. https://doi.org/10. 1378/chest.117.5.1271 1222. Glower DD, Speier RH, White WD, Smith LR, Rankin JS, Wolfe WG. Management and long-term outcome of aortic dissection. Ann Surg 1991;214:31–41. https://doi. org/10.1097/00000658-199107000-00006 1223. Nallamothu BK, Mehta RH, Saint S, Llovet A, Bossone E, Cooper JV, et al. Syncope in acute aortic dissection: diagnostic, prognostic, and clinical implications. Am J Med 2002;113:468–71. https://doi.org/10.1016/s0002-9343(02)01254-8 1224. Suzuki T, Isselbacher EM, Nienaber CA, Pyeritz RE, Eagle KA, Tsai TT, et al. Type-selective benefits of medications in treatment of acute aortic dissection (from the international registry of acute aortic dissection [IRAD]). Am J Cardiol 2012;109:122–7. https://doi.org/10.1016/j.amjcard.2011.08.012 1225. Palmer J, Gelmann D, Engelbrecht-Wiggans E, Hollis G, Hart E, Ali A, et al. Invasive arterial blood pressure monitoring may aid in the medical management of hypertensive patients with acute aortic disease. Am J Emerg Med 2022;59:85–93. https://doi. org/10.1016/j.ajem.2022.06.054 1226. Nienaber CA, Kische S, Rousseau H, Eggebrecht H, Rehders TC, Kundt G, et al. Endovascular repair of type B aortic dissection: long-term results of the randomized investigation of stent grafts in aortic dissection trial. Circ Cardiovasc Interv 2013;6: 407–16. https://doi.org/10.1161/circinterventions.113.000463 1227. Fattori R, Montgomery D, Lovato L, Kische S, Di Eusanio M, Ince H, et al. Survival after endovascular therapy in patients with type B aortic dissection: a report from the international registry of acute aortic dissection (IRAD). JACC Cardiovasc Interv 2013;6:876–82. https://doi.org/10.1016/j.jcin.2013.05.003 1228. Durham CA, Cambria RP, Wang LJ, Ergul EA, Aranson NJ, Patel VI, et al. The natural history of medically managed acute type B aortic dissection. J Vasc Surg 2015;61: 1192–8. https://doi.org/10.1016/j.jvs.2014.12.038 1229. Lou X, Chen EP, Duwayri YM, Veeraswamy RK, Jordan WD, Zehner CA, et al. The impact of thoracic endovascular aortic repair on long-term survival in type B aortic dissection. Ann Thorac Surg 2018;105:31–8. https://doi.org/10.1016/j.athoracsur. 2017.06.016 1230. Lou X, Duwayri YM, Chen EP, Jordan WD, Forcillo J, Zehner CA, et al. Predictors of failure of medical management in uncomplicated type B aortic dissection. Ann Thorac Surg 2019;107:493–8. https://doi.org/10.1016/j.athoracsur.2018.08.012 1231. Lou X, Duwayri YM, Jordan WD, Jr, Chen EP, Veeraswamy RK, Leshnower BG. The safety and efficacy of extended TEVAR in acute type B aortic dissection. Ann Thorac Surg 2020;110:799–806. https://doi.org/10.1016/j.athoracsur.2019.12.036 1232. Hirst AE, Jr, Johns VJ, Jr, Kime SW, Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 1958;37:217–79. https://doi.org/10.1097/00005792-195809000- 00003 1233. Chiappini B, Schepens M, Tan E, Amore AD, Morshuis W, Dossche K, et al. Early and late outcomes of acute type A aortic dissection: analysis of risk factors in 487 consecutive patients. Eur Heart J 2005;26:180–6. https://doi.org/10.1093/eurheartj/ ehi024 1234. Harris KM, Nienaber CA, Peterson MD, Woznicki EM, Braverman AC, Trimarchi S, et al. Early mortality in type A acute aortic dissection: insights from the international registry of acute aortic dissection. JAMA Cardiol 2022;7:1009–15. https://doi.org/10. 1001/jamacardio.2022.2718 1235. Zhu Y, Lingala B, Baiocchi M, Tao JJ, Toro Arana V, Khoo JW, et al. Type A aortic dissection-experience over 5 decades: JACC historical breakthroughs in perspective. J Am Coll Cardiol 2020;76:1703–13. https://doi.org/10.1016/j.jacc.2020.07.061
ESC Guidelines 3691
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.155
1236. Czerny M, Siepe M, Beyersdorf F, Feisst M, Gabel M, Pilz M, et al. Prediction of mortality rate in acute type A dissection: the German registry for acute type A aortic dissection score. Eur J Cardiothorac Surg 2020;58:700–6. https://doi.org/10.1093/ejcts/ ezaa156 1237. Perko MJ, Nørgaard M, Herzog TM, Olsen PS, Schroeder TV, Pettersson G. Unoperated aortic aneurysm: a survey of 170 patients. Ann Thorac Surg 1995;59: 1204–9. https://doi.org/10.1016/0003-4975(95)00132-5 1238. Wolfe SB, Sundt TM, III, Isselbacher EM, Cameron DE, Trimarchi S, Bekeredjian R, et al. Survival after operative repair of acute type A aortic dissection varies according to the presence and type of preoperative malperfusion. J Thorac Cardiovasc Surg 2024; 168:37–49.e6. https://doi.org/10.1016/j.jtcvs.2022.09.034 1239. Trimarchi S, Eagle KA, Nienaber CA, Rampoldi V, Jonker FHW, De Vincentiis C, et al. Role of age in acute type A aortic dissection outcome: report from the international registry of acute aortic dissection (IRAD). J Thorac Cardiovasc Surg 2010;140:784–9. https://doi.org/10.1016/j.jtcvs.2009.11.014 1240. Shrestha M, Khaladj N, Haverich A, Hagl C. Is treatment of acute type A aortic dissection in septuagenarians justifiable? Asian Cardiovasc Thorac Ann 2008;16:33–6. https://doi.org/10.1177/021849230801600109 1241. Bonser RS, Ranasinghe AM, Loubani M, Evans JD, Thalji NMA, Bachet JE, et al. Evidence, lack of evidence, controversy, and debate in the provision and performance of the surgery of acute type A aortic dissection. J Am Coll Cardiol 2011;58:2455–74. https://doi.org/10.1016/j.jacc.2011.06.067 1242. Subramanian S, Leontyev S, Borger MA, Trommer C, Misfeld M, Mohr FW. Valve-sparing root reconstruction does not compromise survival in acute type A aortic dissection. Ann Thorac Surg 2012;94:1230–4. https://doi.org/10.1016/j.athoracsur. 2012.04.094 1243. Urbanski PP, Hijazi H, Dinstak W, Diegeler A. Valve-sparing aortic root repair in acute type A dissection: how many sinuses have to be repaired for curative surgery? Eur J Cardiothorac Surg 2013;44:439–43; discussion 443–4. https://doi.org/10.1093/ ejcts/ezt042 1244. Shrestha M, Baraki H, Maeding I, Fitzner S, Sarikouch S, Khaladj N, et al. Long-term results after aortic valve-sparing operation (David I). Eur J Cardiothorac Surg 2012; 41:56–61; discussion 61–2. https://doi.org/10.1016/j.ejcts.2011.04.012 1245. Tsagakis K, Pacini D, Di Bartolomeo R, Gorlitzer M, Weiss G, Grabenwoger M, et al. Multicenter early experience with extended aortic repair in acute aortic dissection: is simultaneous descending stent grafting justified? J Thorac Cardiovasc Surg 2010;140: S116–20; discussion S142–S146. https://doi.org/10.1016/j.jtcvs.2010.07.066 1246. Tsagakis K, Pacini D, Grabenwöger M, Borger MA, Goebel N, Hemmer W, et al. Results of frozen elephant trunk from the international E-vita Open registry. Ann Cardiothorac Surg 2020;9:178–88. https://doi.org/10.21037/acs-2020-fet-25 1247. Beckmann E, Martens A, Kaufeld T, Natanov R, Krueger H, Rudolph L, et al. Frozen elephant trunk in acute aortic type a dissection: risk analysis of concomitant root replacement. Eur J Cardiothorac Surg 2022;62:ezac051. https://doi.org/10.1093/ejcts/ ezac051 1248. Cruz I, Stuart B, Caldeira D, Morgado G, Gomes AC, Almeida AR, et al. Controlled pericardiocentesis in patients with cardiac tamponade complicating aortic dissection: experience of a centre without cardiothoracic surgery. Eur Heart J Acute Cardiovasc Care 2015;4:124–8. https://doi.org/10.1177/2048872614549737 1249. Hayashi T, Tsukube T, Yamashita T, Haraguchi T, Matsukawa R, Kozawa S, et al. Impact of controlled pericardial drainage on critical cardiac tamponade with acute type A aortic dissection. Circulation 2012;126:S97–101. https://doi.org/10.1161/ CIRCULATIONAHA.111.082685 1250. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The international registry of acute aortic dissection (IRAD): new insights into an old disease. JAMA 2000;283:897–903. https://doi.org/10.1001/jama.283.7.897 1251. Saczkowski R, Malas T, Mesana T, de Kerchove L, El Khoury G, Boodhwani M. Aortic valve preservation and repair in acute type A aortic dissection. Eur J Cardiothorac Surg 2014;45:e220–226. https://doi.org/10.1093/ejcts/ezu099 1252. Hysi I, Juthier F, Fabre O, Fouquet O, Rousse N, Banfi C, et al. Aortic root surgery improves long-term survival after acute type A aortic dissection. Int J Cardiol 2015; 184:285–90. https://doi.org/10.1016/j.ijcard.2015.02.020 1253. Peterss S, Dumfarth J, Rizzo JA, Bonaros N, Fang H, Tranquilli M, et al. Sparing the aortic root in acute aortic dissection type A: risk reduction and restored integrity of the untouched root. Eur J Cardiothorac Surg 2016;50:232–9. https://doi.org/10. 1093/ejcts/ezw012 1254. Chen SK, Qiu ZH, Fang GH, Wu XJ, Chen LW. Reported outcomes after aortic valve resuspension for acute type A aortic dissection: a systematic review and meta-analysis. Interact Cardiovasc Thorac Surg 2019;29:331–8. https://doi.org/10. 1093/icvts/ivz080 1255. Qiu J, Wu J, Xie E, Luo X, Chen JF, Gao W, et al. Surgical management and outcomes of the aortic root in acute type A aortic dissection. Ann Thorac Surg 2020;110: 136–43. https://doi.org/10.1016/j.athoracsur.2019.10.014 1256. Umana-Pizano JB, Nissen AP, Sandhu HK, Miller CC, Loghin A, Safi HJ, et al. Acute type A dissection repair by high-volume vs low-volume surgeons at a high-volume aortic center. Ann Thorac Surg 2019;108:1330–6. https://doi.org/10.1016/j. athoracsur.2019.04.040 1257. Goldstone AB, Chiu P, Baiocchi M, Lingala B, Lee J, Rigdon J, et al. Interfacility transfer of medicare beneficiaries with acute type A aortic dissection and regionalization of care in the United States. Circulation 2019;140:1239–50. https://doi.org/10.1161/ circulationaha.118.038867 1258. Mosbahi S, Stak D, Gravestock I, Burgstaller JM, Steurer J, Eckstein F, et al. A systemic review and meta-analysis: Bentall versus David procedure in acute type A aortic dissection. Eur J Cardiothorac Surg 2019;55:201–9. https://doi.org/10.1093/ejcts/ezy266 1259. Beckmann E, Martens A, Pertz J, Kaufeld T, Umminger J, Hanke JS, et al. Valve-sparing David I procedure in acute aortic type A dissection: a 20-year experience with more than 100 patients. Eur J Cardiothorac Surg 2017;52:319–24. https://doi.org/10.1093/ ejcts/ezx170 1260. Weiss G, Tsagakis K, Jakob H, Di Bartolomeo R, Pacini D, Barberio G, et al. The frozen elephant trunk technique for the treatment of complicated type B aortic dissection with involvement of the aortic arch: multicentre early experience. Eur J Cardiothorac Surg 2015;47:106–14; discussion 114. https://doi.org/10.1093/ejcts/ ezu067 1261. Iafrancesco M, Goebel N, Mascaro J, Franke UFW, Pacini D, Di Bartolomeo R, et al. Aortic diameter remodelling after the frozen elephant trunk technique in aortic dissection: results from an international multicentre registry. Eur J Cardiothorac Surg 2017;52:310–8. https://doi.org/10.1093/ejcts/ezx131 1262. Tsagakis K, Wendt D, Dimitriou AM, Thielmann M, Shehada S-D, El Gabry M, et al. The frozen elephant trunk treatment is the operation of choice for all kinds of arch disease. J Cardiovasc Surg (Torino) 2018;59:540–6. https://doi.org/10.23736/s0021- 9509.18.10597-0 1263. Widenka KJ, Kosiorowska M, Jakob H, Pacini D, Hemmer W, Grabenwoeger M, et al. Early and midterm results of frozen elephant trunk operation with Evita open stentgraft in patients with Marfan syndrome: results of a multicentre study. BMC Cardiovasc Disord 2022;22:333. https://doi.org/10.1186/s12872-022-02777-5 1264. Jakob H, Shehada SE, Dohle D, Wendt D, El Gabry M, Schlosser T, et al. New 3-zone hybrid graft: first-in-man experience in acute type I dissection. J Thorac Cardiovasc Surg 2022;163:568–74.e1. https://doi.org/10.1016/j.jtcvs.2020.04.113 1265. Tsagakis K, Osswald A, Weymann A, Demircioglu A, Schmack B, Wendt D, et al. The frozen elephant trunk technique: impact of proximalization and the four-sites perfusion technique. Eur J Cardiothorac Surg 2021;61:195–203. https://doi.org/10.1093/ ejcts/ezab295 1266. Rampoldi V, Trimarchi S, Eagle KA, Nienaber CA, Oh JK, Bossone E, et al. Simple risk models to predict surgical mortality in acute type A aortic dissection: the international registry of acute aortic dissection score. Ann Thorac Surg 2007;83:55–61. https://doi. org/10.1016/j.athoracsur.2006.08.007 1267. Lawton JS, Liu J, Kulshrestha K, Moon MR, Damiano RJ, Maniar H, et al. The impact of surgical strategy on survival after repair of type A aortic dissection. J Thorac Cardiovasc Surg 2015;150:294–301.e1. https://doi.org/10.1016/j.jtcvs.2015.03.023 1268. Malvindi PG, Modi A, Miskolczi S, Kaarne M, Velissaris T, Barlow C, et al. Open and closed distal anastomosis for acute type A aortic dissection repair. Interact Cardiovasc Thorac Surg 2016;22:776–83. https://doi.org/10.1093/icvts/ivw044 1269. Geirsson A, Shioda K, Olsson C, Ahlsson A, Gunn J, Hansson EC, et al. Differential outcomes of open and clamp-on distal anastomosis techniques in acute type A aortic dissection. J Thorac Cardiovasc Surg 2019;157:1750–8. https://doi.org/10.1016/j.jtcvs. 