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Circulation. 2024;150:e351–e442. DOI: 10.1161/CIR.0000000000001285 November 5, 2024 e351

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*Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry may apply; see Appendix 1 for detailed information. †Former ACC/AHA Joint Committee on Clinical Practice Guidelines member; current member during the writing effort. ‡ACC/AHA Joint Committee on Clinical Practice Guidelines.  §AHA/ACC Joint Committee on Clinical Data Standards. ‖Society for Vascular Medicine representative. ¶Society of Cardiovascular Computed Tomography representative. #Society of Cardiovascular Anesthesiologists representative. **AHA/ACC Joint Committee on Performance Measures. ††Society for Cardiovascular Magnetic Resonance representative. ‡‡Heart Rhythm Society representative. §§American College of Surgeons representative. ‖‖American Society of Nuclear Cardiology representative. Peer Review Committee Members and AHA/ACC Joint Committee on Clinical Practice Guidelines Members, see page e413. The American Heart Association requests that this document be cited as follows: Thompson A, Fleischmann KE, Smilowitz NR, Aggarwal NR, Ahmad FS, Allen RB, Altin SE, Auerbach A, Berger JS, Chow B, Dakik HA, de las Fuentes L, Eisenstein EL, Gerhard-Herman M, Ghadimi K, Kachulis B, Leclerc J, Lee CS, Macaulay TE, Mates G, Merli GJ, Mukherjee D; Parwani P, Poole JE, Rich MW, Ruetzler K, Stain SC, Sweitzer B, Talbot AW, Vallabhajosyula S, Whittle J, Williams KA Sr. 2024 AHA/ACC/ACS/ ASNC/HRS/SCA/SCCT/SCMR/SVM guideline for perioperative cardiovascular management for noncardiac surgery: a report of the American College of Cardiology/ American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;150:e351–e442. doi: 10.1161/CIR.0000000000001285 © 2024 by the American Heart Association, Inc., and the American College of Cardiology Foundation.

CLINICAL PRACTICE GUIDELINES

2024 AHA/ACC/ACS/ASNC/HRS/SCA/

SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Developed in Collaboration With and Endorsed by the American College of Surgeons, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society of Cardiovascular Computed Tomography, Society for Cardiovascular Magnetic Resonance, and the Society for Vascular Medicine

Writing Committee Members* Annemarie Thompson, MD, MBA, FAHA, Chair; Kirsten E. Fleischmann, MD, MPH, FACC, Vice Chair; Nathaniel R. Smilowitz, MD, MS, FACC, Vice Chair; Lisa de las Fuentes, MD, MS, FAHA, JC Liaison†; Debabrata Mukherjee, MD, MS, FACC, FAHA, JC Liaison‡; Niti R. Aggarwal, MD, FACC, FASNC; Faraz S. Ahmad, MD, MS, FACC, FAHA§; Robert B. Allen, JD; S. Elissa Altin, MD, FACC, FSVM‖; Andrew Auerbach, MD, MPH; Jeffrey S. Berger, MD, MS, FAHA, FACC; Benjamin Chow, MD, PhD, FACC, FASNC, MSCCT¶; Habib A. Dakik, MD, FACC; Eric L. Eisenstein, DBA; Marie Gerhard-Herman, MD, FACC, FAHA; Kamrouz Ghadimi, MD, MHSc, FAHA; Bessie Kachulis, MD#; Jacinthe Leclerc, RN, PhD, FAHA; Christopher S. Lee, PhD, RN, FAHA**; Tracy E. Macaulay, PharmD, FACC; Gail Mates, BS; Geno J. Merli, MD, FSVM; Purvi Parwani, MBBS, MPH, FACC††; Jeanne E. Poole, MD, FACC, FHRS‡‡; Michael W. Rich, MD, FACC; Kurt Ruetzler, MD, PhD, FAHA; Steven C. Stain, MD, FACS§§; BobbieJean Sweitzer, MD; Amy W. Talbot, MPH; Saraschandra Vallabhajosyula, MD, MSc, FAHA, FACC; John Whittle, MD; Kim Allan Williams Sr., MD, MACC, FAHA, MASNC‖‖

AIM: The “2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery” provides recommendations to guide clinicians in the perioperative cardiovascular evaluation and management of adult patients undergoing noncardiac surgery. METHODS: A comprehensive literature search was conducted from August 2022 to March 2023 to identify clinical studies, reviews, and other evidence conducted on human subjects that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline.

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STRUCTURE: Recommendations from the “2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery” have been updated with new evidence consolidated to guide clinicians; clinicians should be advised this guideline supersedes the previously published 2014 guideline. In addition, evidence-based management strategies, including pharmacological therapies, perioperative monitoring, and devices, for cardiovascular disease and associated medical conditions, have been developed.

Key Words: AHA Scientific Statements ◼ anesthetics ◼ biomarkers ◼ cardiac ◼ preoperative evaluation ◼ cardiovascular ◼ diagnostic testing ◼ cardiovascular diseases ◼ cardiovascular risk score ◼ heart failure ◼ heart valve diseases ◼ intraoperative period ◼ major adverse cardiovascular events ◼ myocardial protection ◼ noncardiac surgery ◼ perioperative management ◼ postoperative complications

◼ preoperative care ◼ revascularization ◼ risk assessment ◼ treatment outcome

TABLE OF CONTENTS

Abstract ������������������������������������������������������������������������������e351 Top Take-Home Messages��������������������������������������������e353 Preamble. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . e353 1.	 Introduction����������������������������������������������������������������e355 1.1. Methodology and Evidence Review��������e355 1.2. Composition of the Writing Committee������������������������������������������������������e355 1.3. Guideline Review and Approval����������������e355 1.4. Scope of the Guideline��������������������������������e355 1.5. Definitions of Surgical Timing and Risk����������������������������������������������������������e357 1.6. Class of Recommendations and Level of Evidence����������������������������������������������������e357 1.7. Abbreviations��������������������������������������������������e358 2.	 Epidemiology of Cardiovascular Disease and Complications in Patients Undergoing Noncardiac Surgery������������������������������������������������������������������������e359 2.1. Team Based Care����������������������������������������e360 2.2. Quality of Life������������������������������������������������e360 3.	 Risk Calculators��������������������������������������������������������e360 3.1. Cardiovascular Risk Indices����������������������e360 3.2. Functional Capacity Assessment������������e362 3.3. Frailty����������������������������������������������������������������e363 3.4. Preoperative Biomarkers for Risk Stratification ��������������������������������������������������e364 4.	 Preoperative Cardiovascular Diagnostic Testing������������������������������������������������������������������������e365 4.1. 12-Lead Electrocardiogram����������������������e365 4.2. Assessment of Ventricular Function��������e366 4.2.1.	 Left Ventricular Function��������������e366 4.2.2.	 Right Ventricular Function ����������e367 4.3. Stress Testing������������������������������������������������e367 4.4. Cardiopulmonary Exercise Testing����������e368 4.5. Coronary Computed Tomography Angiography��������������������������������������������������e369 4.6. Invasive Coronary Angiography����������������e370 5.	 Approach to Perioperative Cardiac Testing������������������������������������������������������������������������e370 5.1. Stepwise Approach to Perioperative Cardiac Assessment������������������������������������e370 6.	 Cardiovascular Comorbidities and

Perioperative Management������������������������������������e372 6.1. Coronary Artery Disease����������������������������e372 6.1.1.	 Coronary Revascularization ��������e372 6.2. Hypertension and Perioperative Blood Pressure Management��������������������e373 6.3. Heart Failure��������������������������������������������������e375 6.3.1.	 Hypertrophic Cardiomyopathy����e376 6.3.2.	 Pulmonary Hypertension��������������e376 6.3.3.	 Adult Congenital Heart

Disease���������������������������������������������e378 6.3.4.	 Left Ventricular Assist Devices����������������������������������������������e379 6.3.5.	 Heart Transplantation Recipients����������������������������������������e380 6.4. Valvular Heart Disease��������������������������������e380 6.4.1.	 Aortic Stenosis��������������������������������e380 6.4.2.	 Mitral Stenosis��������������������������������e382 6.4.3.	 Chronic Aortic and Mitral

Regurgitation ����������������������������������e383 6.4.4.	 Previous Transcatheter

Aortic Valve Implantation or Mitral Valve Transcatheter Edge-to-Edge Repair��������������������e384 6.5. Atrial Fibrillation��������������������������������������������e385 6.6. Cardiovascular Implantable Electronic Devices����������������������������������������e386 6.7. Previous Stroke or Transient Ischemic Attack��������������������������������������������e389 6.8. Obstructive Sleep Apnea����������������������������e389 7.	 Perioperative Medical Therapy������������������������������e390 7.1. Statins��������������������������������������������������������������e390 7.2. Renin-Angiotensin-Aldosterone System Inhibitors������������������������������������������e391 7.3. Calcium Channel Blockers������������������������e392 7.4. Alpha-2 Receptor Agonists������������������������e392 7.5. Antiplatelet Therapy and Timing of Noncardiac Surgery in Patients With Coronary Artery Disease����������������������������e393 7.6. Oral Anticoagulants��������������������������������������e396 7.7. Perioperative Beta Blockers����������������������e399 7.8. Perioperative Management of Blood Glucose ����������������������������������������������e400 8.	 Anesthetic Considerations and Intraoperative

Management��������������������������������������������������������������e401

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8.1. Choice of Anesthetic Technique and Agent��������������������������������������������������������e401 8.2. Perioperative Pain Management��������������e402 8.3. Intraoperative Monitoring Techniques������������������������������������������������������e403 8.3.1.	 Echocardiography��������������������������e403 8.3.2.	 Body Temperature������������������������e404 8.3.3.	 Temporary Mechanical

Circulatory Support������������������������e404 8.3.4.	 Pulmonary Artery

Catheters������������������������������������������e404 8.4. Perioperative Anemia Management��������������������������������������������������e405 9.	 Perioperative Surveillance and Management of Myocardial Injury and Infarction���������������������������������������������������������������������e406 9.1. Myocardial Injury After Noncardiac Surgery Surveillance and Management��������������������������������������������������e406 9.2. Management of Postoperative STEMI/NSTEMI��������������������������������������������e408 10.	 Special Populations��������������������������������������������������e409

10.1 Preoperative Evaluation Prior to

Liver and Kidney Transplantation������������e409 10.2.	 Obesity and Bariatric Surgery��������������������e410 11.	 Cost Value Considerations������������������������������������e410

11.1.	 Cost Value Considerations������������������������e410

11.1.1 Cost Value Considerations for

Biomarkers��������������������������������������e410 11.1.2.	Cost Value Considerations for 12-Lead ECG����������������������������������e411 11.1.3.	Cost Value Considerations for CCTA������������������������������������������e411 11.1.4.	Cost Value Considerations

for Stress Testing��������������������������e411 12.	 Evidence Gaps and Future Research Directions��������������������������������������������������������������������e411 References��������������������������������������������������������������������������e414 Appendix������������������������������������������������������������������������������e435 Author Relationships With Industry and Other Entities��������������������������������������������������������������e435 Appendix������������������������������������������������������������������������������e441

Peer Review Committee Relationships With Industry and Other Entities��������������������������e441

TOP TAKE-HOME MESSAGES

1 A stepwise approach to perioperative cardiac

assessment assists clinicians in determining when surgery should proceed or when a pause for fur­ ther evaluation is warranted. 2.	 Cardiovascular screening and treatment of patients

undergoing noncardiac surgery should adhere to the same indications as nonsurgical patients, care­ fully timed to avoid delays in surgery and chosen in ways to avoid overscreening and overtreatment. 3 Stress testing should be performed judiciously in

patients undergoing noncardiac surgery, especially those at lower risk, and only in patients in whom testing would be appropriate independent of planned surgery. 4.	 Team-based care should be emphasized when managing patients with complex anatomy or unsta­ ble cardiovascular disease. 5.	 New therapies for management of diabetes, heart failure, and obesity have significant periopera­ tive implications. Sodium-glucose cotransporter 2 inhibitors should be discontinued 3 to 4 days before surgery to minimize the risk of perioperative ketoacidosis associated with their use. 6.	 Myocardial injury after noncardiac surgery is a newly identified disease process that should not be ignored because it portends real consequences for affected patients. 7.	 Patients with newly diagnosed atrial fibrillation identified during or after noncardiac surgery have an increased risk of stroke. These patients should be followed closely after surgery to treat reversible causes of arrhythmia and to assess the need for rhythm control and long-term anticoagulation. 8.	 Perioperative bridging of oral anticoagulant therapy should be used selectively only in those patients at highest risk for thrombotic complications and is not recommended in the majority of cases. 9.	 In patients with unexplained hemodynamic instabil­

ity and when clinical expertise is available, emer­ gency focused cardiac ultrasound can be used for perioperative evaluation; however, focused cardiac ultrasound should not replace comprehensive transthoracic echocardiography.

PREAMBLE

Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health. These guidelines, which are based on systematic meth­ ods to evaluate and classify evidence, provide a founda­ tion for the delivery of quality cardiovascular care. The ACC and AHA sponsor the development and publication of clinical practice guidelines without commercial sup­ port, and members volunteer their time to the writing and review efforts. Guidelines are official policy of the ACC and AHA. For some guidelines, the ACC and AHA col­ laborate with other organizations.

Intended Use Clinical practice guidelines provide recommendations applicable to patients with or at risk of developing cardio­ vascular disease (CVD). The focus is on medical practice in the United States, but these guidelines are relevant to

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Thompson et al 2024 Perioperative Cardiovascular Management for Noncardiac Surgery Guideline

patients throughout the world. Although guidelines may be used to inform regulatory or payer decisions, the in­ tent is to improve quality of care and align with patients’ interests. Guidelines are intended to define practices meeting the needs of patients in most, but not all, cir­ cumstances and should not replace clinical judgment.

Clinical Implementation Management, in accordance with guideline recommen­ dations, is effective only when followed by both practitio­ ners and patients. Adherence to recommendations can be enhanced by shared decision-making between clini­ cians and patients, with patient engagement in select­ ing interventions based on individual values, preferences, and associated conditions and comorbidities.

