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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