2018.09.020 1270. Yan Y, Xu L, Zhang H, Xu Z-Y, Ding X-Y, Wang S-W, et al. Proximal aortic repair versus extensive aortic repair in the treatment of acute type A aortic dissection: a meta-analysis. Eur J Cardiothorac Surg 2016;49:1392–401. https://doi.org/10.1093/ ejcts/ezv351 1271. Poon SS, Theologou T, Harrington D, Kuduvalli M, Oo A, Field M. Hemiarch versus total aortic arch replacement in acute type A dissection: a systematic review and meta-analysis. Ann Cardiothorac Surg 2016;5:156–73. https://doi.org/10.21037/acs. 2016.05.06 1272. Hsieh WC, Kan CD, Yu HC, Aboud A, Lindner J, Henry BM, et al. Ascending aorta replacement vs. total aortic arch replacement in the treatment of acute type A dissection: a meta-analysis. Eur Rev Med Pharmacol Sci 2019;23:9590–611. https://doi. org/10.26355/eurrev_201911_19454 1273. Preventza O, Cervera R, Cooley DA, Bakaeen FG, Mohamed AS, Cheong BYC, et al. Acute type I aortic dissection: traditional versus hybrid repair with antegrade stent delivery to the descending thoracic aorta. J Thorac Cardiovasc Surg 2014;148: 119–25. https://doi.org/10.1016/j.jtcvs.2013.07.055 1274. Roselli EE, Idrees JJ, Bakaeen FG, Tong MZ, Soltesz EG, Mick S, et al. Evolution of simplified frozen elephant trunk repair for acute DeBakey type I dissection: midterm outcomes. Ann Thorac Surg 2018;105:749–55. https://doi.org/10.1016/j.athoracsur.2017. 08.037 1275. Berretta P, Trimarchi S, Patel HJ, Gleason TG, Eagle KA, Di Eusanio M. Malperfusion syndromes in type A aortic dissection: what we have learned from IRAD. J Vis Surg 2018;4:65. https://doi.org/10.21037/jovs.2018.03.13 1276. Benedetto U, Mohamed H, Vitulli P, Petrou M. Axillary versus femoral arterial cannulation in type A acute aortic dissection: evidence from a meta-analysis of comparative studies and adjusted risk estimates. Eur J Cardiothorac Surg 2015;48:953–9. https://doi. org/10.1093/ejcts/ezv035 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.156
1277. Geirsson A, Szeto WY, Pochettino A, McGarvey ML, Keane MG, Woo YJ, et al. Significance of malperfusion syndromes prior to contemporary surgical repair for acute type A dissection: outcomes and need for additional revascularizations. Eur J Cardiothorac Surg 2007;32:255–62. https://doi.org/10.1016/j.ejcts.2007.04.012 1278. Yang B, Norton EL, Rosati CM, Wu X, Kim KM, Khaja MS, et al. Managing patients with acute type A aortic dissection and mesenteric malperfusion syndrome: a 20-year experience. J Thorac Cardiovasc Surg 2019;158:675–87.e4. https://doi.org/ 10.1016/j.jtcvs.2018.11.127 1279. Yang B, Rosati CM, Norton EL, Kim KM, Khaja MS, Dasika N, et al. Endovascular fenestration/stenting first followed by delayed open aortic repair for acute type A aortic dissection with malperfusion syndrome. Circulation 2018;138:2091–103. https://doi. org/10.1161/circulationaha.118.036328 1280. Leshnower BG, Keeling WB, Duwayri YM, Jordan WD, Jr, Chen EP. The “thoracic endovascular aortic repair-first” strategy for acute type A dissection with mesenteric malperfusion: initial results compared with conventional algorithms. J Thorac Cardiovasc Surg 2019;158:1516–24. https://doi.org/10.1016/j.jtcvs.2019.01.116 1281. Rylski B, Szeto WY, Bavaria JE, Branchetti E, Moser W, Milewski RK. Development of a single endovascular device for aortic valve replacement and ascending aortic repair. J Card Surg 2014;29:371–6. https://doi.org/10.1111/jocs.12348 1282. Kreibich M, Rylski B, Kondov S, Morlock J, Scheumann J, Kari FA, et al. Endovascular treatment of acute type A aortic dissection-the Endo Bentall approach. J Vis Surg 2018;4:69. https://doi.org/10.21037/jovs.2018.03.14 1283. Brown CR, Chen Z, Khurshan F, Kreibich M, Bavaria J, Groeneveld P, et al. Outcomes after thoracic endovascular aortic repair in patients with chronic kidney disease in the Medicare population. J Thorac Cardiovasc Surg 2020;159:402–13. https://doi.org/10. 1016/j.jtcvs.2019.01.118 1284. Trimarchi S, Nienaber CA, Rampoldi V, Myrmel T, Suzuki T, Bossone E, et al. Role and results of surgery in acute type B aortic dissection: insights from the international registry of acute aortic dissection (IRAD). Circulation 2006;114:I357–64. https://doi. org/10.1161/circulationaha.105.000620 1285. Tolenaar JL, Froehlich W, Jonker FH, Upchurch GR, Rampoldi V, Tsai TT, et al. Predicting in-hospital mortality in acute type B aortic dissection: evidence from international registry of acute aortic dissection. Circulation 2014;130:S45–50. https://doi. org/10.1161/circulationaha.113.007117 1286. Martin G, Patel N, Grant Y, Jenkins M, Gibbs R, Bicknell C. Antihypertensive medication adherence in chronic type B aortic dissection is an important consideration in the management debate. J Vasc Surg 2018;68:693–9.e2. https://doi.org/10.1016/j.jvs.2017. 12.063 1287. Brooke BS, Griffin CL, Glotzbach JP, Horns JJ, Patel S, Kraiss LW, et al. Predictors of adherence to anti-impulse therapy among patients treated for acute type-B aortic dissections. Ann Vasc Surg 2021;76:95–103. https://doi.org/10.1016/j.avsg.2021.04. 011 1288. Zeeshan A, Woo EY, Bavaria JE, Fairman RM, Desai ND, Pochettino A, et al. Thoracic endovascular aortic repair for acute complicated type B aortic dissection: superiority relative to conventional open surgical and medical therapy. J Thorac Cardiovasc Surg 2010;140:S109–115; discussion S142–S146. https://doi.org/10.1016/j.jtcvs.2010.06. 024 1289. Steuer J, Eriksson MO, Nyman R, Björck M, Wanhainen A. Early and long-term outcome after thoracic endovascular aortic repair (TEVAR) for acute complicated type B aortic dissection. Eur J Vasc Endovasc Surg 2011;41:318–23. https://doi.org/10.1016/j. ejvs.2010.11.024 1290. Zipfel B, Czerny M, Funovics M, Coppi G, Ferro C, Rousseau H, et al. Endovascular treatment of patients with types A and B thoracic aortic dissection using Relay thoracic stent-grafts: results from the RESTORE patient registry. J Endovasc Ther 2011;18: 131–43. https://doi.org/10.1583/10-3233mr.1 1291. Hanna JM, Andersen ND, Ganapathi AM, McCann RL, Hughes GC. Five-year results for endovascular repair of acute complicated type B aortic dissection. J Vasc Surg 2014;59:96–106. https://doi.org/10.1016/j.jvs.2013.07.001 1292. Stelzmueller ME, Nolz R, Mahr S, Beitzke D, Wolf F, Funovics M, et al. Thoracic endovascular repair for acute complicated type B aortic dissections. J Vasc Surg 2019;69: 318–26. https://doi.org/10.1016/j.jvs.2018.05.234 1293. Wilson-Smith AR, Muston B, Kamalanathan H, Yung A, Chen C-HJ, Sahai P, et al. Endovascular repair of acute complicated type B aortic dissection-systematic review and meta-analysis of long-term survival and reintervention. Ann Cardiothorac Surg 2021;10:723–30. https://doi.org/10.21037/acs-2021-taes-17 1294. MacGillivray TE, Gleason TG, Patel HJ, Aldea GS, Bavaria JE, Beaver TM, et al. The Society of Thoracic Surgeons/American Association for Thoracic Surgery clinical practice guidelines on the management of type B aortic dissection. J Thorac Cardiovasc Surg 2022;163:1231–49. https://doi.org/10.1016/j.jtcvs.2021.11.091 1295. Brunkwall J, Kasprzak P, Verhoeven E, Heijmen R, Taylor P, Alric P, et al. Endovascular repair of acute uncomplicated aortic type B dissection promotes aortic remodelling: 1 year results of the ADSORB trial. Eur J Vasc Endovasc Surg 2014;48:285–91. https:// doi.org/10.1016/j.ejvs.2014.05.012 1296. Hossack M, Patel S, Gambardella I, Neequaye S, Antoniou GA, Torella F. Endovascular vs. medical management for uncomplicated acute and sub-acute type B aortic dissection: a meta-analysis. Eur J Vasc Endovasc Surg 2020;59:794–807. https://doi.org/10.1016/j.ejvs.2019.08.003 1297. Sa MP, Jacquemyn X, Van den Eynde J, Chu D, Serna-Gallegos D, Singh MJ, et al. Midterm outcomes of endovascular vs. medical therapy for uncomplicated type B aortic dissection: meta-analysis of reconstructed time to event data. Eur J Vasc Endovasc Surg 2023;66:609–19. https://doi.org/10.1016/j.ejvs.2023.07.004 1298. Sa MP, Jacquemyn X, Brown JA, Ahmad D, Serna-Gallegos D, Arnaoutakis GJ, et al. Thoracic endovascular aortic repair for hyperacute, acute, subacute and chronic type B aortic dissection: meta-analysis of reconstructed time-to-event data. Trends Cardiovasc Med 2023:S1050-1738(23)00113-5. https://doi.org/10.1016/j.tcm.2023. 12.005 1299. Jubouri M, Al-Tawil M, Yip HCA, Bashir A, Tan SZCP, Bashir M, et al. Mid- and longterm outcomes of thoracic endovascular aortic repair in acute and subacute uncomplicated type B aortic dissection. J Card Surg 2022;37:1328–39. https://doi.org/10. 1111/jocs.16349 1300. Torrent DJ, McFarland GE, Wang G, Malas M, Pearce BJ, Aucoin V, et al. Timing of thoracic endovascular aortic repair for uncomplicated acute type B aortic dissection and the association with complications. J Vasc Surg 2021;73:826–35. https://doi.org/ 10.1016/j.jvs.2020.05.073 1301. Schwartz SI, Durham C, Clouse WD, Patel VI, Lancaster RT, Cambria RP, et al. Predictors of late aortic intervention in patients with medically treated type B aortic dissection. J Vasc Surg 2018;67:78–84. https://doi.org/10.1016/j.jvs.2017.05.128 1302. Onitsuka S, Akashi H, Tayama K, Okazaki T, Ishihara K, Hiromatsu S, et al. Long-term outcome and prognostic predictors of medically treated acute type B aortic dissections. Ann Thorac Surg 2004;78:1268–73. https://doi.org/10.1016/j.athoracsur.2004. 02.031 1303. Hughes GC, Ganapathi AM, Keenan JE, Englum BR, Hanna JM, Schechter MA, et al. Thoracic endovascular aortic repair for chronic DeBakey IIIb aortic dissection. Ann Thorac Surg 2014;98:2092–7; discussion 2098. https://doi.org/10.1016/j.athoracsur. 2014.06.066 1304. Jánosi RA, Tsagakis K, Bettin M, Kahlert P, Horacek M, Al-Rashid F, et al. Thoracic aortic aneurysm expansion due to late distal stent graft-induced new entry. Catheter Cardiovasc Interv 2015;85:E43–53. https://doi.org/10.1002/ccd.25614 1305. Cheng L, Xiang D, Zhang S, Zheng C, Wu X. Reintervention after thoracic endovascular aortic repair of uncomplicated type B aortic dissection. J Clin Med 2023;12: 1418. https://doi.org/10.3390/jcm12041418 1306. Akutsu K, Nejima J, Kiuchi K, Sasaki K, Ochi M, Tanaka K, et al. Effects of the patent false lumen on the long-term outcome of type B acute aortic dissection. Eur J Cardiothorac Surg 2004;26:359–66. https://doi.org/10.1016/j.ejcts.2004.03.026 1307. Tsai TT, Evangelista A, Nienaber CA, Myrmel T, Meinhardt G, Cooper JV, et al. Partial thrombosis of the false lumen in patients with acute type B aortic dissection. N Engl J Med 2007;357:349–59. https://doi.org/10.1056/NEJMoa063232 1308. Dake MD, Thompson M, van Sambeek M, Vermassen F, Morales JP. DISSECT: a new mnemonic-based approach to the categorization of aortic dissection. Eur J Vasc Endovasc Surg 2013;46:175–90. https://doi.org/10.1016/j.ejvs.2013.04.029 1309. Wang J, Jin T, Chen B, Pan Y, Shao C. Systematic review and meta-analysis of current evidence in endograft therapy vs medical treatment for uncomplicated type B aortic dissection. J Vasc Surg 2022;76:1099–108.e3. https://doi.org/10.1016/j.jvs.2022.03. 876 1310. Umaña JP, Lai DT, Mitchell RS, Moore KA, Rodriguez F, Robbins RC, et al. Is medical therapy still the optimal treatment strategy for patients with acute type B aortic dissections? J Thorac Cardiovasc Surg 2002;124:896–910. https://doi.org/10.1067/mtc. 2002.123131 1311. Umaña JP, Miller DC, Mitchell RS. What is the best treatment for patients with acute type B aortic dissections—medical, surgical, or endovascular stent-grafting? Ann Thorac Surg 2002;74:S1840–3; discussion S1857–63. https://doi.org/10.1016/s0003- 4975(02)04140-1 1312. Morello F, Santoro M, Fargion AT, Grifoni S, Nazerian P. Diagnosis and management of acute aortic syndromes in the emergency department. Intern Emerg Med 2021;16: 171–81. https://doi.org/10.1007/s11739-020-02354-8 1313. Marui A, Mochizuki T, Mitsui N, Koyama T, Kimura F, Horibe M. Toward the best treatment for uncomplicated patients with type B acute aortic dissection: a consideration for sound surgical indication. Circulation 1999;100:II275–80. https://doi.org/ 10.1161/01.cir.100.suppl_2.ii-275 1314. Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990;264: 2537–41. 1315. Hata M, Shiono M, Inoue T, Sezai A, Niino T, Negishi N, et al. Optimal treatment of type B acute aortic dissection: long-term medical follow-up results. Ann Thorac Surg 2003;75:1781–4. https://doi.org/10.1016/s0003-4975(03)00113-9 1316. Oda T, Minatoya K, Sasaki H, Tanaka H, Seike Y, Itonaga T, et al. Surgical indication for chronic aortic dissection in descending thoracic and thoracoabdominal aorta. Circ Cardiovasc Interv 2017;10:e004292. https://doi.org/10.1161/circinterventions.116. 004292 1317. Conrad MF, Chung TK, Cambria MR, Paruchuri V, Brady TJ, Cambria RP. Effect of chronic dissection on early and late outcomes after descending thoracic and