Methodology and Modernization The AHA/ACC Joint Committee on Clinical Practice Guidelines (Joint Committee) continuously reviews, up­ dates, and modifies guideline methodology on the basis of published standards from organizations, including the National Academy of Medicine (formerly the Insti­ tute of Medicine),1,2 and on the basis of internal reevalu­ ation. Similarly, presentation and delivery of guidelines are reevaluated and modified in response to evolving technolo­ gies and other factors to optimally facilitate dissemination of information to health care professionals at the point of care. Numerous modifications to the guidelines have been implemented to make them shorter and enhance “user friendliness.” Guidelines are written and presented in a modular recommendation format in which each chunk includes a table of recommendations, a brief synopsis, recommendation-specific supportive text and, when appropriate, flow diagrams or additional tables. Hyper­ linked references are provided for each modular knowl­ edge chunk to facilitate quick access and review. In recognition of the importance of cost–value con­ siderations, in certain guidelines, when appropriate and feasible, an assessment of value for a drug, device, or intervention may be performed in accordance with the ACC/AHA methodology.3 To ensure that guideline recommendations remain cur­ rent, new data will be reviewed on an ongoing basis by the writing committee and staff. When applicable, recom­ mendations will be updated with new evidence, or new recommendations will be created when supported by published evidence-based data. Going forward, targeted sections/knowledge chunks will be revised dynamically after publication and timely peer review of potentially practice-changing science. The previous designations of “full revision” and “focused update” will be phased out. For additional information and policies on guideline devel­ opment, readers may consult the ACC/AHA guideline methodology manual4 and other methodology articles.5–7 Selection of Writing Committee Members

The Joint Committee strives to ensure that the guide­ line writing committee contains requisite content exper­ tise and is representative of the broader cardiovascular community by selection of experts across a spectrum of backgrounds, representing different geographic regions, sexes, races, ethnicities, intellectual perspectives/biases, and clinical practice settings. Organizations and profes­ sional societies with related interests and expertise are invited to participate as collaborators.

Relationships With Industry and Other Entities The ACC and AHA have rigorous policies and methods to ensure that documents are developed without bias or improper influence. The complete policy on relationships with industry and other entities (RWIs) can be found online. Appendix 1 of the guideline lists writing commit­ tee members’ comprehensive and relevant RWIs.

Evidence Review and Evidence Review Committees In developing recommendations, the writing commit­ tee uses evidence-based methodologies that are based on all available data.4,5 Literature searches focus on randomized controlled trials (RCTs) but also include reg­ istries, nonrandomized comparative and descriptive stud­ ies, case series, cohort studies, systematic reviews, and expert opinion. Only key references are cited. An independent evidence review committee is com­ missioned when there are ≥1 questions deemed of utmost clinical importance and merit formal systematic review to determine which patients are most likely to ben­ efit from a drug, device, or treatment strategy, and to what degree. Criteria for commissioning an evidence review committee and formal systematic review include absence of a current authoritative systematic review, feasibility of defining the benefit and risk in a time frame consistent with the writing of a guideline, relevance to a substantial number of patients, and likelihood that the findings can be translated into actionable recommendations. Evidence review committee members may include methodologists, epidemiologists, clinicians, and biostatisticians. Recom­ mendations developed by the writing committee on the basis of the systematic review are marked “SR.”

Guideline-Directed Management and Therapy The term guideline-directed management and therapy (GDMT) encompasses clinical evaluation, diagnostic testing, and both pharmacological and procedural treat­ ments. For these and all recommended drug treatment regimens, the reader should confirm dosage with prod­ uct insert material and evaluate for contraindications and interactions. Recommendations are limited to drugs,

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devices, and treatments approved for clinical use in the United States.

Joshua A. Beckman, MD, MS, FACC, FAHA

Chair, AHA/ACC Joint Committee on

Clinical Practice Guidelines

1 INTRODUCTION

1.1 Methodology and Evidence Review

The recommendations listed in this guideline are, when­ ever possible, evidence based. An initial extensive evi­ dence review—which included literature derived from research involving human subjects, published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Re­ search and Quality, and other selected databases rele­ vant to this guideline—was conducted from August 2022 to March 2023. Key search words included but were not limited to the following: ACC/AHA clinical practice guideline; anesthesia, general; anesthetics; anesthetics, inhalation; anesthetics, intravenous; bariatric surgery; cardiac assessment; cardiac evaluation; cardiac preop­ erative evaluation; cardiac protection; cardiovascular risk prediction; cardiovascular risk score; death; death, sud­ den, cardiac; elective surgical procedures; evaluation; heart function tests; hospital mortality; intraoperative period; intraoperative complications; lifestyle; major ad­ verse cardiovascular events; myocardial injury time fac­ tors; myocardial protection; noncardiac surgery; outcome assessment, health care; patient care team; periopera­ tive; perioperative cardiovascular risk; periprocedural; perioperative assessment; perioperative management; perioperative medicine; perioperative nursing; periopera­ tive period; postoperative complications; predictive value of tests; preoperative care; preoperative stress testing; quality of life; risk assessment; risk, cardiac; risk factors; surgical procedures, operative; treatment outcome. Additional relevant studies, which were published through November 2023 during the guideline writing process, were also considered by the writing commit­ tee and added to the evidence tables when appropri­ ate. The final evidence tables are included in the Online Data Supplement and summarize the evidence used by the writing committee to formulate recommen­ dations. References selected and published in the pres­ ent document are representative and not all-inclusive.

1.2 Organization of the Writing Committee

The writing committee consisted of anesthesiologists, general cardiologists, interventional cardiologists, elec­ trophysiologists, heart failure cardiologists, cardiac im­ aging experts, critical care physicians, internists, internal medicine hospitalists, general surgeons, family practi­ tioners, advance practice nurses, clinical pharmacists, health economists, and patient advocates. The writ­ ing committee included representatives from the AHA, ACC, American College of Surgeons, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society of Cardiovas­ cular Computed Tomography, Society for Cardiovascular Magnetic Resonance, and the Society for Vascular Med­ icine. Appendix 1 of the current document lists writing committee members’ comprehensive and relevant RWIs.

1.3 Guideline Review and Approval

The Joint Committee appointed a peer review commit­ tee to review the document. The peer review committee comprised individuals nominated by the ACC, AHA, and the collaborating organizations. Reviewers’ RWI infor­ mation was distributed to the writing committee and is published in this document (Appendix 2). This docu­ ment was approved for publication by the governing bodies of the ACC and the AHA and was endorsed by the American College of Surgeons, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society of Cardio­ vascular Computed Tomography, Society for Cardiovas­ cular Magnetic Resonance, and the Society for Vascular Medicine.

1.4 Scope of the Guideline

The focus of this clinical practice guideline is the peri­ operative cardiovascular evaluation and management of the adult patient (≥18 years of age) being considered for noncardiac surgery (NCS). This guideline addresses the time spanning from preoperative evaluation through postoperative care and emphasizes risk assessment, evaluation of functional status, appropriate use of car­ diovascular testing and screening, and management of cardiovascular conditions and risks. Also addressed are evidence-based management strategies, including phar­ macological therapies, perioperative monitoring, and de­ vices, for CVD and associated medical conditions. This guideline is intended to inform all clinicians involved in the care of patients being considered for NCS. Preoperative evaluation encompasses the assess­ ment of perioperative risk and determination of the need for additional cardiovascular testing through exercise, imaging, or biomarker assessment. Although the primary goal of the evaluation should be evaluation and reduction of a patient’s immediate surgical risk, follow-up is war­ ranted throughout and beyond the surgical period, when modifiable cardiovascular risk is identified. The preop­ erative cardiovascular evaluation begins with a focused history and physical examination and a careful review of a patient’s medical history. This assessment informs peri­ operative care and can be used to implement changes in management and therapy. Through a patient-centered,

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team-based approach, management changes could be made to medical therapy, lifestyle modifications, interven­ tional treatment, and perioperative monitoring. Additional management strategies may include modifications of the surgical technique or procedure, identification of the appropriate surgery location (ambulatory surgery cen­ ter, outpatient surgery, or inpatient surgery), and optimal disposition and monitoring of the patient after surgery and upon discharge from the hospital. At times, the best decision from a team-based, patient-centered approach might be to pursue noninvasive or palliative strategies. The guideline is developed to assist clinicians in applying an evidence-based, expert-informed approach to the perioperative cardiovascular management of patients being considered for NCS. This optimally occurs when there is communication between all rel­ evant parties: surgeon, anesthesiologist, intensivist, primary clinician, and consultants, and especially the patient. The overarching goal of perioperative evaluation and management is to encourage patient engagement and facilitate shared decision-making through clear and understandable communication of information regarding perioperative cardiovascular risk and recommendations for risk mitigation and management. This guideline is primarily, but not exclusively, focused on the periopera­ tive management of patients referred for elevated-risk NCS. Little evidence exists to support extensive preop­ erative testing in patients planned for low-risk surgeries, and care is rarely improved by additional cardiovas­ cular testing. This is particularly true for very low-risk

Table 1.  Associated Guidelines and Statements

Title Organization Publication Year (Reference) Guidelines Focused update on DAPT with coronary artery disease ACC/AHA 20161 Management of blood cholesterol AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/ APhA/ASPC/NLA/PCNA

20182 Prevention, detection, evaluation, and management of high blood pressure in adults

ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ ASPC/NMA/PCNA

20183 Management of adults with congenital heart disease AHA/ACC 20184

Diagnosis and treatment of patients with hypertrophic cardiomyopathy AHA/ACC 20205 Management of patients with valvular heart disease ACC/AHA 20216 Coronary artery revascularization ACC/AHA/SCAI 20217 Evaluation and diagnosis of chest pain AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR 20218 Prevention of stroke in patients with stroke and transient ischemic attack AHA/ASA 20219 Management of heart failure AHA/ACC/HFSA 202210 Management of patients with chronic coronary disease AHA/ACC/ACCP/ASPC/NLA/PCNA 202311 Management of atrial fibrillation ACC/AHA/ACCP/HRS 202312 Scientific Statements Evaluation and management of right-sided heart failure AHA 201813 Cardiovascular considerations in caring for pregnant patients AHA 202014 Emerging evidence on coronary heart disease screening in kidney and liver trans­ plantation candidates AHA 202215 Diagnosis and management of patients with myocardial injury after noncardiac surgery AHA 202116 Evaluation and management of pulmonary hypertension in noncardiac surgery AHA 202317 Consensus Document/Reports Prevention of premature discontinuation of DAPT in patients with coronary artery stents AHA/ACC/SCAI/ACS/ADA/ACP 200718 Expert consensus statement on perioperative management of patients with im­ plantable defibrillators, pacemakers and arrythmia monitors AHA/ASA/HRS/STS 201119 Expert consensus decision pathway for periprocedural management of anticoagu­ lation in patients with nonvalvular atrial fibrillation ACC 201720 AACVPR indicates American Association of Cardiovascular and Pulmonary Rehabilitation; AAPA, American Academy of Physician Associates; ABC, Association of Black Cardiologists, ACC, American College of Cardiology; ACCP, American College of Clinical Pharmacy; ACP, American College of Chest Physicians; ACPM, American College of Preventive Medicine; ADA, American Diabetes Association; AGS, American Geriatrics Society; AHA, American Heart Association; APhA, American Pharma­ cists Association; ASA, American Society of Anesthesiologists; ASE, American Society of Echocardiography; ASH, American Society of Hematology; ASPC, American Society for Preventive Cardiology; CHEST, American College of Chest Physicians; DAPT, dual antiplatelet therapy; HFSA, Heart Failure Society of America; HRS, Heart Rhythm Society; NLA, National Lipid Association; NMA, National Medical Association; PCNA, Preventive Cardiovascular Nurses Association; SAEM, Society for Aca­ demic Emergency Medicine; SCAI, Society for Coronary Angiography and Interventions; SCCT, Society of Cardiovascular Computed Tomography; SCMR, Society for Cardiovascular Magnetic Resonance; and STS, Society of Thoracic Surgery.

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procedures, including cataract and other ophthalmology surgeries, dental procedures, endoscopic procedures, and skin biopsies. Surgical procedures that are low risk but require general anesthesia may require additional preoperative consideration given the hemodynamic effects of anesthesia. In developing this guideline, the writing committee reviewed previously published guidelines and related sci­ entific statements. Table 1 contains a list of publications deemed pertinent to this writing effort and is intended for use as a resource, obviating the need to repeat existing guideline recommendations, some of which have been carried forward from previously published guidelines. If unchanged, those recommendations remain current. Any changes to the formatting or content of these recom­ mendations are defined as: •	 Modified: formatting changes (eg, minor modi­ fications such as PICO[TS] [patient population, intervention, comparator, outcome, time, setting] structure) •	 Adapted: substantive changes (eg, major adapta­ tions, such as a change in Class of Recommendation [COR], Level of Evidence [LOE], drug or device classification). Changes are depicted in a footnote below the recom­ mendation tables. Clinicians should be advised that this guideline supersedes the previously published “2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery.”21

1.5 Definitions of Surgical Timing and Risk

In describing the temporal necessity of opera­ tions within this guideline, we have developed the definitions in Table 2 by writing committee con­ sensus. Elevated risk encompasses intermediate or high surgical risk and is generally defined as a ≥1% risk of a major adverse cardiovascular event (MACE); however, due to varying populations, risk criteria, and endpoints, there is significant variabil­ ity in the reporting of predicted risk of cardiovascu­ lar complications among the available risk-prediction tools (Section 3.1, “Cardiovascular Risk Indices”).1,2 Although many risk scores exist, data are lacking to support the use of one risk index over another.

NCS can be classified by the risk of major adverse cardiac and cerebral event (MACCE) associated with each surgery. Risk calculator criteria (Section 3.1, “Cardiovascular Risk Indices”) frequently include the type and location of surgery. Suprainguinal vascular, thoracic, transplant, and neurosurgery operations are associated with the highest risk of MACCE. General, otolaryngology, genitourinary, and orthopedic sur­ gery are considered intermediate risk, and endocrine, breast, gynecology, and obstetrics are considered to have the lowest risk of MACCE. This list does not include the breadth of surgical procedures or account for changes in surgical approach and should there­ fore only be used as a guide.3 Additionally, patient comorbidities may also affect the risk of MACCE, and the risk associated with anesthesia in patients with comorbid disease may not be completely captured when solely considering surgery type. Changes in sur­ gical approach can reduce the risk of MACE in some surgeries. For instance, an aortic aneurysm repair has a lower risk of MACE when performed using endo­ vascular techniques rather than an open repair.4 The timing of surgery also affects risks, with emergency surgeries generally associated with a higher risk of MACCE than elective surgeries.