ESC Guidelines 3693
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.157
thoracoabdominal aneurysm repair. J Vasc Surg 2011;53:600–7; discussion 607. https://doi.org/10.1016/j.jvs.2010.09.053 1318. Crawford ES, Crawford JL, Safi HJ, Coselli JS, Hess KR, Brooks B, et al. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-term results of operations in 605 patients. J Vasc Surg 1986;3:389–404. https://doi.org/10.1067/mva.1986.avs0030389 1319. Zoli S, Etz CD, Roder F, Mueller CS, Brenner RM, Bodian CA, et al. Long-term survival after open repair of chronic distal aortic dissection. Ann Thorac Surg 2010;89: 1458–66. https://doi.org/10.1016/j.athoracsur.2010.02.014 1320. Etz CD, Zoli S, Mueller CS, Bodian CA, Di Luozzo G, Lazala R, et al. Staged repair significantly reduces paraplegia rate after extensive thoracoabdominal aortic aneurysm repair. J Thorac Cardiovasc Surg 2010;139:1464–72. https://doi.org/10.1016/j. jtcvs.2010.02.037 1321. Conrad MF, Ergul EA, Patel VI, Paruchuri V, Kwolek CJ, Cambria RP. Management of diseases of the descending thoracic aorta in the endovascular era: a Medicare population study. Ann Surg 2010;252:603–10. https://doi.org/10.1097/SLA. 0b013e3181f4eaef 1322. Sobocinski J, Dias NV, Berger L, Midulla M, Hertault A, Sonesson B, et al. Endograft repair of complicated acute type B aortic dissections. Eur J Vasc Endovasc Surg 2013; 45:468–74. https://doi.org/10.1016/j.ejvs.2013.01.031 1323. Conrad MF, Carvalho S, Ergul E, Kwolek CJ, Lancaster RT, Patel VI, et al. Late aortic remodeling persists in the stented segment after endovascular repair of acute complicated type B aortic dissection. J Vasc Surg 2015;62:600–5. https://doi.org/10.1016/j. jvs.2015.03.064 1324. Thrumurthy SG, Karthikesalingam A, Patterson BO, Holt PJE, Hinchliffe RJ, Loftus IM, et al. A systematic review of mid-term outcomes of thoracic endovascular repair (TEVAR) of chronic type B aortic dissection. Eur J Vasc Endovasc Surg 2011;42: 632–47. https://doi.org/10.1016/j.ejvs.2011.08.009 1325. Boufi M, Patterson BO, Loundou AD, Boyer L, Grima MJ, Loftus IM, et al. Endovascular versus open repair for chronic type B dissection treatment: a meta-analysis. Ann Thorac Surg 2019;107:1559–70. https://doi.org/10.1016/j. athoracsur.2018.10.045 1326. Conway AM, Qato K, Mondry LR, Stoffels GJ, Giangola G, Carroccio A. Outcomes of thoracic endovascular aortic repair for chronic aortic dissections. J Vasc Surg 2018;67: 1345–52. https://doi.org/10.1016/j.jvs.2017.08.098 1327. Tenorio ER, Oderich GS, Farber MA, Schneider DB, Timaran CH, Schanzer A, et al. Outcomes of endovascular repair of chronic postdissection compared with degenerative thoracoabdominal aortic aneurysms using fenestrated-branched stent grafts. J Vasc Surg 2020;72:822–36.e9. https://doi.org/10.1016/j.jvs.2019.10.091 1328. Marques De Marino P, Ibraheem A, Gafur N, Verhoeven EL, Katsargyris A. Outcomes of fenestrated and branched endovascular aortic repair for chronic postdissection thoracoabdominal aortic aneurysms. J Cardiovasc Surg 2020;61:427–34. https://doi.org/10.23736/s0021-9509.20.11367-3 1329. Gallitto E, Faggioli G, Melissano G, Fargion A, Isernia G, Bertoglio L, et al. Fenestrated and branched endografts for post-dissection thoraco-abdominal aneurysms: results of a national multicentre study and literature review. Eur J Vasc Endovasc Surg 2022;64:630–8. https://doi.org/10.1016/j.ejvs.2022.06.019 1330. Geisbüsch S, Kuehnl A, Salvermoser M, Reutersberg B, Trenner M, Eckstein H-H. Editor’s choice—hospital incidence, treatment, and in hospital mortality following open and endovascular surgery for thoraco-abdominal aortic aneurysms in Germany from 2005 to 2014: secondary data analysis of the Nationwide German DRG microdata. Eur J Vasc Endovasc Surg 2019;57:488–98. https://doi.org/10.1016/ j.ejvs.2018.10.030 1331. Genoni M, Paul M, Jenni R, Graves K, Seifert B, Turina M. Chronic beta-blocker therapy improves outcome and reduces treatment costs in chronic type B aortic dissection. Eur J Cardiothorac Surg 2001;19:606–10. https://doi.org/10.1016/s1010-7940(01) 00662-5 1332. Chen SW, Chan YH, Lin CP, Wu VC-C, Cheng Y-T, Chen D-Y, et al. Association of long-term use of antihypertensive medications with late outcomes among patients with aortic dissection. JAMA Netw Open 2021;4:e210469. https://doi.org/10.1001/ jamanetworkopen.2021.0469 1333. Smedberg C, Hultgren R, Leander K, Steuer J. Pharmacological treatment in patients with aortic dissection. Open Heart 2022;9:e002082. https://doi.org/10.1136/openhrt- 2022-002082 1334. Xiong J, Jiang B, Guo W, Wang SM, Tong XY. Endovascular stent graft placement in patients with type B aortic dissection: a meta-analysis in China. J Thorac Cardiovasc Surg 2009;138:865–72.e1. https://doi.org/10.1016/j.jtcvs.2009.02.005 1335. Zhu JM, Ma WG, Peterss S, Wang L-F, Qiao Z-Y, Ziganshin BA, et al. Aortic dissection in pregnancy: management strategy and outcomes. Ann Thorac Surg 2017;103: 1199–206. https://doi.org/10.1016/j.athoracsur.2016.08.089 1336. Yates MT, Soppa G, Smelt J, Fletcher N, van Besouw J-P, Thilaganathan B, et al. Perioperative management and outcomes of aortic surgery during pregnancy. J Thorac Cardiovasc Surg 2015;149:607–10. https://doi.org/10.1016/j.jtcvs.2014.10.038 1337. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, Blomström-Lundqvist C, Cífková R, De Bonis M, et al. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J 2018;39:3165–241. https:// doi.org/10.1093/eurheartj/ehy340 1338. DeMartino RR, Sen I, Huang Y, Bower TC, Oderich GS, Pochettino A, et al. Population-based assessment of the incidence of aortic dissection, intramural hematoma, and penetrating ulcer, and its associated mortality from 1995 to 2015. Circ Cardiovasc Qual Outcomes 2018;11:e004689. https://doi.org/10.1161/circoutcomes. 118.004689 1339. Evangelista A, Dominguez R, Sebastia C, Salas A, Permanyer-Miralda G, Avegliano G, et al. Long-term follow-up of aortic intramural hematoma: predictors of outcome. Circulation 2003;108:583–9. https://doi.org/10.1161/01.Cir.0000081776.49923.5a 1340. Moral S, Ballesteros E, Roque M, Carrato C, Vilardell P, Brugada R, et al. Intimal disruption in type B aortic intramural hematoma. Does size matter? A systematic review and meta-analysis. Int J Cardiol 2018;269:298–303. https://doi.org/10.1016/j.ijcard. 2018.07.111 1341. Moral S, Ballesteros E, Evangelista A. Conservative vs surgical treatment in type A intramural hematoma. What is new? J Card Surg 2020;35:1758–60. https://doi.org/ 10.1111/jocs.14739 1342. Ishizu K, Kaji S, Nakashima M, Kitai T, Kim K, Ehara N, et al. Focal intimal disruption size at multidetector CT and disease progression in type B aortic intramural hematoma. Radiology 2021;301:311–9. https://doi.org/10.1148/radiol.2021204385 1343. Chou AS, Ziganshin BA, Charilaou P, Tranquilli M, Rizzo JA, Elefteriades JA. Long-term behavior of aortic intramural hematomas and penetrating ulcers. J Thorac Cardiovasc Surg 2016;151:361–72, 373.e1. https://doi.org/10.1016/j.jtcvs. 2015.09.012 1344. Evangelista A, Mukherjee D, Mehta RH, O’Gara PT, Fattori R, Cooper JV, et al. Acute intramural hematoma of the aorta: a mystery in evolution. Circulation 2005;111: 1063–70. https://doi.org/10.1161/01.Cir.0000156444.26393.80 1345. Song JK. Update in acute aortic syndrome: intramural hematoma and incomplete dissection as new disease entities. J Cardiol 2014;64:153–61. https://doi.org/10.1016/j. jjcc.2014.05.005 1346. Song JK, Kim HS, Kang DH, Lim T-H, Song M-G, Park S-W, et al. Different clinical features of aortic intramural hematoma versus dissection involving the ascending aorta. J Am Coll Cardiol 2001;37:1604–10. https://doi.org/10.1016/s0735-1097(01)01184-6 1347. Evangelista A, Maldonado G, Moral S, Teixido-Tura G, Lopez A, Cuellar H, et al. Intramural hematoma and penetrating ulcer in the descending aorta: differences and similarities. Ann Cardiothorac Surg 2019;8:456–70. https://doi.org/10.21037/acs. 2019.07.05 1348. Wee I, Varughese RS, Syn N, Choong A. Non-operative management of type A acute aortic syndromes: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2019;58:41–51. https://doi.org/10.1016/j.ejvs.2018.10.015 1349. Chow SCY, Wong RHL, Lakhani I, Wong MV, Tse G, Yu PSY, et al. Management of acute type A intramural hematoma: upfront surgery or individualized approach? A retrospective analysis and meta-analysis. J Thorac Dis 2020;12:680–9. https://doi. org/10.21037/jtd.2019.12.109 1350. Evangelista A, Czerny M, Nienaber C, Schepens M, Rousseau H, Cao P, et al. Interdisciplinary expert consensus on management of type B intramural haematoma and penetrating aortic ulcer. Eur J Cardiothorac Surg 2015;47:209–17. https://doi.org/ 10.1093/ejcts/ezu386 1351. Sa MP, Jacquemyn X, Tasoudis P, Dufendach K, Singh MJ, de la Cruz KI, et al. Five year results of endovascular versus medical therapy in acute type B aortic intramural haematoma: meta-analysis of reconstructed time to event data. Eur J Vasc Endovasc Surg 2024;67:584–92. https://doi.org/10.1016/j.ejvs.2023.12.024 1352. Moral S, Cuéllar H, Avegliano G, Ballesteros E, Salcedo MT, Ferreira-González I, et al. Clinical implications of focal intimal disruption in patients with type B intramural hematoma. J Am Coll Cardiol 2017;69:28–39. https://doi.org/10.1016/j.jacc.2016.10. 045 1353. Chakos A, Twindyawardhani T, Evangelista A, Maldonado G, Piffaretti G, Yan TD, et al. Endovascular versus medical management of type B intramural hematoma: a meta-analysis. Ann Cardiothorac Surg 2019;8:447–55. https://doi.org/10.21037/acs. 2019.06.11 1354. Song JK, Yim JH, Ahn JM, Kim D-H, Kang JW, Lee TY, et al. Outcomes of patients with acute type a aortic intramural hematoma. Circulation 2009;120:2046–52. https://doi. org/10.1161/circulationaha.109.879783 1355. Ahn JM, Kim H, Kwon O, Om SY, Heo R, Lee S, et al. Differential clinical features and long-term prognosis of acute aortic syndrome according to disease entity. Eur Heart J 2019;40:2727–36. https://doi.org/10.1093/eurheartj/ehz153 1356. Kitamura T, Torii S, Miyamoto T, Mishima T, Ohkubo H, Fujioka S, et al. Watch-and-wait strategy for type A intramural haematoma and acute aortic dissection with thrombosed false lumen of the ascending aorta: a Japanese single-centre experience. Eur J Cardiothorac Surg 2020;58:590–7. https://doi.org/10.1093/ejcts/ ezaa080 1357. Jánosi RA, Gorla R, Tsagakis K, Kahlert P, Horacek M, Bruckschen F, et al. Thoracic endovascular repair of complicated penetrating aortic ulcer: an 11-year single-center experience. J Endovasc Ther 2016;23:150–9. https://doi.org/10.1177/ 1526602815613790 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.158
1358. Nguyen VX, Nguyen BD. PET/CT imaging of abdominal aorta with intramural hematomas, penetrating ulcer, and saccular pseudoaneurysm. Clin Nucl Med 2014;39: 467–9. https://doi.org/10.1097/RLU.0b013e318292f152 1359. Gorla R, Erbel R, Kuehl H, Kahlert P, Tsagakis K, Jakob H, et al. Prognostic value of (18)F-fluorodeoxyglucose PET-CT imaging in acute aortic syndromes: comparison with serological biomarkers of inflammation. Int J Cardiovasc Imaging 2015;31: 1677–85. https://doi.org/10.1007/s10554-015-0725-8 1360. Eggebrecht H, Plicht B, Kahlert P, Erbel R. Intramural hematoma and penetrating ulcers: indications to endovascular treatment. Eur J Vasc Endovasc Surg 2009;38:659–65. https://doi.org/10.1016/j.ejvs.2009.09.001 1361. Salim S, Locci R, Martin G, Gibbs R, Jenkins M, Hamady M, et al. Short- and long-term outcomes in isolated penetrating aortic ulcer disease. J Vasc Surg 2020;72:84–91. https://doi.org/10.1016/j.jvs.2019.09.039 1362. Überall MA, Elling C, Eibl C, Müller-Schwefe GHH, Lefeber C, Heine M, et al. Tapentadol prolonged release in patients with chronic low back pain: real-world data from the German Pain eRegistry. Pain Manag 2022;12:211–27. https://doi.org/ 10.2217/pmt-2021-0058 1363. Ganaha F, Miller DC, Sugimoto K, Do YS, Minamiguchi H, Saito H, et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis. Circulation 2002;106:342–8. https://doi.org/10. 1161/01.cir.0000022164.26075.5a 1364. DeCarlo C, Latz CA, Boitano LT, Waller HD, Kim Y, Sumpio BJ, et al. Natural history of penetrating atherosclerotic ulcers in aortic branch vessels. J Vasc Surg 2021;74: 1904–9. https://doi.org/10.1016/j.jvs.2021.06.035 1365. Piazza M, Squizzato F, Porcellato L, Casali E, Grego F, Antonello M. Predictors of intervention in acute type B aortic penetrating ulcer and intramural hematoma. Semin Thorac Cardiovasc Surg 2022;36:1–10. https://doi.org/10.1053/j.semtcvs.2022. 07.009 1366. Kotsis T, Spyropoulos BG, Asaloumidis N, Christoforou P, Katseni K, Papaconstantinou I. Penetrating atherosclerotic ulcers of the abdominal aorta: a case report and review of the literature. Vasc Specialist Int 2019;35:152–9. https:// doi.org/10.5758/vsi.2019.35.3.152 1367. DeCarlo C, Latz CA, Boitano LT, Kim Y, Tanious A, Schwartz SI, et al. Prognostication of asymptomatic penetrating aortic ulcers: a modern approach. Circulation 2021;144: 1091–101. https://doi.org/10.1161/circulationaha.121.054710 1368. Demetriades D, Velmahos GC, Scalea TM, Jurkovich GJ, Karmy-Jones R, Teixeira PG, et al. Operative repair or endovascular stent graft in blunt traumatic thoracic aortic injuries: results of an American Association for the Surgery of Trauma Multicenter Study. J Trauma 2008;64:561–70; discussion 570–1. https://doi.org/10.1097/TA. 0b013e3181641bb3 1369. Katzenschlager R, Ugurluoglu A, Ahmadi A, Hülsmann M, Koppensteiner R, Larch E, et al. Incidence of pseudoaneurysm after diagnostic and therapeutic angiography. Radiology 1995;195:463–6. https://doi.org/10.1148/radiology.195.2.7724767 1370. Mulder EJ, van Bockel JH, Maas J, van den Akker PJ, Hermans J. Morbidity and mortality of reconstructive surgery of noninfected false aneurysms detected long after aortic prosthetic reconstruction. Arch Surg 1998;133:45–9. https://doi.org/10.1001/ archsurg.133.1.45 1371. Chaud GJ, Mohammadi S, Cervetti MR, Guimaron S, Sebestyen A, Dagenais F, et al. Aortic pseudoaneurysm after type A aortic dissection: results of conservative management. Semin Thorac Cardiovasc Surg 2022;35:457–64. https://doi.org/10.1053/j. semtcvs.2022.04.004 1372. Richens D, Kotidis K, Neale M, Oakley C, Fails A. Rupture of the aorta following road traffic accidents in the United Kingdom 1992–1999. The results of the co-operative crash injury study. Eur J Cardiothorac Surg 2003;23:143–8. https://doi.org/10.1016/ s1010-7940(02)00720-0 1373. Harky A, Bleetman D, Chan JSK, Eriksen P, Chaplin G, MacCarthy-Ofosu B, et al. A systematic review and meta-analysis of endovascular versus open surgical repair for the traumatic ruptured thoracic aorta. J Vasc Surg 2020;71:270–82. https://doi.org/10. 1016/j.jvs.2019.05.011 1374. Heneghan RE, Aarabi S, Quiroga E, Gunn ML, Singh N, Starnes BW. Call for a new classification system and treatment strategy in blunt aortic injury. J Vasc Surg 2016; 64:171–6. https://doi.org/10.1016/j.jvs.2016.02.047 1375. Januzzi JL, Sabatine MS, Eagle KA, Evangelista A, Bruckman D, Fattori R, et al. Iatrogenic aortic dissection. Am J Cardiol 2002;89:623–6. https://doi.org/10.1016/ s0002-9149(01)02312-8 1376. Gómez-Moreno S, Sabaté M, Jiménez-Quevedo P, Vázquez P, Alfonso F, Angiolillo DJ, et al. Iatrogenic dissection of the ascending aorta following heart catheterisation: incidence, management and outcome. EuroIntervention 2006;2:197–202. 1377. Dunning DW, Kahn JK, Hawkins ET, O’Neill W. Iatrogenic coronary artery dissections extending into and involving the aortic root. Catheter Cardiovasc Interv 2000; 51:387–93. https://doi.org/10.1002/1522-726x(200012)51:4<387::aid-ccd3>3.0. co;2-b 1378. Bekkers JA, te Riele RJ, Takkenberg JJ, Bol Raap G, Hofland J, Roos-Hesselink JW, et al. Thoracic aortic surgery: an overview of 40 years clinical practice. J Thorac Cardiovasc Surg 2014;147:332–43. https://doi.org/10.1016/j.jtcvs.2012.11.036 1379. Meena RA, Benarroch-Gampel J, Leshnower BG, Escobar GA, Duwayri Y, Jordan WD, et al. Surveillance recommendations after thoracic endovascular aortic repair should be based on initial indication for repair. Ann Vasc Surg 2019;57:51–9. https:// doi.org/10.1016/j.avsg.2018.11.001 1380. Giles KA, Beck AW, Lala S, Patterson S, Back M, Fatima J, et al. Implications of secondary aortic intervention after thoracic endovascular aortic repair for acute and chronic type B dissection. J Vasc Surg 2019;69:1367–78. https://doi.org/10.1016/j.jvs.2018.07. 080 1381. Kimura N, Itoh S, Yuri K, Adachi K, Matsumoto H, Yamaguchi A, et al. Reoperation for enlargement of the distal aorta after initial surgery for acute type A aortic dissection. J Thorac Cardiovasc Surg 2015;149:S91–8.e1. https://doi.org/10.1016/j.jtcvs.2014. 08.008 1382. Ameli-Renani S, Das R, Morgan RA. Thoracic endovascular aortic repair for the treatment of aortic dissection: post-operative imaging, complications and secondary interventions. Cardiovasc Intervent Radiol 2015;38:1391–404. https://doi.org/10.1007/ s00270-015-1072-9 1383. Fleischmann D, Afifi RO, Casanegra AI, Elefteriades JA, Gleason TG, Hanneman K, et al. Imaging and surveillance of chronic aortic dissection: a scientific statement from the American Heart Association. Circ Cardiovasc Imaging 2022;15:e000075. https://doi.org/10.1161/hci.0000000000000075 1384. Colacchio EC, Squizzato F, Piazza M, Menegolo M, Grego F, Antonello M. Clinical and imaging predictors of disease progression in type B aortic intramural hematomas and penetrating aortic ulcers: a systematic review. Diagnostics (Basel) 2022;12:2727. https://doi.org/10.3390/diagnostics12112727 1385. Vapnik JS, Kim JB, Isselbacher EM, Ghoshhajra BB, Cheng Y, Sundt TM, et al. Characteristics and outcomes of ascending versus descending thoracic aortic aneurysms. Am J Cardiol 2016;117:1683–90. https://doi.org/10.1016/j.amjcard.2016.02.048 1386. Gökalp AL, Takkenberg JJM. Decision-making in thoracic aortic aneurysm surgeryclinician and patient view. Semin Thorac Cardiovasc Surg 2019;31:638–42. https://doi. org/10.1053/j.semtcvs.2019.05.032 1387. Treasure T, King A, Hidalgo Lemp L, Golesworthy T, Pepper J, Takkenberg JJM. Developing a shared decision support framework for aortic root surgery in Marfan syndrome. Heart 2018;104:480–6. https://doi.org/10.1136/heartjnl-2017-311598 1388. Jondeau G, Ropers J, Regalado E, Braverman A, Evangelista A, Teixedo G, et al. International registry of patients carrying TGFBR1 or TGFBR2 mutations: results of the MAC (Montalcino Aortic Consortium). Circ Cardiovasc Genet 2016;9: 548–58. https://doi.org/10.1161/circgenetics.116.001485 1389. Thakker PD, Braverman AC. Cardiogenetics: genetic testing in the diagnosis and management of patients with aortic disease. Heart 2021;107:619–26. https://doi.org/10. 1136/heartjnl-2020-317036 1390. Loeys BL, Schwarze U, Holm T, Callewaert BL, Thomas GH, Pannu H, et al. Aneurysm syndromes caused by mutations in the TGF-beta receptor. N Engl J Med 2006;355:788–98. https://doi.org/10.1056/NEJMoa055695 1391. Regalado ES, Morris SA, Braverman AC, Hostetler EM, De Backer J, Li R, et al. Comparative risks of initial aortic events associated with genetic thoracic aortic disease. J Am Coll Cardiol 2022;80:857–69. https://doi.org/10.1016/j.jacc.2022.05.054 1392. Huguenard AL, Johnson GW, Desai RR, Osbun JW, Dacey RG, Braverman AC. Relationship between phenotypic features in Loeys-Dietz syndrome and the presence of intracranial aneurysms. J Neurosurg 2022;138:1385–92. https://doi.org/10. 3171/2022.9.Jns221373 1393. Lopez-Sainz A, Mila L, Rodriguez-Palomares J, Limeres J, Granato C, La Mura L, et al. Aortic branch aneurysms and vascular risk in patients with Marfan syndrome. J Am Coll Cardiol 2021;77:3005–12. https://doi.org/10.1016/j.jacc.2021.04.054 1394. Kaw A, Kaw K, Hostetler EM, Beleza-Meireles A, Smith-Collins A, Armstrong C, et al. Expanding ACTA2 genotypes with corresponding phenotypes overlapping with smooth muscle dysfunction syndrome. Am J Med Genet A 2022;188:2389–96. https://doi.org/10.1002/ajmg.a.62775 1395. Velvin G, Wilhelmsen JE, Johansen H, Bathen T, Geirdal AO. Systematic review of quality of life in persons with hereditary thoracic aortic aneurysm and dissection diagnoses. Clin Genet 2019;95:661–76. https://doi.org/10.1111/cge.13522 1396. Mariscalco G, Debiec R, Elefteriades JA, Samani NJ, Murphy GJ. Systematic review of studies that have evaluated screening tests in relatives of patients affected by nonsyndromic thoracic aortic disease. J Am Heart Assoc 2018;7:e009302. https://doi.org/10. 1161/jaha.118.009302 1397. Cecchi AC, Boerio ML, Marin I, Pinard A, Milewicz DM. Preventing acute aortic dissections: the power of familial screening and risk assessment. J Am Heart Assoc 2022; 11:e025441. https://doi.org/10.1161/jaha.122.025441 1398. Abbasciano RG, Mariscalco G, Barwell J, Owens G, Zakkar M, Joel-David L, et al. Evaluating the feasibility of screening relatives of patients affected by nonsyndromic thoracic aortic diseases: the REST study. J Am Heart Assoc 2022;11:e023741. https://doi.org/10.1161/jaha.121.023741 1399. Musunuru K, Hershberger RE, Day SM, Klinedinst NJ, Landstrom AP, Parikh VN, et al. Genetic testing for inherited cardiovascular diseases: a scientific statement from the American Heart Association. Circ Genom Precis Med 2020;13:e000067. https://doi. org/10.1161/hcg.0000000000000067
ESC Guidelines 3695
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.159
1400. Albornoz G, Coady MA, Roberts M, Davies RR, Tranquilli M, Rizzo JA, et al. Familial thoracic aortic aneurysms and dissections—incidence, modes of inheritance, and phenotypic patterns. Ann Thorac Surg 2006;82:1400–5. https://doi.org/10.1016/j. athoracsur.2006.04.098 1401. Biddinger A, Rocklin M, Coselli J, Milewicz DM. Familial thoracic aortic dilatations and dissections: a case control study. J Vasc Surg 1997;25:506–11. https://doi.org/10.1016/ s0741-5214(97)70261-1 1402. Robertson EN, van der Linde D, Sherrah AG, Vallely MP, Wilson M, Bannon PG, et al. Familial non-syndromal thoracic aortic aneurysms and dissections—incidence and family screening outcomes. Int J Cardiol 2016;220:43–51. https://doi.org/10.1016/j. ijcard.2016.06.086 1403. De Backer J, Bondue A, Budts W, Evangelista A, Gallego P, Jondeau G, et al. Genetic counselling and testing in adults with congenital heart disease: a consensus document of the ESC Working Group of Grown-Up Congenital Heart Disease, the ESC Working Group on Aorta and Peripheral Vascular Disease and the European Society of Human Genetics. Eur J Prev Cardiol 2020;27:1423–35. https://doi.org/10. 