1.6 Class of Recommendations and Level of

Evidence The COR indicates the strength of recommendation and encompasses the estimated magnitude and certainty of benefit in proportion to risk. The LOE is a measure

Table 2.  Definitions of Surgical Timing and Surgical Risk Timing Definition Emergency Immediate threat to life or limb without surgical intervention, where there is very limited or no time for preoperative clinical evaluation, typically <2 h. Urgent Threat to life or limb without surgical intervention, where there may be time for preoperative clinical evaluation to allow interventions that could reduce risk of MACE or other postoperative complications, typically ≥2 to <24 h. Time-sensitive Surgery may be delayed up to 3 mo to allow for preoperative evaluation and management without negatively impacting outcomes. Elective The surgical procedure can be delayed to permit a complete preoperative evaluation and appropriate management. Risk Category* Definition Low risk Combined surgical and patient characteristics predict a low risk of MACE of <1%.* Elevated risk† Combined surgical and patient characteristics predict an elevated risk of MACE of ≥1%.* *Determining elevated calculated risk depends on the calculator used. Traditionally a RCRI >1 or a calculated risk of MACE with any perioperative risk calculator >1% is used as a threshold to identify patients at elevated risk.

†Encompasses patients at intermediate or high surgical risk. MACE indicates major adverse cardiovascular event; and RCRI, Revised Cardiac Risk Index.

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of the quality of scientific evidence supporting the in­ tervention on the basis of the type, quantity, and con­ sistency of data from clinical trials and other sources (Table 3).1

1.7 Abbreviations

Abbreviations Meaning/Phrase ACEi angiotensin-converting enzyme inhibitors ACHD adult congenital heart disease ACS acute coronary syndrome AF atrial fibrillation AR aortic regurgitation ARB angiotensin receptor blocker AS aortic stenosis ASCVD atherosclerotic cardiovascular disease AVR aortic valve replacement BMS bare-metal stent BNP B-type natriuretic peptide BP blood pressure CAD coronary artery disease CCB calcium channel blocker CCD chronic coronary disease CCTA coronary computed tomography angiography CHD congenital heart disease CIED cardiovascular implantable electronic device CKD chronic kidney disease CPET cardiopulmonary exercise testing CT computed tomography cTn cardiac troponin CVD cardiovascular disease DAPT dual antiplatelet therapy DASI Duke Activity Status Index DBP diastolic blood pressure DES drug-eluting stent DOAC direct oral anticoagulants ECG electrocardiogram EF ejection fraction EMI electromagnetic interference ESU electrosurgery unit FDA US Food and Drug Administration FoCUS focused cardiac ultrasound GDMT guideline-directed management and therapy GLP-1 glucagon-like polypeptide-1 HCM hypertrophic cardiomyopathy HF heart failure HFrEF heart failure with reduced ejection fraction HR hazard ratio Abbreviations Meaning/Phrase

ICA invasive coronary angiography ICD implantable cardioverter-defibrillator LV left ventricular LVAD left ventricular assist device LVEF left ventricular ejection fraction LVOT left ventricular outflow tract MACCE major adverse cardiac and cerebral event MACE major adverse cardiovascular event MAP mean arterial pressure MCS mechanical circulatory support METs metabolic equivalents MI myocardial infarction MICA myocardial infarction and cardiac arrest MINS myocardial injury after noncardiac surgery MR mitral regurgitation MS mitral stenosis MV mitral valve NCS noncardiac surgery NSQIP National Surgical Quality Improvement Program NSTEMI non–ST segment elevation myocardial infarction NT-proBNP N-terminal pro-B-type natriuretic peptide NYHA New York Heart Association OAC oral anticoagulant/anticoagulation OR odds ratio OSA obstructive sleep apnea P2Y12 platelet adenosine diphosphate receptor PA pulmonary artery PAH pulmonary arterial hypertension PCI percutaneous coronary intervention PH pulmonary hypertension POAF perioperative/postoperative atrial fibrillation QOL quality of life RAASi renin-angiotensin-aldosterone system inhibitors RCT randomized controlled trial RCRI Revised Cardiac Risk Index RV right ventricular SBP systolic blood pressure SGLT2i sodium-glucose cotransporter-2 inhibitors STEMI ST-segment elevation myocardial infarction TAVI transcatheter aortic valve implantation TEA thoracic epidural analgesia TEE transesophageal echocardiography TEER transcatheter edge-to-edge repair TTE transthoracic echocardiogram VHD valvular heart disease VKA vitamin K antagonist

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2 EPIDEMIOLOGY OF CARDIOVASCULAR

DISEASE AND COMPLICATIONS IN PATIENTS UNDERGOING NONCARDIAC SURGERY

Each year, approximately 14.4 million inpatient and 19.2 million ambulatory surgeries are performed in the United States, with an estimated 313 million surgeries performed worldwide.1–3 Cardiovascular risk factors and disease are prevalent among adults undergoing NCS, and perioperative cardiovascular complications are an important cause of morbidity and mortality. Multiple car­ diovascular risk factors are reported in 45% of surgical inpatients age ≥45 years, with an increasing prevalence reported over time.4 Atherosclerotic cardiovascular dis­ ease (ASCVD) is diagnosed in nearly 25% of surgical inpatients.4 Between 2008 and 2013, the proportion of surgical inpatients with elevated cardiovascular risk, defined by a Revised Cardiac Risk Index (RCRI) ≥3, in­ creased from 6.6% to 7.7%.4

In a large retrospective analysis of adults ≥45 years undergoing in-hospital surgery, perioperative death, myo­ cardial infarction (MI), or ischemic stroke occurred in 1 of every 33 surgical admissions, corresponding to >150 000 annual perioperative events in the United States.5

Table 3.  Applying the American College of Cardiology/American Heart Association Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, or Diagnostic Testing in Patient Care (Updated May 2019)

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Although orthopedic (40.0%), general (21.4%), and vas­ cular (10.7%) surgeries were the most commonly per­ formed, patients undergoing vascular, thoracic, and solid organ transplantation surgeries had the highest incidence of cardiovascular events.5 Irrespective of the surgical subtype, perioperative cardiovascular complications are associated with prolonged inpatient hospitalizations, sig­ nificantly higher medical costs, and increased mortality.6–9

2.1 Team-Based Care

Synopsis Multidisciplinary care models are increasingly used to manage complex conditions and care pathways in periop­ erative medicine. Team-based care models in the perioper­ ative setting span the pre-, intra-, and posthospital phases of care and are important parts of the care delivery system, providing efficiency of care, ability to improve broad clinical outcomes, and alignment with patient-centered care goals, such as recovery at home. Few data exist demonstrating that interdisciplinary models improve perioperative cardiac care quality or outcomes, but they provide the framework that is critical to meaningful quality and outcome improve­ ments. These models are often described as “pathways” that standardize perioperative cardiac care practices and accelerate the coordination of recovery activities (eg, early mobilization and feeding, use of opioid-sparing pain regimens, deep venous thrombosis prophylaxis). Although there are concerns about patients leaving the hospital af­ ter a shorter inpatient stay, these concerns have largely been offset by focusing on improved pain control and earlier rehabilitation and recovery.1–9 Few data from these meta-analyses support whether standardized protocols or enhanced recovery pathways specifically reduce the risk for cardiovascular complications of surgery, GDMT, or use of preoperative cardiac testing.1–10 In the contem­ porary era, screening and preoperative planning is often conducted by phone or video visits, with trends acceler­ ated during the coronavirus disease-2019 pandemic.10–13 Similar to the results for enhanced recovery pathways, substantial evidence supports the use of remote visits/ televisits to lower rates of case cancellation and improve patient satisfaction, although the impact of remote visits on cardiovascular outcomes, guideline-concordant pre­ operative testing practices, or how remote preoperative consultations might be used to coordinate specialty care for higher risk patients has not been reported.2–4,6–9,14–20 The role of telemedicine, remote monitoring (gathering patient weights, oxygen saturation, or physical activity data remotely), and mobile (“m-health”) interventions in manag­ ing chronic illnesses such as heart failure (HF) is increas­ ingly described.21 The evidence base for similar models for the postoperative care of patients undergoing NCS is still early in its development.22–30 Available evidence supports the benefit to readmission and patient satisfaction with use of these approaches.4,28,31–36 2.2 Quality of Life

Synopsis The World Health Organization defines quality of life (QOL) as “an individual's perception of their position in life in the context of the culture and value systems in which they live and about their goals, expectations, standards and concerns.”1 Assessment of QOL may im­ prove patient experiences and outcomes of health care procedures and treatments. Patient-reported outcome measures can be used to survey patients’ health-related QOL. Instruments specific to the therapeutic area may be more sensitive than those that are generic.2,3 Although questionnaires are commonly employed, lis­ tening to patients and inquiring about their priorities is extremely important to tailor care to their unique needs. Because surgery confers risks of complications, espe­ cially for high-risk patients with existing CVD, discussing patients’ goals and priorities with respect to QOL may guide perioperative planning.4 In the last decades, a few groups have assessed interventions that might impact perioperative QOL.5,6 Unfortunately, solid evidence is still lacking to formulate actionable recommendations aimed at improving QOL in patients undergoing NCS. Although long-term benefits on QOL from an NCS may outweigh short-term cardiac risks for some patients, this ratio is unevenly balanced in the literature. Greater patient sat­ isfaction has been associated with perioperative assess­ ment that involves shared decision-making.7

3 RISK CALCULATORS

3.1 Cardiovascular Risk Indices

Recommendation for Cardiovascular Risk Indices Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendation

2a B-NR 1 In patients with known CVD being considered

for NCS, a validated risk-prediction tool can be useful to estimate the risk of perioperative MACE.1–4

Synopsis Preoperative cardiovascular risk assessment can help estimate the likelihood of perioperative adverse out­ comes. Several risk indices have been developed based on multivariable analyses of large observational data and have been validated in large datasets (Table 4). Com­ monly used cardiovascular risk scores include the RCRI,2 the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) perioperative MI and cardiac arrest (MICA) risk calculator,5 and the univer­ sal American College of Surgeons NSQIP surgical risk calculator.3 Risk calculators can be used in addition or as an alternative to the assessment of separately discussed

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Table 4.  Risk Scores and Calculators

Goldman Index of Cardiac Risk16 (1977) RCRI2 (1999) Gupta NSQIP Risk Calculator for Perioperative MICA5 (2011) American College of Surgeons NSQIP Surgical Risk Calculator3,13 (2023) Surgical Outcome Risk Tool12 (2014) NSQIP Geriatric- Sensitive Perioperative Cardiac Risk Index17 (2017) AUB-HAS2 Cardiovascular Risk Index14 (2019)

Criteria Age >70 y (5 points)

Recent MI within 6 mo (10 points) Jugular venous distention or a third heart sound on auscultation (11 points) ≥5 PVCs per minute (7 points) Nonsinus rhythm or PACs on preoperative ECG (7 points) Aortic stenosis (3 points) Intraperitoneal, intrathoracic, or aortic surgery (3 points) Any emergency surgery (4 points) Ischemic heart disease

Cerebrovascular disease History of HF Insulin therapy for diabetes Serum creatinine ≥2.0 mg/dL Planned highrisk procedure (intraperitoneal, intrathoracic, or vascular surgery) (1 point for each criterion) Age

ASA class Preoperative function Creatinine Procedure type (anorectal surgery, aortic, bariatric, brain, breast, cardiac, ENT, foregut/ hepatopancreatobiliary, gallbladder/ap­ pendix/adrenal/ spleen, intestinal, neck, obstetric/ gynecologic, orthopedic, other abdomen, periph­ eral vascular, skin, spine, thoracic, urology, vein) Age group

Sex ASA class Functional status Emergency case Steroid use for chronic condition Ascites within 30 d preoperatively System sepsis within 48 h preoperatively Ventilator dependent Disseminated cancer Diabetes Hypertension requiring medication Previous cardiac event HF in 30 d preoperatively Dyspnea Current smoker within 1 y History of COPD Dialysis Acute renal failure BMI class CPT-specific linear risk Age group

ASA class Urgency of surgery Specialty Severity of surgery Cancer ASA class

History of HF History of stroke Diabetes Functional status (partially versus totally dependent) Creatinine >1.5 mg/dL Surgical category Age ≥75 y

History of heart disease Symptoms of angina/ dyspnea Hemoglobin <12 mg/dL Vascular surgery Emergency surgery

Score Range Class I: 0-5 points (lowest risk)

Class II: 6-12 points Class III: 13-25 points Class IV: ≥26 points (highest risk) Class I: RCRI 0 (lowest risk)

Class II: RCRI 1 Class III: RCRI 2 Class IV: RCRI 3+ (highest risk) 0%-100%

(0% lowest risk, 100% highest risk) 0%-100%

(0% lowest risk, 100% highest risk) 0%-100%

(0% lowest risk, 100% highest risk) 0%-100%

(0% lowest risk, 100% highest risk) CVRI Score 0 (lowest risk)

CVRI Score 1 CVRI Score 2 CVRI Score 3 CVRI Score >3 (highest risk)

Threshold Denoting Elevated Risk Class II or higher (≥6 points) RCRI >1 >1% >1% >1% CVRI Score ≥2 Outcome Intraoperative/ postoperative MI, pulmonary edema, VT, cardiac death MI, pulmonary edema, ventricular fibrillation, com­ plete heart block, cardiac death Intraoperative/ postoperative MI or cardiac arrest within 30 d Cardiac arrest, MI, allcause mortality within 30 d 30-d mortality Cardiac arrest, MI, all-cause mortality within 30 d Death, MI, or stroke at 30 d Derivation (n) 1001 1422 211 410 1 414 006 19 097 584 931 3284 Derivation Set ROC 0.61 0.76 0.88 0.90 (cardiac arrest or MI)

0.94 (mortality) N/A 0.90

Validation Set ROC 0.70 0.81

0.75† 0.87* 0.88 (cardiac arrest or MI)* 0.94 (mortality)* 0.91‡ 0.83*

(0.76 in adults age ≥65 y) 0.82*

Adapted with permission from Smilowitz et al.1 Copyright 2020 American Medical Association. All rights reserved. *Validated using the NSQIP database. †Pooled validation studies assessing the performance of the RCRI in mixed noncardiac surgery. ‡Derived and validated using the NCEPOD Knowing the Risk study. ASA indicates American Society of Anesthesiologists; AUB, American University of Beirut; BMI, body mass index; COPD, chronic obstructive pulmonary disease; CPT, current procedural terminology; CVRI, Coronary Vascular Resistance Index; ECG, electrocardiogram; ENT, ear, nose, and throat; HF, heart failure; MI, myocardial infarction; MICA, MI and cardiac arrest; NCEPOD, National Confidential Enquiry into Patient Outcome and Death; NSQIP, National Surgical Quality Improvement Program; PAC, pre­ mature atrial contraction; PVC, premature ventricular complex; RCRI, Revised Cardiac Risk Index; ROC, receiver operating characteristic; and VT, ventricular tachycardia.

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surgery-related (eg, anesthesia type, surgery type) and patient-related (eg, physical activity, physical examina­ tion) risk factors. Combined, there is significant variability in the predicted risk of cardiovascular complications us­ ing different risk-prediction tools.1,6 Evaluated endpoints were not consistent in all risk scores (Table 4). Although many risk scores exist, data are lacking to support the use of one risk index over another, and research is un­ derway to further refine perioperative risk. For example, a recently published study has shown that perioperative risk stratification may be enhanced by combining tra­ ditional risk indices with estimates of coronary calcium burden from existing, nongated chest computed tomog­ raphy (CT) imaging in the year before NCS.4 Differences in surgical populations may also affect risk prediction. Risk scores have poorer discrimination in patients under­ going vascular surgery, likely due to the underestimation of the risk of MI.7–9 Despite their reasonable ability to predict perioperative risk of MACE, there have been few studies in which perioperative treatment strategies were modified based on preoperative risk prediction tools; fu­ ture studies are needed to inform this practice.

Recommendation-Specific Supportive Text

1 There are several indices available for periopera­

tive cardiovascular risk prediction. The American Society of Anesthesiologists (ASA) Physical Status Classification System classifies patients into categories according to their overall health status.10 With 6 predictors of risk (1 point assigned for each criterion), the RCRI is a simple, validated, and commonly used tool to assess perioperative risk of major cardiac complications.3 In a pooled analysis of 24 validation studies, the RCRI had modest risk discrimination for cardiac events in patients undergoing NCS, although there is dis­ cordance among the various risk-prediction tools in identifying low-risk patients, defined as hav­ ing an estimated risk of MACE of <1%.7,11 The Surgical Outcome Risk Tool estimates 30-day mortality after NCS based on the ASA Physical Status grade, urgency of surgery, surgical spe­ cialty and severity, cancer, and age ≥65 years.12 The 21-component universal NSQIP surgical risk calculator may provide superior predictive discrimi­ nation.13 The AUB (American University of Beirut)- HAS2 cardiovascular risk index is easily calculated and used to assess 30-day event risk, stratifying patients undergoing NCS into low (score 0-1), intermediate (score 2-3), and high risk (score >3) based on 6 data elements.14 A simplified method using 3 traditional risk factors for hypertension, diabetes, and current smoking identified a low incidence of MI (0.10%) among patients without risk factors who underwent NCS.15 3.2 Functional Capacity Assessment

Recommendation for Functional Capacity Assessment Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendation

2a B-NR 1 In patients undergoing elevated-risk NCS, a

structured assessment of functional capac­ ity (such as the Duke Activity Status Index [DASI]) is reasonable to stratify the risk of perioperative adverse cardiovascular events.1–8

Synopsis Functional capacity is an important predictor of risk of adverse cardiovascular events after NCS.1–9 It is usually measured in metabolic equivalents (METs) of task, with 4 METs considered the threshold for poor functional capacity. Functional capacity is commonly assessed by asking patients if they can climb 2 flights of stairs (an activity associated with >4 METs) or by using a patientreported instrument such as the DASI (Table 5), a semi­ quantitative tool to assess functional capacity based on patients’ reported ability to perform a set of 12 daily activities.6 In selected cases, exercise stress testing (Section 4.3, “Stress Testing”) can provide an objec­ tive assessment of functional capacity. Patients with poor functional capacity are at increased risk of cardiac events post surgery. Assessments of functional capac­ ity can be used to identify patients who may warrant additional preoperative cardiovascular risk stratification before surgery. In most cases, functional, asymptomatic

Table 5.  Duke Activity Status Index (DASI) Activity: Can you... Weight take care of yourself (eg, eating, dressing, bathing, or using the toilet)?

2.75 walk indoors, such as around your house? 1.75 walk a block or 2 on level ground? 2.75 climb a flight of stairs or walk a hill? 5.5 run a short distance? 8 do light work around the house (eg, dusting, washing dishes)? 2.7 do moderate work around the house (eg, vacuuming, sweeping floors, carrying in groceries)?

3.5 do heavy work around the house (eg, scrubbing floors, lifting or moving heavy furniture)?

8 do yardwork (eg, raking leaves, weeding, pushing a power mower)?

4.5 have sexual relations? 5.25 participate in moderate recreational activities (eg, golf, bowling, dancing, doubles tennis, throwing a baseball or football)?

6 participate in strenuous sports (eg, swimming, singles tennis, basketball, skiing)?

7.5

The DASI score is calculated by adding the points of all performed activi­ ties together. The higher the score (range, 0-58.2), the higher the functional status. Reprinted from Hlatky et al.6 Copyright 1989 Elsevier, with permission from Elsevier.

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patients may proceed with planned NCS without further cardiovascular testing.

Recommendation-Specific Supportive Text

1 In a study of 600 patients undergoing NCS, self-

reported poor functional capacity, defined as the inability to walk 4 blocks or climb 2 flights of stairs, was associated with an almost 2-fold greater risk of in-hospital cardiovascular events (9.6% versus 5.2%; P=0.04).1 The BASEL-PMI (Incidence and Outcome of Perioperative Myocardial Injury After Noncardiac Surgery) study (n=4560) included patients at elevated cardiovascular risk (ASA class ≥3) and showed that functional capacity <2 flights of stairs was associated with a 1.63 higher rate of death, MI, acute HF, or life-threatening arryth­ mias at 30 days.2 Furthermore, the addition of the functional capacity data to the RCRI significantly increased its predictive power. In a large analy­ sis from NSQIP (n=211 410), functional capacity comprised 1 of 5 elements in a multivariate model predicting MI/MICA at 30 days after surgery.4 Functional capacity was classified into 3 catego­ ries: independent, partially dependent, and totally dependent. Using the same classification, a ret­ rospective observational cohort study (n=12 324) from the US Department of Veterans Affairs Surgical Quality Improvement Project demon­ strated that functional capacity was independently associated with mortality and added discriminatory power to traditional ASA classification.5 The METs study compared the power of the DASI score for predicting death or MI at 30 days after major NCS with cardiopulmonary exercise testing (CPET) and a subjective assessment of functional capacity by the anesthesiologist, classified as good (>10), moderate (4-10), or poor (<4).7 Subjective assess­ ment of functional capacity by the clinician was not associated with outcomes, whereas the DASI score was associated with death or MI at 30 days after surgery (N=1401, mean age 65 years).7 DASI scores ≤34 were associated with increased odds of 30-day death or MI.8

3.3 Frailty

Recommendation for Frailty Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendation

2a B-NR 1.	 In all patients ≥65 years of age and in those <64

years with perceived frailty who are undergoing elevated-risk NCS, preoperative frailty assessment using a validated tool can be useful for evaluating perioperative risk and guiding management.1–5 Synopsis

Older patients undergoing NCS are at increased risk for numerous cardiac and noncardiac complications, including myocardial injury and infarction, atrial fibril­ lation (AF), acute kidney injury, and delirium. Frailty is a syndrome characterized by physiological declines across multiple organ systems that result in increased vulnerability to stressors. It is an independent risk fac­ tor for adverse outcomes after NCS across the age spectrum, including cardiac complications, infections, bleeding, falls, functional decline, increased length of stay, and mortality.1,3,4 In a systematic review of 21 studies, the weighted prevalence of frailty was 10.7% among community-dwelling individuals ≥65 years of age.6 That rate exceeds 25% among communitydwelling adults ≥85 years of age. Women have an almost 2-fold higher prevalence of frailty than men,6 and the rates are markedly higher among older pa­ tients with HF (>40%).7,8 A formal diagnosis of frailty using a validated screen instrument (Table 6) may im­ pact perioperative management and inform benefit-risk discussions with patients and their families.2,9 Emerg­ ing evidence suggests that prehabilitation (ie, physical conditioning, nutritional support, or both) before NCS may be associated with improved outcomes in selected patients with frailty.10,11

Recommendation-Specific Supportive Text

1 Frailty is a risk marker for adverse outcomes after

NCS and for reduced benefit after cardiac proce­ dures.1,3,4 In a meta-analysis of 56 studies involv­ ing 1.1 million older adults undergoing NCS, frailty was associated with an increased risk of 30-day mortality (relative risk, 3.71 [95% CI, 2.89-4.77]) and 30-day complications (relative risk, 2.39 [95% CI, 2.02-2.83]).4 Several validated tools are avail­ able to assess for frailty (Table 6).12 Although most comparative studies have been neutral, 1 prospec­ tive evaluation found that the Clinical Frailty Scale outperformed the Fried phenotype and the Frailty Index for predicting death, disability, prolonged length of stay, or nonhome discharge after NCS in older adults.5 In a single-center observational study involving 9153 patients undergoing major NCS, incorporation of routine frailty screening into the preoperative assessment was associated with a significant reduction in 30-day mortality.2 In some cases, older patients with advanced frailty, poor functional status, and reduced life expectancy may derive limited benefit from surgery; in these patients, goals of care and shared decision-making should be integrated into preoperative planning.13 In selected patients, prehabilitation before NCS may be associated with improved outcomes.9–11,14

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3.4 Preoperative Biomarkers for Risk

Stratification Recommendations for Preoperative Biomarkers for Risk Stratification Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2a B-NR 1 In patients with known CVD, or age ≥65 years, or

age ≥45 years with symptoms suggestive of CVD undergoing elevated-risk NCS, it is reasonable to measure B-type natriuretic peptide (BNP) or Nterminal pro–B-type natriuretic peptide (NT-proBNP) before surgery to supplement evaluation of perioperative risk.1–3

2b B-NR 2.	 In patients with known CVD, or age ≥65 years,

or age ≥45 years with symptoms suggestive of CVD undergoing elevated-risk NCS, it may be reasonable to measure cardiac troponin (cTn) before surgery to supplement evaluation of peri­ operative risk.4–6

Synopsis cTn and BNP are inexpensive and widely available biomarkers that can detect and quantify myocardial injury and cardiac wall stress, respectively. Several large prospective studies have demonstrated that both biomarkers have high prognostic value and excellent negative predictive value for perioperative cardiac complications. To date, there have been no studies in patients with elevated preoperative biomarkers to recommend management that improves perioperative cardiovascular outcomes. The utility of preoperative biomarkers in low-risk patients has not been evalu­ ated. Biomarker measurement poses the potential for increased risk via downstream tests predicated on the resulting value. For cost–value consideration, please refer to Section 11.1.1 (“Cost–Value Considerations for Biomarkers”). Recommendation-Specific Supportive Text

1 Several prospective observational studies and

meta-analyses have documented the use of pre­ operative BNP and NT-proBNP concentrations to predict postoperative complications in selected patients undergoing NCS. Both preoperative and postoperative natriuretic peptide levels were inde­ pendent predictors of the composite outcome of death or nonfatal MI at 30 days and at 180 days of follow-up.3 In a nested substudy of VISION (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation), preoperative NT-proBNP con­ centrations >100 pg/mL were independently asso­ ciated with all-cause mortality.1 Optimal threshold values of BNP or NT-proBNP for perioperative risk prediction are not clearly established. However, in a recent cohort study evaluating 3597 patients undergoing NCS, the addition of NT-proBNP to traditional risk scores did not significantly improve risk prediction beyond that of risk scores combined with self-reported measures of functional status.7

2 Preoperative high-sensitivity cTn concentrations in

patients without symptoms or signs of ischemia can identify patients with chronic myocardial injury as well as those at increased risk during and after the procedure.4,8 There is no action predicated on this knowledge alone, although preoperative baseline tro­ ponin concentrations also inform the interpretation of postoperative troponin measurements and can help confirm a diagnosis of acute myocardial injury in the postoperative setting. There is limited evidence from heterogenous populations that preoperative cTn can predict short- or long-term adverse outcomes.4 The predictive performance of the RCRI to identify patients who develop perioperative MACE is improved with the addition of preoperative cTn concentrations.5

Table 6.  Frailty Assessment Tools Name Items Scoring Physical Frailty Phenotype (Fried phenotype)15 Slowness, low activity, weight loss, exhaustion, weakness (1 point each) 0=Nonfrail

1-2=Prefrail 3-5=Frail

Deficit Accumulation Index16 Variable; typically 30-70 items from multiple domains Number of deficits/number of items scored; higher scores indicate greater frailty Edmonton Frail Scale17 10 items across multiple domains Sum of scores/17; higher scores indicate greater frailty FRAIL Scale18 Fatigue, stair climb, ambulation, illnesses >5, weight loss ≥5% (1 point each) 0=Nonfrail

1-2=Intermediate 3-5=Frail

Clinical Frailty Scale19 9 categories ranging from very fit to terminally ill as assessed by clinicians Categories 5-8 indicate mild, moderate, severe, and very severe frailty SPPB20 Gait speed, chair stands, balance tests Maximum 4 points per item, range, 0-12 points; ≥10=Nonfrail, 3-9=Frail, ≤2=Disabled Adapted with permission from frailtyscience.org. Copyright 2021 FrailtyScience.org. SPPB indicates Short Physical Performance Battery.