1177/2047487319854552 1404. Wolford BN, Hornsby WE, Guo D, Zhou W, Lin M, Farhat L, et al. Clinical implications of identifying pathogenic variants in individuals with thoracic aortic dissection. Circ Genom Precis Med 2019;12:e002476. https://doi.org/10.1161/circgen.118.002476 1405. Renard M, Francis C, Ghosh R, Scott AF, Witmer PD, Adès LC, et al. Clinical validity of genes for heritable thoracic aortic aneurysm and dissection. J Am Coll Cardiol 2018; 72:605–15. https://doi.org/10.1016/j.jacc.2018.04.089 1406. De Backer J, Jondeau G, Boileau C. Genetic testing for aortopathies: primer for the nongeneticist. Curr Opin Cardiol 2019;34:585–93. https://doi.org/10.1097/hco. 0000000000000669 1407. Milewicz DM, Guo D, Hostetler E, Marin I, Pinard AC, Cecchi AC, et al. Update on the genetic risk for thoracic aortic aneurysms and acute aortic dissections: implications for clinical care. J Cardiovasc Surg 2021;62:203–10. https://doi.org/10.23736/ s0021-9509.21.11816-6 1408. Chou EL, Lindsay ME. The genetics of aortopathies: hereditary thoracic aortic aneurysms and dissections. Am J Med Genet C Semin Med Genet 2020;184:136–48. https:// doi.org/10.1002/ajmg.c.31771 1409. Harris SL, Lindsay ME. Role of clinical genetic testing in the management of aortopathies. Curr Cardiol Rep 2021;23:10. https://doi.org/10.1007/s11886-020-01435-6 1410. Regalado ES, Guo DC, Prakash S, Bensend TA, Flynn K, Estrera A, et al. Aortic disease presentation and outcome associated with ACTA2 mutations. Circ Cardiovasc Genet 2015;8:457–64. https://doi.org/10.1161/circgenetics.114.000943 1411. Teixidó-Tura G, Franken R, Galuppo V, Gutiérrez García-Moreno L, Borregan M, Mulder BJM, et al. Heterogeneity of aortic disease severity in patients with Loeys-Dietz syndrome. Heart 2016;102:626–32. https://doi.org/10.1136/heartjnl- 2015-308535 1412. Baudhuin LM, Kotzer KE, Lagerstedt SA. Increased frequency of FBN1 truncating and splicing variants in Marfan syndrome patients with aortic events. Genet Med 2015;17: 177–87. https://doi.org/10.1038/gim.2014.91 1413. Franken R, Teixido-Tura G, Brion M, Forteza A, Rodriguez-Palomares J, Gutierrez L, et al. Relationship between fibrillin-1 genotype and severity of cardiovascular involvement in Marfan syndrome. Heart 2017;103:1795–9. https://doi.org/10.1136/heartjnl- 2016-310631 1414. Wallace SE, Regalado ES, Gong L, Janda AL, Guo D, Russo CF, et al. MYLK pathogenic variants aortic disease presentation, pregnancy risk, and characterization of pathogenic missense variants. Genet Med 2019;21:144–51. https://doi.org/10.1038/ s41436-018-0038-0 1415. Seike Y, Matsuda H, Ishibashi-Ueda H, Morisaki H, Morisaki T, Minatoya K, et al. Surgical outcome and histological differences between individuals with TGFBR1 and TGFBR2 mutations in Loeys-Dietz syndrome. Ann Thorac Cardiovasc Surg 2021; 27:56–63. https://doi.org/10.5761/atcs.oa.20-00223 1416. Arnaud P, Milleron O, Hanna N, Ropers J, Ould Ouali N, Affoune A, et al. Clinical relevance of genotype-phenotype correlations beyond vascular events in a cohort study of 1500 Marfan syndrome patients with FBN1 pathogenic variants. Genet Med 2021;23:1296–304. https://doi.org/10.1038/s41436-021-01132-x 1417. Silberbach M, Roos-Hesselink JW, Andersen NH, Braverman AC, Brown N, Collins RT, et al. Cardiovascular health in Turner syndrome: a scientific statement from the American Heart Association. Circ Genom Precis Med 2018;11:e000048. https://doi. org/10.1161/hcg.0000000000000048 1418. Gravholt CH, Andersen NH, Conway GS, Dekkers OM, Geffner ME, Klein KO, et al. Clinical practice guidelines for the care of girls and women with Turner syndrome: proceedings from the 2016 Cincinnati International Turner Syndrome Meeting. Eur J Endocrinol 2017;177:G1–70. https://doi.org/10.1530/eje-17-0430 1419. van den Hoven AT, Chelu RG, Duijnhouwer AL, Demulier L, Devos D, Nieman K, et al. Partial anomalous pulmonary venous return in Turner syndrome. Eur J Radiol 2017;95:141–6. https://doi.org/10.1016/j.ejrad.2017.07.024 1420. Carlson M, Airhart N, Lopez L, Silberbach M. Moderate aortic enlargement and bicuspid aortic valve are associated with aortic dissection in Turner syndrome: report of the international Turner syndrome aortic dissection registry. Circulation 2012;126: 2220–6. https://doi.org/10.1161/circulationaha.111.088633 1421. Matura LA, Ho VB, Rosing DR, Bondy CA. Aortic dilatation and dissection in Turner syndrome. Circulation 2007;116:1663–70. https://doi.org/10.1161/circulationaha.106. 685487 1422. Schoemaker MJ, Swerdlow AJ, Higgins CD, Wright AF, Jacobs PA. Mortality in women with Turner syndrome in Great Britain: a national cohort study. J Clin Endocrinol Metab 2008;93:4735–42. https://doi.org/10.1210/jc.2008-1049 1423. Duijnhouwer AL, Bons LR, Timmers H, van Kimmenade RRL, Snoeren M, Timmermans J, et al. Aortic dilatation and outcome in women with Turner syndrome. Heart 2019;105:693–700. https://doi.org/10.1136/heartjnl-2018-313716 1424. Donadille B, Tuffet S, Cholet C, Nedelcu M, Bourcigaux N, Iserin L, et al. Prevalence and progression of aortic dilatation in adult patients with Turner syndrome: a cohort study. Eur J Endocrinol 2020;183:463–70. https://doi.org/10.1530/eje-20-0284 1425. Meccanici F, Schotte MH, Snoeren M, Bons LR, van den Hoven AT, Kardys I, et al. Aortic dilation and growth in women with Turner syndrome. Heart 2023;109: 102–10. https://doi.org/10.1136/heartjnl-2022-320922 1426. Galian-Gay L, Rodriguez-Palomares JF. Turner syndrome and aortic complications: more benign than previously thought. Heart 2022;109:82–3. https://doi.org/10. 1136/heartjnl-2022-321330 1427. Silberbach M, Braverman AC, Prakash SK, Roos-Hesselink JW, Quezada E, Scurlock C. Preventing aortic dissection in Turner syndrome: who faces the risk? Int J Cardiol 2023;377:44. https://doi.org/10.1016/j.ijcard.2023.01.075 1428. Prakash S, Gen TACRI, Milewicz D. Turner syndrome-specific and general population Z-scores are equivalent for most adults with Turner syndrome. Am J Med Genet A 2017;173:1094–6. https://doi.org/10.1002/ajmg.a.38100 1429. Corbitt H, Maslen C, Prakash S, Morris SA, Silberbach M. Allometric considerations when assessing aortic aneurysms in Turner syndrome: implications for activity recommendations and medical decision-making. Am J Med Genet A 2018;176:277–82. https://doi.org/10.1002/ajmg.a.38584 1430. Quigley CA, Fechner PY, Geffner ME, Eugster EA, Ross JL, Habiby RL, et al. Prevention of growth failure in Turner syndrome: long-term results of early growth hormone treatment in the “Toddler Turner” Cohort. Horm Res Paediatr 2021;94: 18–35. https://doi.org/10.1159/000513788 1431. Klein KO, Rosenfield RL, Santen RJ, Gawlik AM, Backeljauw PF, Gravholt CH, et al. Estrogen replacement in Turner syndrome: literature review and practical considerations. J Clin Endocrinol Metab 2018;103:1790–803. https://doi.org/10.1210/jc.2017- 02183 1432. Quigley CA, Wan X, Garg S, Kowal K, Cutler GB, Ross JL. Effects of low-dose estrogen replacement during childhood on pubertal development and gonadotropin concentrations in patients with Turner syndrome: results of a randomized, double-blind, placebo-controlled clinical trial. J Clin Endocrinol Metab 2014;99:E1754–1764. https:// doi.org/10.1210/jc.2013-4518 1433. Davenport ML, Crowe BJ, Travers SH, Rubin K, Ross JL, Fechner PY, et al. Growth hormone treatment of early growth failure in toddlers with Turner syndrome: a randomized, controlled, multicenter trial. J Clin Endocrinol Metab 2007;92:3406–16. https://doi.org/10.1210/jc.2006-2874 1434. Stephure DK; Canadian Growth Hormone Advisory Committee. Impact of growth hormone supplementation on adult height in Turner syndrome: results of the Canadian randomized controlled trial. J Clin Endocrinol Metab 2005;90:3360–6. https://doi.org/10.1210/jc.2004-2187 1435. Campens L, Baris L, Scott NS, Broberg CS, Bondue A, Jondeau G, et al. Pregnancy outcome in thoracic aortic disease data from the registry of pregnancy and cardiac disease. Heart 2021;107:1704–9. https://doi.org/10.1136/heartjnl-2020-318183 1436. Grewal J, Valente AM, Egbe AC, Wu FM, Krieger EV, Sybert VP, et al. Cardiovascular outcomes of pregnancy in Turner syndrome. Heart 2021;107:61–6. https://doi.org/ 10.1136/heartjnl-2020-316719 1437. Thompson T, Zieba B, Howell S, Karakash W, Davis S. A mixed methods study of physical activity and quality of life in adolescents with Turner syndrome. Am J Med Genet A 2020;182:386–96. https://doi.org/10.1002/ajmg.a.61439 1438. Pepin M, Schwarze U, Superti-Furga A, Byers PH. Clinical and genetic features of Ehlers-Danlos syndrome type IV, the vascular type. N Engl J Med 2000;342: 673–80. https://doi.org/10.1056/nejm200003093421001 1439. Byers PH, Belmont J, Black J, De Backer J, Frank M, Jeunemaitre X, et al. Diagnosis, natural history, and management in vascular Ehlers-Danlos syndrome. Am J Med Genet C Semin Med Genet 2017;175:40–7. https://doi.org/10.1002/ajmg.c.31553 1440. Oderich GS, Panneton JM, Bower TC, Lindor NM, Cherry KJ, Noel AA, et al. The spectrum, management and clinical outcome of Ehlers-Danlos syndrome type IV: a 30-year experience. J Vasc Surg 2005;42:98–106. https://doi.org/10.1016/j.jvs.2005. 03.053 1441. Frank M, Adham S, Seigle S, Legrand A, Mirault T, Henneton P, et al. Vascular Ehlers-Danlos syndrome: long-term observational study. J Am Coll Cardiol 2019;73: 1948–57. https://doi.org/10.1016/j.jacc.2019.01.058 1442. Pepin MG, Schwarze U, Rice KM, Liu M, Leistritz D, Byers PH. Survival is affected by mutation type and molecular mechanism in vascular Ehlers-Danlos syndrome (EDS type IV). Genet Med 2014;16:881–8. https://doi.org/10.1038/gim.2014.72 1443. van de Laar I, Baas AF, De Backer J, Blankenstein JD, Dulfer E, Helderman-van den Enden ATJM, et al. Surveillance and monitoring in vascular Ehlers-Danlos syndrome Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.160
in European reference network for rare vascular diseases (VASCERN). Eur J Med Genet 2022;65:104557. https://doi.org/10.1016/j.ejmg.2022.104557 1444. Baderkhan H, Wanhainen A, Stenborg A, Stattin EL, Bjorck M. Celiprolol treatment in patients with vascular Ehlers-Danlos syndrome. Eur J Vasc Endovasc Surg 2021;61: 326–31. https://doi.org/10.1016/j.ejvs.2020.10.020 1445. Ong KT, Perdu J, De Backer J, Bozec E, Collignon P, Emmerich J, et al. Effect of celiprolol on prevention of cardiovascular events in vascular Ehlers-Danlos syndrome: a prospective randomised, open, blinded-endpoints trial. Lancet 2010;376:1476–84. https://doi.org/10.1016/s0140-6736(10)60960-9 1446. Murray ML, Pepin M, Peterson S, Byers PH. Pregnancy-related deaths and complications in women with vascular Ehlers-Danlos syndrome. Genet Med 2014;16:874–80. https://doi.org/10.1038/gim.2014.53 1447. Loeys BL, Dietz HC, Braverman AC, Callewaert BL, De Backer J, Devereux RB, et al. The revised Ghent nosology for the Marfan syndrome. J Med Genet 2010;47:476–85. https://doi.org/10.1136/jmg.2009.072785 1448. Yildiz M, Nucera M, Jungi S, Heinisch PP, Mosbahi S, Becker D, et al. Outcome of Stanford type B dissection in patients with Marfan syndrome. Eur J Cardiothorac Surg 2023;64:ezad178. https://doi.org/10.1093/ejcts/ezad178 1449. Narula N, Devereux RB, Arbustini E, Ma X, Weinsaft JW, Girardi L, et al. Risk of type B dissection in Marfan syndrome: the Cornell aortic aneurysm registry. J Am Coll Cardiol 2023;82:2009–17. https://doi.org/10.1016/j.jacc.2023.08.055 1450. Senemaud J, Gaudry M, Jouve E, Blanchard A, Milleron O, Dulac Y, et al. Primary nonaortic lesions are not rare in Marfan syndrome and are associated with aortic dissection independently of age. J Clin Med 2023;12:2902. https://doi.org/10.3390/ jcm12082902 1451. Judge DP, Rouf R, Habashi J, Dietz HC. Mitral valve disease in Marfan syndrome and related disorders. J Cardiovasc Transl Res 2011;4:741–7. https://doi.org/10.1007/ s12265-011-9314-y 1452. Demolder A, Bianco L, Caruana M, Cervi E, Evangelista A, Jondeau G, et al. Arrhythmia and impaired myocardial function in heritable thoracic aortic disease: an international retrospective cohort study. Eur J Med Genet 2022;65:104503. https://doi.org/10.1016/j.ejmg.2022.104503 1453. Pyeritz RE. Marfan syndrome: improved clinical history results in expanded natural history. Genet Med 2019;21:1683–90. https://doi.org/10.1038/s41436-018-0399-4 1454. Jondeau G, Detaint D, Tubach F, Arnoult F, Milleron O, Raoux F, et al. Aortic event rate in the Marfan population: a cohort study. Circulation 2012;125:226–32. https:// doi.org/10.1161/circulationaha.111.054676 1455. Requejo-Garcia L, Martinez-Lopez R, Plana-Andani E, Medina-Badenes P, Hernándiz-Martínez A, Torres-Blanco A, et al. Extrathoracic aneurysms in Marfan syndrome: a systematic review of the literature. Ann Vasc Surg 2022;87:548–59. https://doi.org/10.1016/j.avsg.2022.08.005 1456. Guala A, Teixidó-Tura G, Rodríguez-Palomares J, Ruiz-Muñoz A, Dux-Santoy L, Villalva N, et al. Proximal aorta longitudinal strain predicts aortic root dilation rate and aortic events in Marfan syndrome. Eur Heart J 2019;40:2047–55. https://doi. org/10.1093/eurheartj/ehz191 1457. Teixido-Tura G, Redheuil A, Rodríguez-Palomares J, Gutiérrez L, Sánchez V, Forteza A, et al. Aortic biomechanics by magnetic resonance: early markers of aortic disease in Marfan syndrome regardless of aortic dilatation? Int J Cardiol 2014;171:56–61. https://doi.org/10.1016/j.ijcard.2013.11.044 1458. Kuijpers JM, Mulder BJ. Aortopathies in adult congenital heart disease and genetic aortopathy syndromes: management strategies and indications for surgery. Heart 2017;103:952–66. https://doi.org/10.1136/heartjnl-2015-308626 1459. Milewicz DM, Braverman AC, De Backer J, Morris SA, Boileau C, Maumenee IH, et al. Marfan syndrome. Nat Rev Dis Primers 2021;7:64. https://doi.org/10.1038/s41572- 021-00298-7 1460. Doyle JJ, Doyle AJ, Wilson NK, Habashi JP, Bedja D, Whitworth RE, et al. A deleterious gene-by-environment interaction imposed by calcium channel blockers in Marfan syndrome. Elife 2015;4:e08648. https://doi.org/10.7554/eLife.08648 1461. Lacro RV, Dietz HC, Sleeper LA, Yetman AT, Bradley TJ, Colan SD, et al. Atenolol versus losartan in children and young adults with Marfan’s syndrome. N Engl J Med 2014;371:2061–71. https://doi.org/10.1056/NEJMoa1404731 1462. Teixido-Tura G, Forteza A, Rodríguez-Palomares J, González Mirelis J, Gutiérrez L, Sánchez V, et al. Losartan versus atenolol for prevention of aortic dilation in patients with Marfan syndrome. J Am Coll Cardiol 2018;72:1613–8. https://doi.org/10.1016/j. jacc.2018.07.052 1463. Pitcher A, Spata E, Emberson J, Davies K, Halls H, Holland L, et al. Angiotensin receptor blockers and β blockers in Marfan syndrome: an individual patient data meta-analysis of randomised trials. Lancet 2022;400:822–31. https://doi.org/10. 