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4 PREOPERATIVE CARDIOVASCULAR

DIAGNOSTIC TESTING

4.1 12-Lead Electrocardiogram

Recommendations for 12-Lead Electrocardiogram Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendations

2a B-NR 1 For patients with known coronary heart disease, signifi­

cant arrhythmia, peripheral arterial disease, cerebrovas­ cular disease, other significant structural heart disease, or symptoms* of CVD undergoing elevated-risk sur­ gery, a preoperative resting 12-lead electrocardiogram (ECG) is reasonable to establish a preoperative base­ line and guide perioperative management.1,2

2a B-NR 2 In patients undergoing NCS with a preoperative

ECG exhibiting new abnormalities,† further evalu­ ation is reasonable to refine assessment of cardio­ vascular risk.3–8

2b B-NR 3 For asymptomatic patients undergoing elevated-risk

surgeries without known CVD, a preoperative rest­ ing 12-lead ECG may be considered to establish a baseline and guide perioperative management.3,9,10

3: No benefit B-NR 4 For asymptomatic patients undergoing low-risk surgi­

cal procedures, a routine preoperative resting 12-lead ECG is not recommended to improve outcomes.11

*Active symptoms and signs of CVD include chest pain, dyspnea, undiagnosed palpitations, tachycardia, syncope, or murmurs. †Abnormalities may include ST-segment elevation, ST depression, T-wave inversions, left ventricular (LV) hypertrophy, significant pathologic Q-waves, Mo­ bitz type II or higher atrioventricular block, bundle branch block, QT prolonga­ tion, or AF.

Synopsis The resting 12-lead ECG may contain important prognos­ tic information related to short- and long-term morbidity and mortality among patients with coronary heart dis­ ease undergoing NCS.1 However, it rarely adds prognos­ tic information beyond what can be determined with risk assessment tools. For clarification of low-, intermediate-, or high-risk surgery and associated risk assessment tools, please refer to Section 1.5 (“Definitions of Surgical Timing and Risk”) and Section 3 (“Risk Calculators”) of this guideline. For cost–value consideration, please refer to Section 11.1.2 (“Cost–Value Considerations for 12- Lead ECG”).

Recommendation-Specific Supportive Text

1 A preoperative 12-lead ECG is likely to be more

valuable for patients planned for elevated-risk surgi­ cal procedures.2,3 This is particularly true for patients with known coronary heart disease, arrhythmias, peripheral arterial disease, cerebrovascular dis­ ease, or other significant structural heart disease. Comparing a preoperative ECG with previous elec­ trocardiographic tracings may be helpful whenever relevant abnormalities are identified, with the preop­ erative ECG serving as a baseline if postoperative complications develop. 2 The prognostic significance of several electrocar­

diographic abnormalities, including arrhythmias, significant pathologic Q-waves, LV hypertrophy, ST-segment depressions, QTc prolongation, and bundle branch blocks has been identified in obser­ vational studies.4,5 Most studies, however, report little to no added prognostication of ECGs beyond clinical risk assessment. The abnormalities on the ECG that should prompt the preoperative clinician to request further information, consultation, or testing are not well defined; however, notable abnormalities include significant Q-waves, LV hypertrophy, ST-segment elevation, ST depression, T-wave inversion, Mobitz type II or higher block, bundle branch blocks, AF, or QT interval prolongation.9,12 The likelihood of abnor­ malities on a preoperative 12-lead ECG increases with patient age and when risk factors for heart dis­ ease are present, but a standard age or risk factor cutoff for recommending a preoperative ECG has not been defined. Likewise, the optimal time interval between obtaining a 12-lead ECG and elective NCS is unknown. 3.	 In general, an abnormal preoperative ECG may not substantially alter perioperative management, except for second-degree Mobitz type II or higher atrioventricular block,13 AF with rapid ventricu­ lar response or new-onset AF, or a prolonged QT interval.4,10,14 Recognition of a prolonged QT inter­ val may inform the selection of anesthetics, postop­ erative antiemetics, or antibiotic therapy. Incidental findings of Q-waves or bundle branch block on a preoperative ECG in an asymptomatic patient may indicate coronary artery disease (CAD) but should not lead to a decision to perform coronary revascularization before NCS. Another important reason to obtain a preoperative ECG in asymptom­ atic patients undergoing elevated- risk NCS with increased risk of MACE is to establish a baseline ECG for comparison should a postoperative ECG be abnormal. 4.	 Clinical risk assessment using validated tools is

more useful to guide management and predict outcomes than are the findings of a single resting preoperative ECG. Available data suggest that in low-risk patients, a routine preoperative ECG has little effect on treatment or complication rates and should be omitted from standard preoperative eval­ uation.11,13 One study assessed 30 892 patients undergoing NCS with shockwave lithotripsy for nephrolithiasis, in which a preoperative ECG trig­ gered the cancellation of 13 (0.04%) treatments in low-risk patients (1 with new AF and 12 with ischemia or previous infarction). Of these patients, only 1 had a subsequent abnormal cardiac workup, and the remaining 11 ultimately underwent NCS without complications. The study concluded that in patients at low risk for cardiac complications,

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preoperative ECG triggered very few cancellations and did not predict cardiac complications after NCS.11 Avoiding unnecessary testing can signifi­ cantly save resources.15

4.2 Assessment of Ventricular Function

4.2.1 Left Ventricular Function

Recommendations for Assessment of Left Ventricular Function Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendations

1 B-NR 1.	 In patients undergoing NCS with new dyspnea,

physical examination findings of HF, or suspected new/worsening ventricular dysfunction, it is recom­ mended to perform preoperative evaluation of LV function to help guide perioperative management.1–8

2a C-LD 2 In patients with a known diagnosis of HF with wors­

ening dyspnea or other change in clinical status undergoing NCS, preoperative assessment of LV function is reasonable to help guide perioperative management.1,4,7,9–11

3: No benefit B-NR 3 In asymptomatic and clinically stable patients undergo­

ing NCS, routine preoperative evaluation of LV func­ tion is not recommended due to lack of benefit.12–15

Synopsis Abnormal LV systolic or diastolic function is associated with increased perioperative MACE in NCS.1–8,16–18 The risk of perioperative MACE is higher with lower LV ejec­ tion fraction (LVEF), in higher surgical risk procedures, and in patients with additional comorbid risk factors.1,7,18 In a 5% sample of Medicare beneficiaries, a preopera­ tive diagnosis of HF conferred increased 30-day op­ erative mortality and readmission rates after major NCS compared with control patients and patients with CAD without HF (n=1757).2 An analysis of a US Department of Veterans Affairs database found that patients with symptomatic and asymptomatic HF, regardless of LVEF, had increased 90-day mortality compared with patients without HF.4 A study of patients with isolated diastolic dysfunction undergoing NCS (n=2976) found a 70% higher risk of MACE in those with grade 3 compared with grades 1 to 2 diastolic dysfunction.18 Assessment of LV function is indicated in patients with unexplained cardiac symptoms and may be reasonable in the setting of elevated preoperative BNP or NT-proBNP concentra­ tions. Evidence is lacking to support routine preoperative assessment of LV function in stable patients. Recommendation-Specific Supportive Text

1 HF is an established risk factor for poor outcomes

after NCS.1–4,8,16–18 In a perioperative cohort of 159 237 patients undergoing NCS, 18% of the procedures were performed in patients with HF, and 34% were performed in patients with CAD. A signif­ icantly higher risk of mortality and HF readmissions was found in patients with HF compared to patients with CAD.1 In a retrospective analysis, 723 patients underwent preoperative 12-lead ECG, hemoglobin blood tests, and preoperative transthoracic echo­ cardiogram (TTE).17 After multivariate analysis, higher-risk NCS, reduced hemoglobin level, and decreased LVEF were independently associated with poorer outcomes.17 In a prospective analysis of 570 patients who had preoperative echocardiogra­ phy before NCS, risk models including the echocar­ diographic elements performed better than models using clinical variables alone (c statistic, 0.73 versus 0.68; P<0.05); however, the incremental benefit of preoperative echocardiography was observed only in the higher-risk patients.16 Diastolic dysfunction is also associated with a higher perioperative risk of MACE in many18–20 but not all15 studies. In a retro­ spective cohort of 2976 patients undergoing NCS, TTE-detected grade 3 diastolic dysfunction had a higher risk of perioperative MACE than grades 1 to 2 diastolic dysfunction.18

2 The risk of perioperative mortality is higher in patients

with HF compared with those without HF.1,4 Although even asymptomatic patients with HF have been shown to have an increased risk of MACE in some studies,4,6 symptomatic patients with lower LVEF who are undergoing higher-risk procedures have been shown to be at highest risk.7,17 In a retrospec­ tive review of 174 patients undergoing intermediateand high-risk procedures, severely reduced LVEF ≤30% identified with preoperative echocardiogra­ phy was an independent predictor of 30-day mor­ tality.7 In a retrospective cohort of 609 735 patients undergoing NCS, the 90-day mortality for those with symptomatic HF was 5.49%, 4.9% for asymptom­ atic HF, and 1.2% for those with no history of HF history.4 Preoperative point-of-care assessment of LV function using handheld focused cardiac ultra­ sound (FoCUS) has been considered in several small studies as a screening method to identify both systolic and diastolic dysfunction.9–11 FoCUS may be considered to identify patients who may need addi­ tional preoperative evaluation to reduce periopera­ tive risk only when performed by trained individuals. In 100 patients with known CVD or considered high risk undergoing hip surgery, perioperative manage­ ment was changed in 54 patients as a result of the use of handheld ultrasound.10 In a subsequent small RCT of 100 patients undergoing NCS, 1-year mor­ tality rate was lower in those who had preoperative FoCUS (18.4%) compared with 29.4% in the con­ trol group.9 Larger RCTs are needed to support the routine use of FoCUS in the preoperative evalua­ tion, and comprehensive TTE remains the standard of care for assessment of perioperative LV function. 3.	 Large retrospective cohorts have not identified a

benefit of preoperative assessment of LV function

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in clinically stable patients undergoing NCS, even in patients at higher risk.12–15 In a large retrospec­ tive multicenter study of 264 823 patients under­ going intermediate- or high-risk NCS, 40 084 had preoperative echocardiography.12 In a propensity score-matched cohort of 70 996 patients, including symptomatic and asymptomatic individuals, perfor­ mance of a TTE was not associated with improved outcomes.12 Similarly, data from a US Department of Veterans Affairs health care system reported that preoperative echocardiography (16.4%) was not associated with improved survival or shorter hospital stays after major NCS.14 As such, there is currently insufficient evidence to recommend rou­ tine assessment of LV function in stable patients undergoing NCS. In high-risk patients undergoing high-risk NCS, physician judgment may be used when the results of LV assessment are expected to alter perioperative management or inform periop­ erative risk in patients undergoing elective NCS.

4.2.2 Right Ventricular Function

Synopsis Patients with mitral regurgitation (MR), tricuspid regur­ gitation, and/or pulmonary hypertension (PH) can have reduced right ventricular (RV) function, which has been independently associated with adverse cardiovascular outcomes in NCS.1,2 Echocardiography is often the first diagnostic test to assess RV function. Cardiovascular magnetic resonance imaging is considered the gold standard for quantitative assessment of RV volume and function and may be appropriate in selected cases. Routine preoperative evaluation of RV function is not recommended in asymptomatic and clinically stable patients.

4.3 Stress Testing

Recommendations for Stress Testing Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendations

2b B-NR 1 For patients undergoing elevated-risk NCS with

poor or unknown functional capacity and elevated risk for perioperative cardiovascular events based on a validated risk tool, stress testing may be consid­ ered to evaluate for inducible myocardial ischemia.1

3: No benefit B-R 2 In patients who are at low risk for perioperative

cardiovascular events, have adequate* functional capacity with stable symptoms, or who are undergo­ ing low-risk procedures, routine stress testing before NCS is not recommended due to lack of benefit.1–3

*Poor functional capacity is considered <4 METs or a DASI score of ≤34.

Synopsis The presence of reversible myocardial ischemia on a preoperative stress test is associated with increased risk for perioperative cardiac events.1 However, the positive predictive value of an abnormal test is modest, and it is not clear that an abnormal test provides incremental prognostic value beyond standard risk assessment tools (eg, RCRI) or biomarkers (eg, natriuretic peptides).1,4–11 Testing is also expensive and may lead to unnecessary downstream testing or delays in performing the indicated surgery.12 Moreover, preoperative revascularization has not been shown to reduce perioperative MACE or car­ diac mortality, and there is high potential for overtesting and overtreatment unless further perioperative testing is limited to patients in whom high-risk coronary lesions are likely.3,13,14 Therefore, the goal of preoperative testing for ischemia is not to identify undiagnosed CAD but to identify patients for whom revascularization is believed to improve clinical outcomes, specifically those with left main disease or severe multivessel disease with a re­ duced LVEF.13 These patients have been excluded from studies of preoperative revascularization, and the utility of revascularization in this context is unknown. Thus, in select patients in whom high-risk ischemia is suspected based on symptoms or other factors, stress testing may be useful for risk stratification and to guide manage­ ment.1,15,16 However, an abnormal stress test should not prompt coronary angiography or revascularization unless the study has high-risk features.7,8,11,17 For cost–value consideration, please refer to Section 11.1.4 (“Cost– Value Considerations for Stress Testing”).

Recommendation-Specific Supportive Text

1 Functional capacity of <4 METs (eg, patients unable

to climb 1-2 flights of stairs or walk on a flat sur­ face at ≥3 mph) is associated with increased risk for perioperative cardiac events regardless of the cause of the disability (eg, CAD, HF, or a noncardiac condition such as arthritis, chronic lung disease, or obesity).18,19 In patients with elevated risk for peri­ operative cardiovascular events, as determined by a validated risk score (Section 3.1, “Cardiovascular Risk Indices”), and functional capacity <4 METs or indeterminate functional capacity, a stress test (exercise or pharmacological, with or without imag­ ing depending on the clinical context) may be con­ sidered in select patients undergoing elevated-risk surgery, if high-risk myocardial ischemia is sus­ pected (eg, left main disease or severe multivessel disease with reduced EF) or there is an indication for testing independent of planned surgery.1,15,16 There is, however, limited evidence to support coronary revascularization before NCS in stable patients.3,14,20,21 In general, an exercise stress test is preferable to a pharmacological stress test if the patient is able to exercise.15,16 In patients unable to exercise, selection of a pharmacological stress test modality should be based on patient factors and local availability and expertise.12,15,16

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2 Stable patients with exercise capacity ≥4 METs

are at relatively low risk for perioperative cardiac events.2 In addition, although some observational studies have suggested that preoperative revas­ cularization of patients with abnormal stress test findings may be associated with a reduction in post­ operative ischemic complications, other studies have found no benefit.14 In the CARP (Coronary Artery Revascularization Prophylaxis) trial, 510 patients with documented CAD (at least 1 lesion with ≥70% stenosis) were randomly assigned to coronary revas­ cularization or medical therapy before undergoing major vascular surgery.3 Patients in the revascular­ ization group experienced a 36-day delay in time to vascular surgery. There was no difference in the inci­ dence of perioperative MI at 30 days or in all-cause mortality at a median follow-up of 2.7 years.3 More contemporary large RCTs have demonstrated that routine coronary revascularization does not reduce mortality or risk for MI.20,22,23 Because the benefits of preoperative revascularization appear to be lim­ ited, routine preoperative stress testing should not be performed in patients with adequate functional capacity. Similarly, preoperative stress testing is not recommended in low-risk patients (eg, RCRI=0; see Section 3.1, “Cardiovascular Risk Indices”) or in stable patients undergoing low-risk NCS because it is costly, may lead to a delay in surgery, and has not been shown to improve clinical outcomes. 2,14,16,24 This applies to patients with or without known or suspected CAD or cardiovascular risk factors.