1016/s0140-6736(22)01534-3 1464. Groenink M, den Hartog AW, Franken R, Radonic T, de Waard V, Timmermans J, et al. Losartan reduces aortic dilatation rate in adults with Marfan syndrome: a randomized controlled trial. Eur Heart J 2013;34:3491–500. https://doi.org/10.1093/ eurheartj/eht334 1465. Nucera M, Kreibich M, Yildiz M, Berger T, Kolb RK, Kondov S, et al. Endovascular aortic repair in patients with Marfan and Loeys-Dietz syndrome is safe and durable when employed by a multi-disciplinary aortic team. Eur J Cardiothorac Surg 2024;65: ezae069. https://doi.org/10.1093/ejcts/ezae069 1466. Czerny M, Grabenwoger M, Berger T, Aboyans V, Della Corte A, Chen EP, et al. EACTS/STS Guidelines for diagnosing and treating acute and chronic syndromes of the aortic organ. Eur J Cardiothorac Surg 2024;65:ezad426. https://doi.org/10.1093/ ejcts/ezad426 1467. Milleron O, Arnoult F, Delorme G, Detaint D, Pellenc Q, Raffoul R, et al. Pathogenic FBN1 genetic variation and aortic dissection in patients with Marfan syndrome. J Am Coll Cardiol 2020;75:843–53. https://doi.org/10.1016/j.jacc.2019.12.043 1468. Baumgartner H, De Backer J, Babu-Narayan SV, Budts W, Chessa M, Diller G-P, et al. 2020 ESC Guidelines for the management of adult congenital heart disease. Eur Heart J 2021;42:563–645. https://doi.org/10.1093/eurheartj/ehaa554 1469. Martín C, Evangelista A, Serrano-Fiz S, Villar S, Ospina V, Martínez D, et al. Aortic complications in Marfan syndrome: should we anticipate preventive aortic root surgery? Ann Thorac Surg 2020;109:1850–7. https://doi.org/10.1016/j.athoracsur.2019. 08.096 1470. Roman MJ, Pugh NL, Hendershot TP, Devereux RB, Dietz H, Holmes K, et al. Aortic complications associated with pregnancy in Marfan syndrome: the NHLBI national registry of genetically triggered thoracic aortic aneurysms and cardiovascular conditions (GenTAC). J Am Heart Assoc 2016;5:e004052. https://doi.org/10.1161/jaha.116. 004052 1471. Braverman AC, Mittauer E, Harris KM, Evangelista A, Pyeritz RE, Brinster D, et al. Clinical features and outcomes of pregnancy-related acute aortic dissection. JAMA Cardiol 2021;6:58–66. https://doi.org/10.1001/jamacardio.2020.4876 1472. Narula N, Devereux RB, Malonga GP, Hriljac I, Roman MJ. Pregnancy-related aortic complications in women with Marfan syndrome. J Am Coll Cardiol 2021;78:870–9. https://doi.org/10.1016/j.jacc.2021.06.034 1473. Davis MB, Arendt K, Bello NA, Brown H, Briller J, Epps K, et al. Team-based care of women with cardiovascular disease from pre-conception through pregnancy and postpartum: JACC focus seminar 1/5. J Am Coll Cardiol 2021;77:1763–77. https:// doi.org/10.1016/j.jacc.2021.02.033 1474. Meijboom LJ, Vos FE, Timmermans J, Boers GH, Zwinderman AH, Mulder BJM. Pregnancy and aortic root growth in the Marfan syndrome: a prospective study. Eur Heart J 2005;26:914–20. https://doi.org/10.1093/eurheartj/ehi103 1475. Kuperstein R, Cahan T, Yoeli-Ullman R, Ben Zekry S, Shinfeld A, Simchen MJ. Risk of aortic dissection in pregnant patients with the Marfan syndrome. Am J Cardiol 2017; 119:132–7. https://doi.org/10.1016/j.amjcard.2016.09.024 1476. Roberts EA, Pistner A, Osobamiro O, Banning S, Shalhub S, Albright C, et al. Beta-blocker use during pregnancy correlates with less aortic root dilatation in patients with Marfan’s syndrome. Aorta (Stamford) 2023;11:63–70. https://doi.org/10. 1055/a-2072-0469 1477. Roman MJ, Devereux RB. Aortic dissection risk in Marfan syndrome. J Am Coll Cardiol 2020;75:854–6. https://doi.org/10.1016/j.jacc.2019.12.042 1478. Quan A. Fetopathy associated with exposure to angiotensin converting enzyme inhibitors and angiotensin receptor antagonists. Early Hum Dev 2006;82:23–8. https://doi. org/10.1016/j.earlhumdev.2005.11.001 1479. Walfisch A, Al-maawali A, Moretti ME, Nickel C, Koren G. Teratogenicity of angiotensin converting enzyme inhibitors or receptor blockers. J Obstet Gynaecol 2011;31: 465–72. https://doi.org/10.3109/01443615.2011.579197 1480. Cooper WO, Hernandez-Diaz S, Arbogast PG, Dudley JA, Dyer S, Gideon PS, et al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N Engl J Med 2006;354:2443–51. https://doi.org/10.1056/NEJMoa055202 1481. Mas-Stachurska A, Siegert AM, Batlle M, Gorbenko del Blanco D, Meirelles T, Rubies C, et al. Cardiovascular benefits of moderate exercise training in Marfan syndrome: insights from an animal model. J Am Heart Assoc 2017;6:e006438. https://doi.org/10. 1161/jaha.117.006438 1482. Gibson C, Nielsen C, Alex R, Cooper K, Farney M, Gaufin D, et al. Mild aerobic exercise blocks elastin fiber fragmentation and aortic dilatation in a mouse model of Marfan syndrome associated aortic aneurysm. J Appl Physiol 2017;123:147–60. https://doi.org/10.1152/japplphysiol.00132.2017 1483. Selamet Tierney ES, Chung S, Stauffer KJ, Brabender J, Collins RT, Folk R, et al. Can 10 000 healthy steps a day slow aortic root dilation in pediatric patients with Marfan syndrome? J Am Heart Assoc 2022;11:e027598. https://doi.org/10.1161/jaha.122.027598 1484. Jouini S, Milleron O, Eliahou L, Jondeau G, Vitiello D. Effects of a personalized homebased training program among patients suffering from Marfan syndrome: a pilot randomized and controlled study. Intractable Rare Dis Res 2021;10:263–8. https://doi.org/ 10.5582/irdr.2021.01080 1485. Benninghoven D, Hamann D, von Kodolitsch Y, Rybczynski M, Lechinger J, Schroeder F, et al. Inpatient rehabilitation for adult patients with Marfan syndrome: an observational pilot study. Orphanet J Rare Dis 2017;12:127. https://doi.org/10.1186/s13023- 017-0679-0 1486. Fuglsang S, Heiberg J, Hjortdal VE, Laustsen S. Exercise-based cardiac rehabilitation in surgically treated type-A aortic dissection patients. Scand Cardiovasc J 2017;51: 99–105. https://doi.org/10.1080/14017431.2016.1257149 1487. Loeys BL, Chen J, Neptune ER, Judge DP, Podowski M, Holm T, et al. A syndrome of altered cardiovascular, craniofacial, neurocognitive and skeletal development caused
ESC Guidelines 3697
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.161
by mutations in TGFBR1 or TGFBR2. Nat Genet 2005;37:275–81. https://doi.org/10. 1038/ng1511 1488. MacCarrick G, Black JH, III, Bowdin S, El-Hamamsy I, Frischmeyer-Guerrerio PA, Guerrerio AL, et al. Loeys-Dietz syndrome: a primer for diagnosis and management. Genet Med 2014;16:576–87. https://doi.org/10.1038/gim.2014.11 1489. Lindsay ME, Schepers D, Bolar NA, Doyle JJ, Gallo E, Fert-Bober J, et al. Loss-of-function mutations in TGFB2 cause a syndromic presentation of thoracic aortic aneurysm. Nat Genet 2012;44:922–7. https://doi.org/10.1038/ng.2349 1490. Boileau C, Guo DC, Hanna N, Regalado ES, Detaint D, Gong L, et al. TGFB2 mutations cause familial thoracic aortic aneurysms and dissections associated with mild systemic features of Marfan syndrome. Nat Genet 2012;44:916–21. https://doi.org/ 10.1038/ng.2348 1491. van der Linde D, van de Laar IM, Bertoli-Avella AM, Oldenburg RA, Bekkers JA, Mattace-Raso FUS, et al. Aggressive cardiovascular phenotype of aneurysms-osteoarthritis syndrome caused by pathogenic SMAD3 variants. J Am Coll Cardiol 2012;60:397–403. https://doi.org/10.1016/j.jacc.2011.12.052 1492. Hostetler EM, Regalado ES, Guo DC, Hanna N, Arnaud P, Muiño-Mosquera L, et al. SMAD3 pathogenic variants: risk for thoracic aortic disease and associated complications from the Montalcino Aortic Consortium. J Med Genet 2019;56:252–60. https:// doi.org/10.1136/jmedgenet-2018-105583 1493. Renard M, Callewaert B, Malfait F, Campens L, Sharif S, del Campo M, et al. Thoracic aortic-aneurysm and dissection in association with significant mitral valve disease caused by mutations in TGFB2. Int J Cardiol 2013;165:584–7. https://doi.org/10. 1016/j.ijcard.2012.09.029 1494. Bertoli-Avella AM, Gillis E, Morisaki H, Verhagen JMA, de Graaf BM, van de Beek G, et al. Mutations in a TGF-beta ligand, TGFB3, cause syndromic aortic aneurysms and dissections. J Am Coll Cardiol 2015;65:1324–36. https://doi.org/10.1016/j.jacc.2015.01. 040 1495. Marsili L, Overwater E, Hanna N, Baujat G, Baars MJH, Boileau C, et al. Phenotypic spectrum of TGFB3 disease-causing variants in a Dutch-French cohort and first report of a homozygous patient. Clin Genet 2020;97:723–30. https://doi.org/10.1111/ cge.13700 1496. Guo DC, Pannu H, Tran-Fadulu V, Papke CL, Yu RK, Avidan N, et al. Mutations in smooth muscle alpha-actin (ACTA2) lead to thoracic aortic aneurysms and dissections. Nat Genet 2007;39:1488–93. https://doi.org/10.1038/ng.2007.6 1497. Guo DC, Papke CL, Tran-Fadulu V, Regalado ES, Avidan N, Johnson RJ, et al. Mutations in smooth muscle alpha-actin (ACTA2) cause coronary artery disease, stroke, and Moyamoya disease, along with thoracic aortic disease. Am J Hum Genet 2009;84:617–27. https://doi.org/10.1016/j.ajhg.2009.04.007 1498. van de Laar I, Arbustini E, Loeys B, Björck E, Murphy L, Groenink M, et al. European reference network for rare vascular diseases (VASCERN) consensus statement for the screening and management of patients with pathogenic ACTA2 variants. Orphanet J Rare Dis 2019;14:264. https://doi.org/10.1186/s13023-019-1186-2 1499. Brownstein AJ, Ziganshin BA, Kuivaniemi H, Body Simon, Bale A, Elefteriades J. Genes associated with thoracic aortic aneurysm and dissection: an update and clinical implications. Aorta (Stamford) 2017;5:11–20. https://doi.org/10.12945/j.aorta.2017.17.003 1500. Bray JJH, Freer R, Pitcher A, Kharbanda R. Family screening for bicuspid aortic valve and aortic dilatation: a meta-analysis. Eur Heart J 2023;44:3152–64. https://doi.org/10. 1093/eurheartj/ehad320 1501. Michelena HI, Vallabhajosyula S, Prakash SK. Nosology spectrum of the bicuspid aortic valve condition: complex-presentation valvulo-aortopathy. Circulation 2020;142: 294–9. https://doi.org/10.1161/circulationaha.120.046892 1502. Prakash SK, Bosse Y, Muehlschlegel JD, Michelena HI, Limongelli G, Della Corte A, et al. A roadmap to investigate the genetic basis of bicuspid aortic valve and its complications: insights from the International BAVCon (Bicuspid Aortic Valve Consortium). J Am Coll Cardiol 2014;64:832–9. https://doi.org/10.1016/j.jacc.2014. 04.073 1503. Fulmer D, Toomer K, Guo L, Moore K, Glover J, Moore R, et al. Defects in the exocyst-cilia machinery cause bicuspid aortic valve disease and aortic stenosis. Circulation 2019;140:1331–41. https://doi.org/10.1161/circulationaha.119.038376 1504. Luyckx I, Kumar AA, Reyniers E, Dekeyser E, Vanderstraeten K, Vandeweyer G, et al. Copy number variation analysis in bicuspid aortic valve-related aortopathy identifies TBX20 as a contributing gene. Eur J Hum Genet 2019;27:1033–43. https://doi.org/10. 1038/s41431-019-0364-y 1505. Xu YJ, Di RM, Qiao Q, Li X-M, Huang R-T, Xue S, et al. GATA6 loss-of-function mutation contributes to congenital bicuspid aortic valve. Gene 2018;663:115–20. https:// doi.org/10.1016/j.gene.2018.04.018 1506. Gehlen J, Stundl A, Debiec R, Fontana F, Krane M, Sharipova D, et al. Elucidation of the genetic causes of bicuspid aortic valve disease. Cardiovasc Res 2023;119:857–66. https://doi.org/10.1093/cvr/cvac099 1507. Gago-Díaz M, Brion M, Gallego P, Calvo F, Robledo-Carmona J, Saura D, et al. The genetic component of bicuspid aortic valve and aortic dilation. An exome-wide association study. J Mol Cell Cardiol 2017;102:3–9. https://doi.org/10.1016/j.yjmcc.2016. 11.012 1508. Girdauskas E, Geist L, Disha K, Kazakbaev I, Groß T, Schulz S, et al. Genetic abnormalities in bicuspid aortic valve root phenotype: preliminary results. Eur J Cardiothorac Surg 2017;52:156–62. https://doi.org/10.1093/ejcts/ezx065 1509. Mansoorshahi S, Yetman AT, Bissell MM, Kim YY, Michelena H, Hui DS, et al. Whole exome sequencing uncovers the genetic complexity of bicuspid aortic valve in families with early onset complications. medRxiv 2024. https://doi.org/10.1101/2024.02.07. 24302406. 1510. Michelena HI, Della Corte A, Evangelista A, Maleszewski JJ, Edwards WD, Roman MJ, et al. International consensus statement on nomenclature and classification of the congenital bicuspid aortic valve and its aortopathy, for clinical, surgical, interventional and research purposes. Eur J Cardiothorac Surg 2021;60:448–76. https://doi.org/10. 1093/ejcts/ezab038 1511. Verma S, Siu SC. Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med 2014;370:1920–9. https://doi.org/10.1056/NEJMra1207059 1512. Yang LT, Ye Z, Wajih Ullah M, Maleszewski JJ, Scott CG, Padang R, et al. Bicuspid aortic valve: long-term morbidity and mortality. Eur Heart J 2023;44:4549–62. https://doi. org/10.1093/eurheartj/ehad477 1513. Guo MH, Appoo JJ, Saczkowski R, Smith HN, Ouzounian M, Gregory AJ, et al. Association of mortality and acute aortic events with ascending aortic aneurysm: a systematic review and meta-analysis. JAMA Netw Open 2018;1:e181281. https://doi. org/10.1001/jamanetworkopen.2018.1281 1514. Dayan V, Zuasnabar A, Citro R, Bossone E, Michelena HI, Parma G, et al. Aortopathy and regurgitation in bicuspid valve patients increase the risk of aortopathy in relatives. Int J Cardiol 2019;286:117–20. https://doi.org/10.1016/j.ijcard.2019.03.031 1515. Galian-Gay L, Carro Hevia A, Teixido-Turà G, Rodríguez Palomares J, Gutiérrez-Moreno L, Maldonado G, et al. Familial clustering of bicuspid aortic valve and its relationship with aortic dilation in first-degree relatives. Heart 2019;105: 603–8. https://doi.org/10.1136/heartjnl-2018-313802 1516. Tessler I, Leshno M, Shmueli A, Shpitzen S, Durst R, Gilon D. Cost-effectiveness analysis of screening for first-degree relatives of patients with bicuspid aortic valve. Eur Heart J Qual Care Clin Outcomes 2021;7:447–57. https://doi.org/10.1093/ehjqcco/ qcab047 1517. Girdauskas E, Rouman M, Disha K, Espinoza A, Misfeld M, Borger MA, et al. Aortic dissection after previous aortic valve replacement for bicuspid aortic valve disease. J Am Coll Cardiol 2015;66:1409–11. https://doi.org/10.1016/j.jacc.2015.07.022 1518. Masri A, Kalahasti V, Svensson LG, Alashi A, Schoenhagen P, Roselli EE, et al. Aortic cross-sectional area/height ratio and outcomes in patients with bicuspid aortic valve and a dilated ascending aorta. Circ Cardiovasc Imaging 2017;10:e006249. https://doi. org/10.1161/circimaging.116.006249 1519. Della Corte A, Michelena HI, Citarella A, Votta E, Piatti F, Lo Presti F, et al. Risk stratification in bicuspid aortic valve aortopathy: emerging evidence and future perspectives. Curr Probl Cardiol 2021;46:100428. https://doi.org/10.1016/j.cpcardiol.2019.06. 002 1520. Ye Z, Lane C, Beachey JD. Clinical outcomes in patients with bicuspid aortic valves and ascending aorta ≥50 mm under surveillance. JACC: Advances 2023;2:100626. https://doi.org/10.1016/j.jacadv.2023.100626. 1521. Michelena HI, Khanna AD, Mahoney D, Margaryan E, Topilsky Y, Suri RM, et al. Incidence of aortic complications in patients with bicuspid aortic valves. JAMA 2011;306:1104–12. https://doi.org/10.1001/jama.2011.1286 1522. Michelena HI, Desjardins VA, Avierinos JF, Russo A, Nkomo VT, Sundt TM, et al. Natural history of asymptomatic patients with normally functioning or minimally dysfunctional bicuspid aortic valve in the community. Circulation 2008;117:2776–84. https://doi.org/10.1161/CIRCULATIONAHA.107.740878 1523. Girdauskas E, Disha K, Secknus M, Borger M, Kuntze T. Increased risk of late aortic events after isolated aortic valve replacement in patients with bicuspid aortic valve insufficiency versus stenosis. J Cardiovasc Surg (Torino) 2013;54:653–9. 1524. Cortenbach KRG, Yosofi B, Rodwell L, Meek J, Patel R, Prakash SK, et al. Editor’s choice—therapeutic options and outcomes in midaortic syndrome: a systematic review and meta-analysis. Eur J Vasc Endovasc Surg 2023;65:120–30. https://doi.org/10. 1016/j.ejvs.2022.10.017 1525. Teo LL, Cannell T, Babu-Narayan SV, Hughes M, Mohiaddin RH. Prevalence of associated cardiovascular abnormalities in 500 patients with aortic coarctation referred for cardiovascular magnetic resonance imaging to a tertiary center. Pediatr Cardiol 2011;32:1120–7. https://doi.org/10.1007/s00246-011-9981-0 1526. Spaziani G, Girolami F, Arcieri L, Calabri GB, Porcedda G, Di Filippo C, et al. Bicuspid aortic valve in children and adolescents: a comprehensive review. Diagnostics (Basel) 2022;12:1751. https://doi.org/10.3390/diagnostics12071751 1527. Raissadati A, Nieminen H, Haukka J, Sairanen H, Jokinen E. Late causes of death after pediatric cardiac surgery: a 60-year population-based study. J Am Coll Cardiol 2016;68: 487–98. https://doi.org/10.1016/j.jacc.2016.05.038 1528. Panzer J, Bové T, Vandekerckhove K, De Wolf D. Hypertension after coarctation repair–a systematic review. Transl Pediatr 2022;11:270–9. https://doi.org/10.21037/tp- 21-418 1529. Batlivala SP, Goldstein BH. Current transcatheter approaches for the treatment of aortic coarctation in children and adults. Interv Cardiol Clin 2019;8:47–58. https:// doi.org/10.1016/j.iccl.2018.08.001 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.162
1530. Egbe AC, Miranda WR, Bonnichsen CR, Warnes CA, Connolly HM. Potential benefits of ambulatory blood pressure monitoring in coarctation of aorta. J Am Coll Cardiol 2020;75:2089–90. https://doi.org/10.1016/j.jacc.2020.02.053 1531. Luitingh TL, Lee MGY, Jones B, Kowalski R, Weskamp Aguero S, Koleff J, et al. A cross-sectional study of the prevalence of exercise-induced hypertension in childhood following repair of coarctation of the aorta. Heart Lung Circ 2019;28:792–9. https://doi.org/10.1016/j.hlc.2018.03.015 1532. Brown ML, Burkhart HM, Connolly HM, Dearani JA, Cetta F, Li Z, et al. Coarctation of the aorta: lifelong surveillance is mandatory following surgical repair. J Am Coll Cardiol 2013;62:1020–5. https://doi.org/10.1016/j.jacc.2013.06.016 1533. Somers T, Nies H, van Kimmenade RRJ, Bosboom DGH, Geuzebroek GSC, Morshuis WJ. Necessity of life-long follow-up after surgery for coarctation of the aorta: a case series of very late false aneurysm formation. Eur Heart J Case Rep 2022;6:ytac073. https://doi.org/10.1093/ehjcr/ytac073 1534. Padang R, Dennis M, Semsarian C, Bannon PG, Tanous DJ, Celermajer DS, et al. Detection of serious complications by MR imaging in asymptomatic young adults with repaired coarctation of the aorta. Heart Lung Circ 2014;23:332–8. https://doi. org/10.1016/j.hlc.2013.10.055 1535. Bhatt AB, Lantin-Hermoso MR, Daniels CJ, Jaquiss R, Landis BJ, Marino BS, et al. Isolated coarctation of the aorta: current concepts and perspectives. Front Cardiovasc Med 2022;9:817866. https://doi.org/10.3389/fcvm.2022.817866 1536. Erben Y, Oderich GS, Verhagen HJM, Witsenburg M, van den Hoven AT, Debus ES, et al. Multicenter experience with endovascular treatment of aortic coarctation in adults. J Vasc Surg 2019;69:671–9.e1. https://doi.org/10.1016/j.jvs.2018.06.209 1537. Meijs TA, Warmerdam EG, Slieker MG, Krings GJ, Molenschot MMC, Meijboom FJ, et al. Medium-term systemic blood pressure after stenting of aortic coarctation: a systematic review and meta-analysis. Heart 2019;105:1464–70. https://doi.org/10.1136/ heartjnl-2019-314965 1538. Layton KF, Kallmes DF, Cloft HJ, Lindell EP, Cox VS. Bovine aortic arch variant in humans: clarification of a common misnomer. AJNR Am J Neuroradiol 2006;27:1541–2. 1539. Berko NS, Jain VR, Godelman A, Stein EG, Ghosh S, Haramati LB. Variants and anomalies of thoracic vasculature on computed tomographic angiography in adults. J Comput Assist Tomogr 2009;33:523–8. https://doi.org/10.1097/RCT. 0b013e3181888343 1540. Dumfarth J, Peterss S, Kofler M, Plaikner M, Ziganshin BA, Schachner T, et al. In DeBakey type I aortic dissection, bovine aortic arch is associated with arch tears and stroke. Ann Thorac Surg 2017;104:2001–8. https://doi.org/10.1016/j.athoracsur. 2017.05.026 1541. Hornick M, Moomiaie R, Mojibian H, Ziganshin B, Almuwaqqat Z, Lee ES, et al. ‘Bovine’ aortic arch—a marker for thoracic aortic disease. Cardiology 2012;123: 116–24. https://doi.org/10.1159/000342071 1542. Yousef S, Singh S, Alkukhun A, Alturkmani B, Mori M, Chen J, et al. Variants of the aortic arch in adult general population and their association with thoracic aortic aneurysm disease. J Card Surg 2021;36:2348–54. https://doi.org/10.1111/jocs.15563 1543. Tanaka A, Milner R, Ota T. Kommerell’s diverticulum in the current era: a comprehensive review. Gen Thorac Cardiovasc Surg 2015;63:245–59. https://doi.org/10.1007/ s11748-015-0521-3 1544. Upchurch GR, Jr, Escobar GA, Azizzadeh A, Beck AW, Conrad MF, Matsumura JS, et al. Society for Vascular Surgery clinical practice guidelines of thoracic endovascular aortic repair for descending thoracic aortic aneurysms. J Vasc Surg 2021;73:55s–83s. https://doi.org/10.1016/j.jvs.2020.05.076 1545. Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG, Creager MA, Olin JW, et al. Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA 2001;286:1317–24. https://doi.org/10.1001/jama.286.11.1317 1546. Suárez C, Zeymer U, Limbourg T, Baumgartner I, Cacoub P, Poldermans D, et al. Influence of polyvascular disease on cardiovascular event rates. Insights from the REACH registry. Vasc Med 2010;15:259–65. https://doi.org/10.1177/1358863x 10373299 1547. Alberts MJ, Bhatt DL, Mas JL, Ohman EM, Hirsch AT, Rother J, et al. Three-year follow-up and event rates in the international REduction of atherothrombosis for continued health registry. Eur Heart J 2009;30:2318–26. https://doi.org/10.1093/ eurheartj/ehp355 1548. van den Berg MJ, Bhatt DL, Kappelle LJ, de Borst GJ, Cramer MJ, van der Graaf Y, et al. Identification of vascular patients at very high risk for recurrent cardiovascular events: validation of the current ACC/AHA very high risk criteria. Eur Heart J 2017;38: 3211–8. https://doi.org/10.1093/eurheartj/ehx102 1549. Subherwal S, Bhatt DL, Li S, Wang TY, Thomas L, Alexander KP, et al. Polyvascular disease and long-term cardiovascular outcomes in older patients with non-ST-segment-elevation myocardial infarction. Circ Cardiovasc Qual Outcomes 2012;5:541–9. https://doi.org/10.1161/circoutcomes.111.964379 1550. van der Meer MG, Cramer MJ, van der Graaf Y, Appelman Y, Doevendans PA, Nathoe HM. The impact of polyvascular disease on long-term outcome in percutaneous coronary intervention patients. Eur J Clin Invest 2014;44:231–9. https://doi.org/ 10.1111/eci.12222 1551. Steinvil A, Sadeh B, Arbel Y, Justo D, Belei A, Borenstein N, et al. Prevalence and predictors of concomitant carotid and coronary artery atherosclerotic disease. J Am Coll Cardiol 2011;57:779–83. https://doi.org/10.1016/j.jacc.2010.09.047 1552. Ahmed B, Al-Khaffaf H. Prevalence of significant asymptomatic carotid artery disease in patients with peripheral vascular disease: a meta-analysis. Eur J Vasc Endovasc Surg 2009;37:262–71. https://doi.org/10.1016/j.ejvs.2008.10.017 1553. Mukherjee D, Eagle KA, Kline-Rogers E, Feldman LJ, Juliard J-M, Agnelli G, et al. Impact of prior peripheral arterial disease and stroke on outcomes of acute coronary syndromes and effect of evidence-based therapies (from the global registry of acute coronary events). Am J Cardiol 2007;100:1–6. https://doi.org/10.1016/j.amjcard.2007.02. 