4.3.1 Modality Selection for Stress Testing

Synopsis The selection of stress testing is often driven by clini­ cian preference1 and should incorporate patient con­ siderations, including their risk factors. Stress testing is generally avoided in unstable syndromes such as acute coronary syndrome (ACS), decompensated HF, severe/symptomatic aortic stenosis (AS), uncontrolled arrhythmia, severe systemic arterial hypertension (eg, ≥200/110 mm Hg), acute aortic dissection, pericarditis/ myocarditis, pulmonary embolism, severe PH, or in some cases, other acute illness. Additional modality-specific considerations and contraindications are listed in Table 7. Exercise testing is preferred to pharmacological stress testing whenever functional status permits.2 Stress myocardial perfusion imaging has a longstanding role in preoperative risk assessment.3–5 Moderate to large re­ versible defects on myocardial perfusion imaging have moderate sensitivity for postoperative cardiac events, while the absence of reversible defects is an indica­ tion of lower risk for postoperative MI or death.6 Fixed defects do not indicate additional risk for postopera­ tive cardiac events but, as an indicator of CAD, carry prognostic and therapeutic implications for longer-term cardiac and mortality outcomes.7,8

Dobutamine stress echocardiography for preopera­ tive risk assessment before elevated-risk NCS has been evaluated in several studies, predominantly including patients at increased cardiovascular risk, with poor (<4 METs), and/or unknown functional capacity.9–26 Overall, a positive test result for dobutamine stress echocardiogra­ phy was reported in the range of 5% to 50%.9–11,19,23,27,28 In these studies with event rates of 0% to 15%, the abil­ ity of a positive test result to predict perioperative cardio­ vascular events ranged from 0% to 37%, whereas the negative predictive value was typically >90%. Dobuta­ mine stress echocardiography is appropriate for patients unable to exercise and should be avoided in patients with uncontrolled hypertension, serious arrhythmias, unstable or ACS, or hemodynamically significant LV outflow tract (LVOT) obstruction.29 There is limited evidence for other stress testing imaging modalities, including positron emission tomography and cardiac magnetic resonance, in preoperative risk stratification before NCS.

4.4 Cardiopulmonary Exercise Testing

Synopsis In high-risk patients undergoing elevated-risk proce­ dures in whom objective functional capacity is reduced and where additional physiological data are needed to inform perioperative care or guide preoperative optimi­ zation, CPET may be beneficial for risk assessment of perioperative morbidity and mortality.1,2 Reduced cardio­ respiratory fitness increases the risk of postoperative complications.3 CPET is the gold-standard assessment of the physiological response to exercise, providing an objective measure of functional capacity.4 CPET can be used to diagnose the etiology of exercise intolerance

Table 7.  Considerations and Contraindications for Specific Stress Testing Modalities Modality Contraindication* Vasodilator pharmaco­ logical stress imaging Significant arrhythmias (eg, VT, second- or third-degree atrioventricular block), significant hypotension (SBP <90 mm Hg), known or sus­ pected bronchoconstrictive or bronchospastic disease or use of dipyridamole or methylxan­ thines (eg, aminophylline, caffeine) within 12 h Exercise stress testing (with or without imaging) Inability to exercise Dobutamine stress echocardiography Critical aortic stenosis, hemodynamically significant LVOT obstruction *In general, the following contraindications apply to all stress testing modalities: ACS, decompensated HF, severe/symptomatic aortic stenosis, uncontrolled arrhyth­ mia, systemic arterial hypertension (eg, ≥200/110 mm Hg), acute aortic dissections, pericarditis/myocarditis, pulmonary embolism, and severe PH.30 ACS indicates acute coronary syndrome; HF, heart failure; LVOT, left ventricular outflow tract; PH, pulmonary hypertension; SBP, systolic blood pressure; and VT, ventricular tachycardia.

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(cardiac versus pulmonary pathology), guide preopera­ tive optimization, and inform prehabilitation.4 CPET pre­ dicts all-cause morbidity, which is more common than cardiovascular complications alone,5 and supports risk prediction in major abdominal, vascular, bariatric, and tho­ racic surgery, although the definitions of morbidity dif­ fer across studies.1,4 Most studies in perioperative CPET are retrospective and single center and vary in predictive precision.6,7 The thresholds for identifying high-risk pa­ tients also vary between cohorts and surgical proce­ dures. Over time, the risk threshold for reported indices has fallen (eg, the anaerobic threshold decreased from 11 to 9-10 mL/min/kg), reflecting an evolution in surgi­ cal and perioperative practice.8 Alternative measures of functional capacity exist (eg, 6-minute-walk-test) that are also used in risk prediction.9 These have the advantage of being easier to perform than CPET, without the need for specialized equipment. CPET and the 6-minute-walktest demonstrate variable correlation, possibly reflecting the need for both tests to be conducted in a standardized manner by trained personnel.9 Consensus guidance has been released on the indications, organization, conduct, and reporting of perioperative CPET.4 Additional physio­ logical data beyond the 6-minute-walk-test are provided by CPET that may support its use in high-risk patients with objectively reduced functional capacity undergoing elevated-risk procedures.

4.5 Coronary Computed Tomography

Angiography Recommendations for Coronary Computed Tomography Angiography Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendations

2b B-NR 1 For patients undergoing elevated-risk surgery with

poor* or unknown functional capacity, and elevated risk for perioperative cardiovascular events based on a validated risk tool, coronary computed tomog­ raphy angiography (CCTA) for the detection of high-risk coronary anatomy† may be considered.1–4

3: No benefit B-NR 2 In patients who are at low risk for perioperative

cardiovascular events, have adequate* functional capacity with stable symptoms, or who are undergo­ ing low-risk procedures, routine CCTA before NCS is not recommended due to lack of benefit.1,5

*Poor functional capacity is considered <4 METs or a DASI score of ≤34. †High-risk coronary anatomy is defined as patients with obstructive stenosis who have ≥50% left main stenosis or anatomically significant 3-vessel disease (≥70% stenosis).6

Synopsis In patients with acute chest pain and no known CAD, CCTA may be useful to exclude atherosclerotic plaque and obstructive CAD and is recommended as an al­ ternative to invasive angiography.6 However, the role of CCTA in the perioperative setting before NCS is less well established. A positive CCTA has a low pre­ dictive value (ie, overestimates the risk for periopera­ tive MACE), thereby possibly contributing to delays in surgery and potential harm.1 Furthermore, there is no demonstrable benefit of prophylactic coronary re­ vascularization to mitigate the risk of MACE in stable patients undergoing NCS.5 As a result, routine preoper­ ative risk assessment with CCTA is not recommended. Further, if a patient has a prior coronary artery calcium score of 0 within 2 years, proceeding to surgery without additional testing would be reasonable. CCTA may be considered in select patients with elevated risk or to exclude high-risk coronary anatomy in patients under­ going elevated-risk surgery.6 Although CCTA is a costeffective strategy for evaluating patients with chest pain compared with stress testing, the cost analysis has not been evaluated in stable patients undergoing NCS.7 Studies using CT-based vulnerable plaque character­ istics or CT perfusion imaging are currently limited to nonsurgical literature, and their role in perioperative risk assessment are not well established. CCTA is contra­ indicated and may be harmful in patients who require urgent or emergency surgery, as the need and urgent timing for surgery outweighs any benefit that might be obtained by performing a CCTA and delaying surgery.1 For cost–value consideration, please refer to Section 11.1.3 (“Cost–Value Considerations for Coronary Com­ puted Tomography Angiography”).

Recommendation-Specific Supportive Text

1 In patients with elevated risk for perioperative

cardiovascular events, as determined by a vali­ dated risk score (Section 3.1, “Cardiovascular Risk Indices”) and low (<4 METs or a DASI score of ≤34) or indeterminate functional capacity, CCTA may be considered in select cases if high-risk coronary anatomy is suspected and there is a guidelineconcordant indication for testing independent of planned surgery. Risk assessment by CCTA offers incremental risk assessment over clinical risk scores. The Coronary CTA-VISION (Coronary CT Angiography to Predict Vascular Events in NCS Patients Cohort Evaluation) study (N=987) showed that use of CCTA marginally improved the risk estimation for predicting postoperative cardiovascular death and nonfatal MI compared with clinical risk score alone.1 CCTA confers a high negative predictive value for excluding periopera­ tive cardiovascular events.1–4 These results were confirmed in a meta-analysis including 11 stud­ ies and 3480 patients who underwent preopera­ tive CCTA.2 The presence, extent, and severity of coronary atherosclerosis directly correlated with risk of perioperative MACE. On CCTA, patients with single- and multivessel disease demonstrated a

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3-fold and an 8-fold increased risk of perioperative MACE, respectively.2 However, as listed in Section 6.1.1 (“Coronary Revascularization”), evidence sup­ porting routine coronary revascularization before planned surgery is lacking. 2.	 CCTA can improve risk estimation among patients

who will experience perioperative MACE; however, compared with clinical risk scores, CCTA is >5 times as likely to inappropriately overestimate risk among patients who will not experience MACE.1 This over­ estimation of risk may result in a delay or cancellation of surgery and unnecessary increased use of medi­ cal resources, thereby contributing to patient mor­ bidity and mortality and increased medical expenses. Low-risk patients include those at low risk for car­ diovascular events based on validated risk tools and those who are undergoing low-risk noncardiac sur­ gical procedures (Section 3.1, “Cardiovascular Risk Indices,” Section 1.5, “Definitions of Surgical Timing and Risk”). In these patients, or those with functional capacity ≥4 METs with stable symptoms, the prob­ ability of uncovering high-risk coronary anatomy that would adversely affect surgical outcomes is small. This recommendation is applicable to patients with or without known or suspected CAD or cardiovascu­ lar risk factors.

4.6 Invasive Coronary Angiography

Recommendation for Invasive Coronary Angiography

COR LOE Recommendation

3: No benefit C-LD 1 In patients undergoing NCS, routine preoperative

invasive coronary angiography (ICA) is not recom­ mended to improve perioperative outcomes.1,2

Synopsis ICA is used to define epicardial coronary artery anatomy, diagnose atherosclerotic CAD, and assess the location, extent, and severity of obstructive coronary stenoses. ICA is necessary to determine the feasibility and necessity of percutaneous or surgical revascularization.3 Preopera­ tive ICA may be performed in selected patients to de­ tect coronary stenoses that pose significant risks in the perioperative period. Data are insufficient to recommend routine coronary angiography in patients scheduled for NCS, including those undergoing elevated-risk surgery or pretransplant evaluation.4 Even in patients undergoing vascular surgery, independent of preoperative risk, ICA is not consistently associated with improved early postop­ erative clinical outcomes.1,2,5

Recommendation-Specific Supportive Text

1 Routine invasive angiography to assess the need

for coronary revascularization is not recommended in the preoperative evaluation of NCS. The CARP trial of 510 patients assessed the benefit of pre­ operative coronary artery revascularization among patients with chronic CAD scheduled for elective vascular surgery and reported that coronary artery revascularization before elective vascular surgery does not significantly alter long-term outcomes.2 Two small European RCTs also evaluated routine versus selective ICA before vascular surgery. In a trial enrolling 426 patients undergoing carotid endarter­ ectomy without a previous history of CAD, routine preoperative ICA was associated with lower rates of early postoperative MI and improved long-term sur­ vival compared with surgeries without prior ICA.6 In a separate study of 208 patients undergoing major vascular surgery with an RCRI ≥2, in-hospital risk of MACE was not different in patients assigned to routine versus selective ICA, although routine ICA was associated with improved survival and freedom from MACE at approximately 5 years of follow-up.5 Unfortunately, in contrast to the more robust CARP trial, these 2 trials were small, nonblinded, and man­ agement of patients assigned to the selective ICA arms was not clearly defined; these findings have not been replicated in larger, more contemporary studies. In contrast, large trials that are not specific to perioperative care indicate that in the setting of stable CAD, invasive management with coronary revascularization of CAD in epicardial vessels other than the left main does not improve short- or longterm survival versus optimal medical therapy alone.7 Thus, ICA should be reserved for the highest-risk patients. A strategy of routine ICA with an intent to perform revascularization before elective NCS in patients with chronic coronary syndromes cannot be recommended. In general, indications for preop­ erative coronary angiography should be similar to those identified in nonoperative settings, such as ACS, accelerating angina despite maximal antiangi­ nal therapy, newly diagnosed moderate-severe isch­ emia on stress testing, and indicators of obstructive left main disease on noninvasive testing.

5 APPROACH TO PERIOPERATIVE

CARDIAC TESTING

5.1 Stepwise Approach to Perioperative

Cardiac Assessment Figure 1 represents a suggested framework for perioper­ ative risk stratification and management that incorporates best practices and recommendations described through­ out this guideline. Recommendations are supported by various levels of evidence. Clinical outcomes of periop­ erative care guided by this algorithm have not been pro­ spectively studied or validated and therefore should not replace clinical judgment and individualized clinical care.

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Figure 1. Stepwise Approach to Perioperative Cardiac Assessment. *Cardiovascular risk factors: hypertension, smoking, high cholesterol, diabetes, women age >65 y; men age >55 y; obesity; family history of premature CAD. †Determining elevated calculated risk depends on the calculator used. Traditionally, RCRI >1 or a calculated risk of MACE with any perioperative risk calculator >1% is used as a threshold to identify patients at elevated risk. §Abnormal biomarker thresholds: troponin >99th percentile URL for the assay; BNP >92 ng/L, NT-proBNP ≥300 ng/L. ‡Conditions that pose additional risk for MACE. ‖Noninvasive stress testing or CCTA suggestive of LM or multivessel CAD. Colors correspond to Class of Recommendation in Table 3. BNP indicates B-type natriuretic peptide; CABG, coronary artery bypass grafting; CAD, coronary artery disease; CCTA, coronary computed tomography angiography; CIED, cardiovascular implantable electronic device; CVD, cardiovascular disease; DASI, Duke Activity Status Index; ECG, electrocardiogram; GDMT, guideline-directed management and therapy; ICD, implantable cardioverter-defibrillator; LM, left main; MACE, major adverse cardiovascular event; METs, metabolic equivalents; NCS, noncardiac surgery; NT-proBNP, N-terminal pro b-type natriuretic peptide; RCRI, Revised Cardiac Risk Index; and URL, upper reference limit.