046 1554. Fowkes FG, Low LP, Tuta S, Kozak J. Ankle-brachial index and extent of atherothrombosis in 8891 patients with or at risk of vascular disease: results of the international AGATHA study. Eur Heart J 2006;27:1861–7. https://doi.org/10.1093/ eurheartj/ehl114 1555. Durand DJ, Perler BA, Roseborough GS, Grega MA, Borowicz LM, Baumgartner WA, et al. Mandatory versus selective preoperative carotid screening: a retrospective analysis. Ann Thorac Surg 2004;78:159–66; discussion 159–66. https://doi.org/10.1016/j. athoracsur.2004.02.024 1556. Naylor AR, Mehta Z, Rothwell PM, Bell PR. Carotid artery disease and stroke during coronary artery bypass: a critical review of the literature. Eur J Vasc Endovasc Surg 2002;23:283–94. https://doi.org/10.1053/ejvs.2002.1609 1557. Jens S, Koelemay MJ, Reekers JA, Bipat S. Diagnostic performance of computed tomography angiography and contrast-enhanced magnetic resonance angiography in patients with critical limb ischaemia and intermittent claudication: systematic review and meta-analysis. Eur Radiol 2013;23:3104–14. https://doi.org/10.1007/s00330-013- 2933-8 1558. Illuminati G, Schneider F, Greco C, Mangieri E, Schiariti M, Tanzilli G, et al. Long-term results of a randomized controlled trial analyzing the role of systematic pre-operative coronary angiography before elective carotid endarterectomy in patients with asymptomatic coronary artery disease. Eur J Vasc Endovasc Surg 2015;49:366–74. https://doi.org/10.1016/j.ejvs.2014.12.030 1559. Eikelboom JW, Bhatt DL, Fox KAA, Bosch J, Connolly SJ, Anand SS, et al. Mortality benefit of rivaroxaban plus aspirin in patients with chronic coronary or peripheral artery disease. J Am Coll Cardiol 2021;78:14–23. https://doi.org/10.1016/j.jacc.2021.04. 083 1560. Aboyans V, Lacroix P, Postil A, Guilloux J, Rollé F, Cornu E, et al. Subclinical peripheral arterial disease and incompressible ankle arteries are both long-term prognostic factors in patients undergoing coronary artery bypass grafting. J Am Coll Cardiol 2005;46: 815–20. https://doi.org/10.1016/j.jacc.2005.05.066 1561. Rihal CS, Sutton-Tyrrell K, Guo P, Keller NM, Jandova R, Sellers MA, et al. Increased incidence of periprocedural complications among patients with peripheral vascular disease undergoing myocardial revascularization in the bypass angioplasty revascularization investigation. Circulation 1999;100:171–7. https://doi.org/10.1161/01.cir.100. 2.171 1562. Aboyans V, Lacroix P. Indications for carotid screening in patients with coronary artery disease. Presse Med 2009;38:977–86. https://doi.org/10.1016/j.lpm.2009.02.015 1563. Collet JP, Cayla G, Ennezat PV, Leclercq F, Cuisset T, Elhadad S, et al. Systematic detection of polyvascular disease combined with aggressive secondary prevention in patients presenting with severe coronary artery disease: the randomized AMERICA study. Int J Cardiol 2018;254:36–42. https://doi.org/10.1016/j.ijcard.2017.11.081 1564. Neufang A, Dorweiler B, Espinola-Klein C, Savvidis S, Doemland M, Schotten S, et al. Outcomes of complex femorodistal sequential autologous vein and biologic prosthesis composite bypass grafts. J Vasc Surg 2014;60:1543–53. https://doi.org/10. 1016/j.jvs.2014.07.103 1565. Calvet D, Touzé E, Varenne O, Sablayrolles J-L, Weber S, Mas J-L. Prevalence of asymptomatic coronary artery disease in ischemic stroke patients: the PRECORIS study. Circulation 2010;121:1623–9. https://doi.org/10.1161/circulationaha.109. 906958 1566. Hofmann R, Kypta A, Steinwender C, Kerschner K, Grund M, Leisch F. Coronary angiography in patients undergoing carotid artery stenting shows a high incidence of significant coronary artery disease. Heart 2005;91:1438–41. https://doi.org/10. 1136/hrt.2004.050906 1567. Masabni K, Raza S, Blackstone EH, Gornik HL, Sabik JF, III. Does preoperative carotid stenosis screening reduce perioperative stroke in patients undergoing coronary artery bypass grafting? J Thorac Cardiovasc Surg 2015;149:1253–60. https://doi.org/10. 1016/j.jtcvs.2015.02.003 1568. Klarin D, Patel VI, Zhang S, Xian Y, Kosinski A, Yerokun B, et al. Concomitant carotid endarterectomy and cardiac surgery does not decrease postoperative stroke rates. J Vasc Surg 2020;72:589–96.e3. https://doi.org/10.1016/j.jvs.2019.10.072 1569. D’Agostino RS, Svensson LG, Neumann DJ, Balkhy HH, Williamson WA, Shahian DM. Screening carotid ultrasonography and risk factors for stroke in coronary artery surgery patients. Ann Thorac Surg 1996;62:1714–23. https://doi.org/10.1016/s0003- 4975(96)00885-5 1570. Weissler EH, Jones WS, Desormais I, Debus S, Mazzolai L, Espinola-Klein C, et al. Polyvascular disease: a narrative review of current evidence and a consideration of
ESC Guidelines 3699
Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026
p.163
the role of antithrombotic therapy. Atherosclerosis 2020;315:10–7. https://doi.org/10. 1016/j.atherosclerosis.2020.11.001 1571. Alkhalil M, Kuzemczak M, Whitehead N, Kavvouras C, Džavík V. Meta-analysis of intensive lipid-lowering therapy in patients with polyvascular disease. J Am Heart Assoc 2021;10:e017948. https://doi.org/10.1161/jaha.120.017948 1572. Ward RP, Goonewardena SN, Lammertin G, Lang RM. Comparison of the frequency of abnormal cardiac findings by echocardiography in patients with and without peripheral arterial disease. Am J Cardiol 2007;99:499–503. https://doi.org/10.1016/j. amjcard.2006.09.102 1573. Kelly R, Staines A, MacWalter R, Stonebridge P, Tunstall-Pedoe H, Struthers AD. The prevalence of treatable left ventricular systolic dysfunction in patients who present with noncardiac vascular episodes: a case-control study. J Am Coll Cardiol 2002;39: 219–24. https://doi.org/10.1016/s0735-1097(01)01725-9 1574. Samsky MD, Hellkamp A, Hiatt WR, Fowkes FGR, Baumgartner I, Berger JS, et al. Association of heart failure with outcomes among patients with peripheral artery disease: insights from EUCLID. J Am Heart Assoc 2021;10:e018684. https://doi.org/10. 1161/jaha.120.018684 1575. Kahan T. The importance of myocardial fibrosis in hypertensive heart disease. J Hypertens 2012;30:685–7. https://doi.org/10.1097/HJH.0b013e328350e5db 1576. O’Rourke MF, Safar ME, Dzau V. The Cardiovascular Continuum extended: aging effects on the aorta and microvasculature. Vasc Med 2010;15:461–8. https://doi.org/10. 1177/1358863x10382946 1577. Duscha BD, Annex BH, Green HJ, Pippen AM, Kraus WE. Deconditioning fails to explain peripheral skeletal muscle alterations in men with chronic heart failure. J Am Coll Cardiol 2002;39:1170–4. https://doi.org/10.1016/s0735-1097(02)01740-0 1578. Mancini DM, Walter G, Reichek N, Lenkinski R, McCully KK, Mullen JL, et al. Contribution of skeletal muscle atrophy to exercise intolerance and altered muscle metabolism in heart failure. Circulation 1992;85:1364–73. https://doi.org/10.1161/ 01.cir.85.4.1364 1579. Hedberg P, Hammar C, Selmeryd J, Viklund J, Leppert J, Hellberg A, et al. Left ventricular systolic dysfunction in outpatients with peripheral atherosclerotic vascular disease: prevalence and association with location of arterial disease. Eur J Heart Fail 2014;16:625–32. https://doi.org/10.1002/ejhf.95 1580. Sandesara PB, Hammadah M, Samman-Tahhan A, Kelli HM, O’Neal WT. Peripheral artery disease and risk of adverse outcomes in heart failure with preserved ejection fraction. Clin Cardiol 2017;40:692–6. https://doi.org/10.1002/clc.22716 1581. Nakamura Y, Kunii H, Yoshihisa A, Takiguchi M, Shimizu T, Yamauchi H, et al. Impact of peripheral artery disease on prognosis in hospitalized heart failure patients. Circ J 2015;79:785–93. https://doi.org/10.1253/circj.CJ-14-1280 1582. Inglis SC, Bebchuk J, Al-Suhaim SA, Case J, Pfeffer MA, Solomon SD, et al. Peripheral artery disease and outcomes after myocardial infarction: an individual-patient meta-analysis of 28,771 patients in CAPRICORN, EPEHESUS, OPTIMAAL and VALIANT. Int J Cardiol 2013;168:1094–101. https://doi.org/10.1016/j.ijcard.2012.11. 033 1583. Jones WS, Clare R, Ellis SJ, Mills JS, Fischman DL, Kraus WE, et al. Effect of peripheral arterial disease on functional and clinical outcomes in patients with heart failure (from HF-ACTION). Am J Cardiol 2011;108:380–4. https://doi.org/10.1016/j.amjcard.2011. 03.057 1584. van Straten AH, Firanescu C, Soliman Hamad MA, Tan MESH, ter Woorst JFJ, Martens EJ, et al. Peripheral vascular disease as a predictor of survival after coronary artery bypass grafting: comparison with a matched general population. Ann Thorac Surg 2010;89:414–20. https://doi.org/10.1016/j.athoracsur.2009.11.036 1585. Goto S, Bhatt DL, Rother J, Alberts M, Hill MD, Ikeda Y, et al. Prevalence, clinical profile, and cardiovascular outcomes of atrial fibrillation patients with atherothrombosis. Am Heart J 2008;156:855–63, 863.e2. https://doi.org/10.1016/j.ahj.2008.06.029 1586. Olesen JB, Gislason GH, Torp-Pedersen C, Lip GY. Atrial fibrillation and vascular disease—a bad combination. Clin Cardiol 2012;35:15–20. https://doi.org/10.1002/clc. 20955 1587. Parvar SL, Thiyagarajah A, Nerlekar N, King P, Nicholls SJ. A systematic review and meta-analysis of gender differences in long-term mortality and cardiovascular events in peripheral artery disease. J Vasc Surg 2021;73:1456–65.e7. https://doi.org/10.1016/ j.jvs.2020.09.039 1588. Depta JP, Bhatt DL. Atherothrombosis and atrial fibrillation: important and often overlapping clinical syndromes. Thromb Haemost 2010;104:657–63. https://doi.org/ 10.1160/th10-05-0332 1589. Kannel WB, Wolf PA, Benjamin EJ, Levy D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol 1998;82:2n–9n. https://doi.org/10.1016/s0002-9149(98)00583-9 1590. Benjamin EJ, Levy D, Vaziri SM, D’Agostino RB, Belanger AJ, Wolf PA. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham heart study. JAMA 1994;271:840–4. 1591. Zhu J, Tan X, Zhou JZ. Peripheral artery disease and clinical outcomes in patients with atrial fibrillation: a systematic review and meta-analysis. Clin Cardiol 2021;44:1050–7. https://doi.org/10.1002/clc.23678 1592. Olesen JB, Lip GY, Lane DA, Køber L, Hansen ML, Karasoy D, et al. Vascular disease and stroke risk in atrial fibrillation: a nationwide cohort study. Am J Med 2012;125: 826.e13–23. https://doi.org/10.1016/j.amjmed.2011.11.024 1593. Skelding KA, Yakubov SJ, Kleiman NS, Reardon MJ, Adams DH, Huang J, et al. Transcatheter aortic valve replacement versus surgery in women at high risk for surgical aortic valve replacement (from the CoreValve US High Risk Pivotal Trial). Am J Cardiol 2016;118:560–6. https://doi.org/10.1016/j.amjcard.2016.05.051 1594. Gilard M, Eltchaninoff H, Iung B, Donzeau-Gouge P, Chevreul K, Fajadet J, et al. Registry of transcatheter aortic-valve implantation in high-risk patients. N Engl J Med 2012;366:1705–15. https://doi.org/10.1056/NEJMoa1114705 1595. Leon MB, Smith CR, Mack M, Miller DC, Moses JW, Svensson LG, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med 2010;363:1597–607. https://doi.org/10.1056/NEJMoa1008232 1596. Reindl M, Lechner I, Holzknecht M, Tiller C, Fink P, Oberhollenzer F, et al. Cardiac magnetic resonance imaging versus computed tomography to guide transcatheter aortic valve replacement (TAVR-CMR): a randomized, open-label, non-inferiority trial. Circulation 2023;148:1220–30. https://doi.org/10.1161/CIRCULATIONAHA. 123.066498 1597. Hindricks G, Potpara T, Dagres N, Arbelo E, Bax JJ, Blomström-Lundqvist C, et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS): The Task Force for the diagnosis and management of atrial fibrillation of the European Society of Cardiology (ESC) developed with the special contribution of the European Heart Rhythm Association (EHRA) of the ESC. Eur Heart J 2021; 42:373–498. https://doi.org/10.1093/eurheartj/ehaa612 1598. Fanaroff AC, Manandhar P, Holmes DR, Cohen DJ, Harrison JK, Hughes GC, et al. Peripheral artery disease and transcatheter aortic valve replacement outcomes: a report from the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Therapy Registry. Circ Cardiovasc Interv 2017;10:e005456. https://doi. org/10.1161/CIRCINTERVENTIONS.117.005456 Downloaded from academic.oup.com/eurheartj/article/45/36/3538/7738955 by guest on 07 October 2026