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6 CARDIOVASCULAR COMORBIDITIES

AND PERIOPERATIVE MANAGEMENT

6.1 Coronary Artery Disease

Synopsis CAD is prevalent in approximately 18% of patients un­ dergoing major NCS,1 is associated with increased risk of perioperative MACE, and is a common element in pre­ operative risk estimation.2–6 The location, extent, and se­ verity of atherosclerotic CAD informs perioperative risks, and a history of an ACS confers greater perioperative risks than chronic coronary disease (CCD) does. Among >3500 patients included in the RCRI derivation and vali­ dation cohorts, a history of MI was associated with a 3.5fold increased risk of perioperative MACE.4 Patients with CAD treated with coronary stents also have increased risk of MACE.3 In a retrospective cohort of approximately 28 000 patients undergoing NCS, the odds of perioperative MACE was 2-fold higher in patients with coronary stents placed in the prior 2 years compared with matched controls without stents.7 The risks of MACE are inversely proportional to the time interval between coro­ nary revascularization and NCS (Section 6.1.1, “Coronary Revascularization”).8 Careful attention to optimal medical management for ASCVD is important before elective NCS in patients with CAD.9 The perioperative diagnostic evalu­ ation and management of patients with a history of CAD undergoing NCS is outlined in Section 3 through Section 7.

6.1.1 Coronary Revascularization

Recommendations for Coronary Revascularization Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendations

1 C-LD 1 In patients with ACS being considered for elective

NCS, coronary revascularization as appropriate and deferral of surgery is recommended to reduce peri­ operative cardiovascular events.1–9

2a C-LD 2 In patients with CCD and hemodynamically signifi­

cant left main coronary artery stenosis ≥50% who are planning elective NCS, coronary revasculariza­ tion and deferral of surgery is reasonable to reduce perioperative cardiovascular events.10,11

3: No benefit B-R 3 In patients with non–left main CAD who are

planned for NCS, routine preoperative coronary revascularization is not recommended to reduce perioperative cardiovascular events.*12–15

*Modified from the “2021 ACC/AHA/SCAI Guideline for Coronary Artery Re­ vascularization.”16

Synopsis This guideline reviews the role of coronary revascular­ ization before NCS. For further guidance on coronary revascularization, please refer to the “2021 ACC/AHA/ SCAI Guideline for Coronary Artery Revascularization.”16 For patients with ACS ST-segment elevation myocardial infarction (STEMI) or high-risk non–ST-segment eleva­ tion myocardial infarction (NSTEMI) and patients with CCD involving left main CAD, preoperative revascu­ larization can be beneficial in reducing MACE.13–17 For patients experiencing anginal symptoms refractory to op­ timal GDMT, a multidisciplinary heart team approach to revascularization should be considered before planned NCS.15,16 In general, the 2021 revascularization guideline can be applied to NCS patients as long as they are able to safely postpone the surgery to accommodate for the dual antiplatelet therapy (DAPT) recommendations. For pa­ tients undergoing organ transplant surgery, vascular sur­ gery, and/or with multivessel CAD, multidisciplinary team input is recommended for assessing revascularization needs and timing.16 Please refer to Section 7.5 (“Anti­ platelet Therapy and Timing of Noncardiac Surgery in Patients With Coronary Artery Disease”) in this guide­ line for antiplatelet management and timing of NCS after percutaneous coronary intervention (PCI).

Recommendation-Specific Supportive Text

1 Coronary revascularization, either with PCI or coro­

nary artery bypass grafting (CABG), is an important treatment modality for patients with ACS. In patients with STEMI, cardiovascular outcomes are improved by immediate reperfusion therapy with primary PCI and coronary stent placement.7,16,18 Coronary revas­ cularization is also commonly indicated in patients with unstable angina and NSTEMI, particularly in those with (1) cardiogenic shock; (2) ACS charac­ terized by refractory angina, intractable arrhythmias, or hemodynamic instability; or (3) GRACE (Global Registry of Acute Coronary Events) scores >140.16 In patients with ACS who have an indication for NCS, coronary revascularization should be per­ formed as described in the “2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization” and, when possible, NCS should be deferred to reduce perioperative cardiovascular events.16

2 In patients with CCD and left main disease, the

cumulative mortality and morbidity risks of both the coronary revascularization procedure and the NCS should be weighed carefully, taking into consider­ ation the individual patient’s overall health, func­ tional status, and prognosis. Summative evidence from prior RCTs such as ISCHEMIA (International Study of Comparative Health Effectiveness With Medical and Invasive Approaches), COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation), and BARI-2D (Bypass Angioplasty Revascularization Investigation 2 Diabetes) have noted the importance of GDMT and lack of benefit from routine revascularization in most patients with CCD.13–15 However, patients with left main CAD were excluded from these landmark RCTs. Older RCT data suggest that revascularization

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with CABG reduces mortality in patients with left main disease.10,11 In nonrandomized patients with multivessel CAD (including left main) planned for vascular NCS, unprotected left main disease was the only angiographic subset with a survival ben­ efit from preoperative coronary revascularization.19 Furthermore, Bayesian methods support the con­ cept that PCI, like CABG, improves survival for patients with unprotected left main CAD compared with medical therapy.10 Therefore, preoperative coro­ nary revascularization before NCS is a reasonable consideration in patients with CCD and significant left main CAD (defined as >50% stenosis).16,17

3 In the CARP trial, routine prophylactic coronary

revascularization with either PCI or CABG before elective major vascular surgery was not associ­ ated with differences in 30-day or 1-year rates of death or MI.12 Patients with left main CAD, LVEF <20%, or severe AS were excluded from this trial.12 Smaller trials, including a subgroup of abdominal aortic operations from the CARP study, demon­ strated potential benefits from routine coronary angiography and PCI, if indicated, before NCS.20–22 However, a meta-analysis of 3949 patients includ­ ing CARP and 6 other retrospective studies did not show any benefit from routine revascularization before NCS.23 Coronary artery revascularization in patients undergoing vascular surgery has been noted to shift the mortality from cardiovascular to noncardiovascular causes, without an absolute reduction in mortality.24 Bleeding complications are higher with PCI, specifically in the first 6 months after placement of a drug-eluting stent (DES).25

6.2 Hypertension and Perioperative Blood

Pressure Management Recommendations for Hypertension and Perioperative Blood Pressure Management Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations Preoperative Blood Pressure Management

2a C-EO 1 In most* patients with hypertension planned for elec­

tive NCS, it is reasonable to continue medical therapy for hypertension throughout the perioperative period.†

2b C-LD 2 In patients undergoing elective elevated-risk surgery

who have cardiovascular risk factors for periopera­ tive complications‡ and recent history of poorly con­ trolled hypertension (systolic blood pressure [SBP] ≥180 mm Hg or diastolic blood pressure [DBP] ≥110 mm Hg before the day of surgery), deferring surgery may be considered to reduce the risk of perioperative complications.†1,2

Intraoperative Blood Pressure Management

1 B-NR 3 In patients undergoing NCS, maintaining an intraop­

erative mean arterial pressure (MAP) ≥60 to 65 mm Hg or SBP ≥90 mm Hg is recommended to reduce the risk of myocardial injury.3–9 Postoperative Blood Pressure Management

1 B-NR 4 In patients undergoing NCS, treatment of hypoten­

sion (MAP <60-65 or SBP <90 mm Hg) in the postoperative period is recommended to limit the risk of cardiovascular, cerebrovascular, renal events, and mortality.6

1 C-EO 5 In patients with hypertension undergoing NCS, it is

recommended that preoperative antihypertensive medications be restarted as soon as clinically rea­ sonable to avoid complications from postoperative hypertension.

*Caution is advised when continuing antihypertensive therapy in patients with low or low-normal perioperative BPs, older adults (≥65 years),10 and patients in whom the risk for perioperative hypotension is high based on an evaluation of the patient’s overall clinical status, surgery type, and anesthetic plan. †Modified from the “2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ ASH/ASPC/NMA/PCNA High Blood Pressure Guideline.”11 ‡One or more components of the RCRI: CAD, congestive heart failure, cere­ brovascular accident, baseline serum creatinine >2.0 mg/dL, or preoperative in­ sulin treatment.12

Synopsis Perioperative hypertension affects an estimated 25% of patients who undergo major NCS and is a leading cause for postponement of elective surgery.13 Uncon­ trolled hypertension contributes to increased myocar­ dial demand via elevated LV end-diastolic pressure, leading to subendocardial myocardial ischemia. In the perioperative period, uncontrolled hypertension in­ creases the risk of CVD, cerebrovascular events, and bleeding.14,15 Evidence from large cohort studies in­ dicates that intraoperative6,8,16,17 and postoperative6,17 hypotension also increases the risk for adverse car­ diovascular and renal outcomes and death. There are comparatively fewer data that attribute the risk to intra­ operative hypertension5,16 and intraoperative BP vari­ ability.18 However, no high-quality RCTs have shown that acute lowering of perioperative BP reduces rates of cardiovascular events or mortality and, in fact, may be harmful.19 The most appropriate approaches to BP as­ sessment (systolic,2,5,6,20 diastolic,2,5,21,22 mean,4,5,10,23 or pulse pressure24), thresholds (absolute2,4–6,10,20 or rela­ tive4,25), and frequency of measurement26 to guide care have not been established.27 In addition to baseline BP, an assessment of total cardiovascular risk, age, clinical comorbidities, surgery type, anesthetic approach, and short-term risk of complications should be considered when individualizing perioperative BP management.

Recommendation-Specific Supportive Text

1 Uncontrolled hypertension is associated with

increased perioperative complications. In a ret­ rospective analysis of 251 000 adults undergo­ ing elective NCS from the UK Clinical Practice Research Datalink, preoperative DBP >90 mm Hg

Recommendations for Hypertension and Perioperative Blood Pressure Management (Continued) COR LOE Recommendations

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was associated with increased 30-day postopera­ tive mortality.21 Accordingly, ongoing treatment of chronic hypertension is recommended in the peri­ operative period. If hypertensive patients are unable to take oral medications, it is reasonable to use intravenous medications to control BP. Tight BP control mitigates long-term cardiovascular risk, but this strategy may not be appropriate for all patients in the perioperative period. Whereas maintaining an SBP >90 mm Hg may be an acceptable target for younger adults,20 a higher target may be preferred in older adults, those with chronic hypertension, or both.21 The decision whether to hold or continue antihypertensive medications may be specific to drug class. Certain medications (eg, beta block­ ers, clonidine) may be associated with rebound hypertension if discontinued abruptly,28 whereas others have been associated with increased risk of intraoperative hypotension when continued (eg, angiotensin-converting enzyme inhibitors [ACEi], angiotensin-receptor blockers [ARBs]).29,30 Refer to Sections 7.2 through 7.4 for further guidance on specific classes of antihypertensive drugs. 2.	 In patients with untreated or uncontrolled hyper­ tension, induction of anesthesia can trigger sym­ pathetic activity, resulting in labile BP and heart rate.31 In a systematic review and meta-analysis of 30 observational studies, a preoperative diag­ nosis of hypertension was associated with a 35% increase in cardiovascular complications.2 A singlecenter retrospective analysis of 58 276 patients undergoing NCS identified an association between preinduction SBP >160 mm Hg and a composite outcome (cardiac, neurological, or renal complica­ tion or in-hospital mortality) that was only signifi­ cant in patients (n=10 512) with ≥1 components of the RCRI (eg, CAD, congestive HF, cerebrovas­ cular accident, baseline serum creatinine >2.0 mg/ dL, or preoperative insulin treatment).1 However, an elevated BP on the day of surgery may represent a situational (“white coat hypertension”) response.32 Therefore, referring to patients’ baseline ambula­ tory BP is recommended to guide management. In the absence of RCRI components,1 there is little evidence for increased risk of perioperative complications in patients with preoperative BP of <180/110 mm Hg2 or at any preinduction BP. 3.	 Intraoperative hypotension is associated with post­

operative myocardial injury, acute kidney injury, and mortality.4–6,8,23 The harm threshold in observational analyses appears to be roughly a MAP <65 mm Hg or an SBP <90 mm Hg maintained for about 15 minutes.4,33 However, the results of 3 key trials are challenging to interpret. The multicenter, ran­ domized INPRESS (Intraoperative Noradrenaline to Control Arterial Pressure) trial studied 298 high-risk patients and reported a roughly 25% relative risk reduction if SBP was maintained within 10% from baseline versus >80 mm Hg.25 Another single-center trial34 randomized 458 highrisk patients to a MAP ≥60 mm Hg versus MAP ≥75 mm Hg, and POISE-3 (Perioperative Ischemic Evaluation-3)9 randomized 7490 patients to a hypotension-avoidance (target MAP ≥80 mm Hg) versus hypertension-avoidance (target MAP ≥60 mm Hg) intraoperative strategy. Neither of these reported benefit from a strategy targeting higher BP. However, interpretation of the INPRESS study is complicated by lack of details reported with respect to extent of hypotension, especially in the potentially harmful MAP range of 55 to 70 mm Hg. Thus, while the expert opinion is to maintain intraoperative BP targets above MAP ≥60 to 65 or SBP >90 mm Hg, there is currently insufficient trial evidence to support higher BP targets. 4.	 In the POISE-2 (Perioperative Ischemic Evaluation-2) substudy, there was increased risk of the composite outcome of MI and death for increasing duration of SBP <90 mm Hg through postoperative day 4 (OR, 2.83 per 10-minute increase).6 However, anesthetic and hypotension management (eg, fluid boluses, vasoactive drugs, and mechanical support) was at the discretion of the clinical team and not controlled or reported. Closer monitoring of postoperative patients in the intensive care setting may allow for earlier recog­ nition of hypotension.35 A systematic review and meta-analysis on the perioperative use of vasoac­ tive drugs (including inotropic agents and vasocon­ strictors) to treat hypotension concluded that their use may reduce postoperative complications and reduce the length of stay in adult patients having major abdominal surgery.7

5 Postoperative hypertension can occur as a result of

a variety of stimuli, including pain, inflammation, anxi­ ety, hypoxia, volume overload, urinary retention, or as a result of withdrawal of chronic antihypertensive medications.36 Hypertension can increase the risk for myocardial ischemia/infarction, acute decom­ pensated HF, cerebral ischemia, and dysrhythmias.36 Propensity-matched retrospective US Department of Veterans Affairs cohort studies found that delay­ ing the resumption of preoperative ACEi/ARBs was associated with increased 30-day mortality risk.37,38 Chronically taken oral antihypertensive medications should be restarted as soon as clinically reasonable to avoid complications from postoperative hyper­ tension. However, results from a nonrandomized propensity-matched cohort study of men ≥65 years with hypertension caution against intensification of antihypertensive therapy at hospital discharge due to an increased 30-day risk of readmission and serious

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adverse events without improvement in 1-year car­ diovascular events.39

6.3 Heart Failure

Recommendations for Heart Failure Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 C-LD 1.	 In patients with HF undergoing elective NCS,

sodium-glucose cotransporter-2 inhibitors (SGLT2i) should be withheld for 3 to 4 days* before surgery when feasible to reduce the risk of perioperative metabolic acidosis.1–3

2a C-LD 2 In patients with compensated HF undergoing NCS, it

is reasonable to continue GDMT (excluding SGLT2i) in the perioperative period, unless contraindicated, to reduce the risk of worsening HF.4–8

*Canagliflozin, dapagliflozin, and empagliflozin should be stopped ≥3 days and ertugliflozin ≥4 days before scheduled surgery.3

Synopsis Patients with HF are at increased risk for periopera­ tive complications.9,10 In a study of 38 047 patients with nonischemic HF, ischemic HF, CAD, or AF, the crude 30-day postoperative mortality was significantly higher in patients with nonischemic HF (9.3%) or ischemic HF (9.2%) compared with patients with CAD (2.9%), sug­ gesting that patients with HF have a 3-fold greater risk for perioperative death than those with CAD alone.11 In addition, patients with active HF symptoms or signs are at higher risk for adverse outcomes than those with compensated HF or history of HF.9 In another study of patients undergoing NCS, those with an HF diagnosis (n=47 997) had 67% higher adjusted odds of 90-day mortality compared with those without HF (n=561 738), and lower LVEF was associated with higher 90-day mor­ tality (Table 8).10 Accordingly, history of HF has been integrated into both the RCRI and NSQIP preoperative risk assessment indices.

There are established guideline-directed therapies for all forms of HF,12 and there is evidence that optimizing HF treatment before elevated-risk surgery is associ­ ated with reduced risk for perioperative complications.10 Moreover, interruption or discontinuation of HF GDMT without a specific indication to do so is associated with increased mortality.4–7,13 However, SGLT2i have been associated with increased risk for metabolic acidosis in the perioperative period and should be withheld for 3 to 4 days before surgery when feasible.1–3,14 In patients with advanced HF (New York Heart Association [NYHA] class III-IV) who are clinically decompensated or hemo­ dynamically unstable, consideration should be given to postponing elective surgery and obtaining cardiology consultation to assist with perioperative management.

Recommendation-Specific Supportive Text

1 SGLT2i have been associated with metabolic acido­

sis and euglycemic ketoacidosis in the perioperative period, which can lead to serious complications, pro­ longed hospital stay, and death.1,2 The mechanism underlying SGLT2i-induced ketoacidosis is thought to be similar to starvation ketosis, with intensification of the normal metabolic effects of these agents by perioperative fasting. The diagnosis of euglycemic ketoacidosis may be missed because symptoms are often nonspecific, such as nausea, abdominal pain, and shortness of breath, and blood glucose levels may be normal or only mildly elevated. The diagno­ sis should be suspected when there is an anion gap metabolic acidosis and ketones in the blood or urine. In 2022, the US Food and Drug Administration (FDA) updated the labeling for SGLT2i to recom­ mend discontinuing these agents 3 to 4 days before surgery when feasible.3 This recommenda­ tion has been endorsed by the American Diabetes Association and other organizations.14

2 GDMT for HF with reduced EF (HFrEF) includes

4 medication classes that have been shown in multiple trials to reduce mortality and morbidity: (1) renin-angiotensin system inhibition with angio­ tensin receptor-neprilysin inhibitors, ACEi, or ARBs alone; (2) beta blockers; (3) mineralocorticoid receptor antagonists; and (4) SGLT2i.12 There are also guideline-recommended therapies for HF with mildly reduced EF, HF with preserved EF, and HF with improved EF.12 Similarly, patients with stage B pre-HF, including those with asymptomatic sys­ tolic or diastolic dysfunction, should be managed in accordance with guideline recommendations.12 In patients hospitalized for HFrEF, discontinuation of GDMT in the absence of a direct contraindica­ tion has been associated with increased mortality

Table 8.  Association of Heart Failure and Left Ventricular Ejection Fraction With 90-day Mortality in Patients Undergoing Noncardiac Surgery

N Crude Mortality Crude OR Adjusted OR

No heart failure 561 738 1.22% Reference Reference HFpEF, LVEF ≥50% 28 742 4.88% 4.14 (3.90-4.39) 1.51 (1.40-1.62) LVEF 40%-49% 7612 5.11% 4.34 (3.91-4.82) 1.53 (1.38-1.71) LVEF 30%-39% 6048 6.58% 5.68 (5.12-6.31) 1.85 (1.68-2.05) LVEF <30% 4185 8.34% 7.34 (6.56-8.21) 2.35 (2.09-2.63) Adapted with permission from Lerman et al.10 Copyright 2019 American Medi­ cal Association. All rights reserved. HFpEF indicates heart failure with preserved ejection fraction; LVEF, left ven­ tricular ejection fraction; and OR, odds ratio (with 95% CI).

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and readmission.4–8 Thus, continuation of medical therapy for HF is reasonable and likely to be ben­ eficial for most patients undergoing NCS.

6.3.1 Hypertrophic Cardiomyopathy

Recommendation for Hypertrophic Cardiomyopathy COR LOE Recommendation

3: Harm C-LD 1 For patients with hypertrophic cardiomyopathy

(HCM) undergoing NCS, factors that aggravate or trigger dynamic outflow obstructions (eg, positive inotropic agents, tachycardia, or reduced preload) are harmful and should be avoided to reduce the risk of hemodynamic instability.1,2

Synopsis HCM is a common inherited disorder (1 in 500 people in the United States) frequently accompanied by dynamic LVOT obstruction.3 Echocardiography and cardiac magnetic resonance are the preferred di­ agnostic imaging modalities of HCM. Patients with HCM may be asymptomatic at rest but can decom­ pensate from LVOT obstruction in the setting of an­ esthesia, tachycardia, reduced preload, or reduced afterload. Decompensation of HCM can manifest as HF, MI, ischemia, arrhythmia, or sudden cardiac death, and management of established treatment modalities (pharmacotherapy, implantable defibrillators) must be considered in the perioperative management of pa­ tients with HCM. Established negative inotropic agents should be continued into the perioperative period. Use of invasive monitoring (arterial line/central venous pressure) and/or cardiac output measurement may be considered. In most clinical situations, excessive di­ uresis and inotropes should be avoided to avoid the consequent increase in LV outflow gradient (Table 9). When BP support is required, vasopressors are pre­ ferred to inotropic agents. Use of transesophageal echo­ cardiography (TEE) (Section 8.3.1, “Echocardiography”) can be considered in situations of hemodynamic in­ stability to evaluate for LVOT obstruction in patients with HCM. Sinus rhythm should be maintained where possible due to the prevalence of LV hypertrophy and decreased LV compliance in HCM.5–7 For management of other cardiomyopathy conditions, please refer to the 2020 AHA//Multisociety HCM Guideline.3

Recommendation-Specific Supportive Text

1 There is limited evidence about perioperative risk

in patients with HCM undergoing NCS. There are no studies in which intraoperative manage­ ment of HCM has been addressed. Outcomes evidence is mostly derived from cohort studies and case reports, which suffer from small size, single-center composition, and from heterogene­ ity in patient populations and type of surgery.1,2,4–7 These studies report either no or significantly increased perioperative risk, increased risk of developing HF, or both. A recent case-control cohort single-center observational study under­ taken in an institution experienced with HCM1 reported an increase in a composite outcome of 30-day primary events in patients with HCM, but a very low rate of death, MI, or stroke individu­ ally. Higher levels of comorbidity and higher-risk surgery, prolonged intraoperative hypotension, and higher levels of provokable LVOT obstruction appeared to be associated with greatest risk. It may be reasonable to refer patients with HCM to high-volume centers. Postoperative critical care may be indicated in patients with known obstruc­ tive HCM.3

6.3.2 Pulmonary Hypertension

Recommendations for Pulmonary Hypertension Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 C-LD 1 In patients receiving stable doses of targeted medi­

cal therapies* for pulmonary arterial hypertension (PAH) undergoing NCS, it is recommended to con­ tinue these agents to reduce the risk for the devel­ opment of perioperative MACE.1

2a C-LD 2 In patients with severe† PH undergoing elevated-

risk NCS, referral to or consultation with a special­ ized PH center that can support risk assessment, optimization, and postoperative management (with consideration of intensive care after NCS) is reason­ able to reduce perioperative cardiopulmonary compli­ cations.2

2a C-LD 3 In patients with severe† PH undergoing elevated-

risk NCS, invasive hemodynamic monitoring is reasonable to guide intraoperative and postoperative care.3–5

Table 9.  Preoperative and Intraoperative Management Considerations in Patients With Hypertrophic Cardiomyopathy Management Considerations Continue beta blockers and/or nondihydropyridine calcium channel blockers without interruption in the perioperative period Avoid hypovolemia and reduced preload (can worsen LVOT obstruction) Avoid hypotension and reduced afterload (can worsen LVOT obstruction) Avoid tachycardia to ensure adequate LV filling If hypotension develops: Prioritize intravenous fluid administration to correct hypovolemia Use alpha-agonists, such as phenylephrine or vasopressin,7 rather than beta-agonists, which can worsen LVOT obstruction Consider intraoperative echocardiography to evaluate LVOT obstruction in the setting of hypotension In selected cases, intravenous beta-blockade may be necessary to reduce LV myocardial contractility and relieve LVOT obstruction LV indicates left ventricular; and LVOT, left ventricular outflow tract.

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2b C-EO 4 In patients with precapillary PH undergoing elevated-

risk NCS, perioperative administration of short-acting inhaled pulmonary vasodilators (eg, nitric oxide, aero­ solized prostacyclins) may be reasonable to reduce elevated RV afterload and prevent acute decompen­ sated right HF.6

*For example, nitric oxide pathway mediators, endothelin receptor antagonists, prostacyclin pathway agonists, or a combination of these. †Severe PH is defined according to hemodynamics (severe precapillary PH component by right heart catheterization and echocardiography) and additional data derived from clinical assessment, exercise tests, and laboratory biomarkers. Hemodynamically, severe PH displays a mean pulmonary artery (PA) pressure >40 mm Hg, pulmonary vascular resistance >5 Wood units, or echocardiographic evidence of significant RV dysfunction (eg, RV-to-LV diastolic diameter ratio >0.8 or RV dysfunction that is graded as moderate or severe). Although all 5 World Symposium on Pulmonary Hypertension group classifications display some de­ gree of risk for developing severe PH, Group 1 (PAH), Group 3 (PH due to lung disease), and Group 4 (chronic thromboembolic PH) are at high risk for devel­ oping severe PH if left untreated and may be best managed and followed at a center with PH specialists.

Synopsis The role of PH in the development of perioperative MACE in NCS remains largely defined by observational data.1,2,7–17 A recent AHA scientific statement6 provided comprehensive guidance related to the diagnosis, evalu­ ation, and management of PH in patients undergoing NCS, including a thorough review of the 5 clinical group classifications of PH according to the World Sympo­ sium on PH.17 The development of perioperative MACE is consistently higher in patients with any PH subtype compared with those without PH.6 Perioperative risk stratification and optimization should include a re­ view of recent preoperative right heart catheteriza­ tion to determine the presence of precapillary PH (mean PA pressure >20 mm Hg, PA wedge pres­ sure <15 mm Hg, and pulmonary vascular resis­ tance >2 Wood units)18 and echocardiographic data to assess the severity of RV dysfunction to inform management before, during, and after NCS.6 Although patients with PH determined to be at elevated risk for development of perioperative MACE may benefit from invasive hemodynamic monitoring during and after sur­ gery, the choice of invasive monitoring will vary depend­ ing on the patient, surgery, care team, and PH center.

Recommendation-Specific Supportive Text

1 For patients with Group 1 disease (PAH), it is rec­

ommended to continue targeted medical thera­ pies during the perioperative period given the higher risk for MACE compared with patients with non-Group 1 PH undergoing NCS.1,2 A prospec­ tive, international, multicenter, observational study of patients with PAH undergoing nonobstet­ ric NCS at 11 specialized PH centers reported major complications in 6.1% and perioperative mortality in 3.5% of patients.1 Mortality was 15% in emergency procedures compared with 2% in nonemergency surgeries. Although some of the risk factors for major complications were unmodi­ fiable, this study demonstrated the importance of having specialized centers manage patients with PAH undergoing NCS. This study also supported the continuation of PAH-target medical therapies (eg, nitric oxide pathway inhibitors, endothelin receptor antagonists, prostacyclin pathway ago­ nists) in preparation for NCS due to lower morbid­ ity and mortality seen with well-controlled PAH.1

2 A study from 2004 to 2014 of almost 18 million

adult hospitalizations for major NCS in the United States found that, of 143 846 patients with PH hos­ pitalized for NCS (0.81%), PH was associated with a 43% increased odds of death, MI, or stroke and a nearly 2-fold higher risk of cardiogenic shock and cardiac arrest.2 Compared with patients without PH, those with Group 1 disease had a 2.5-fold increase in MACE and a 5-fold greater risk for cardiogenic shock after covariate adjustment.2 This study high­ lights the importance of creating a perioperative management plan for elevated-risk NCS in Group 1 patients within a specialized center that can sup­ port multidisciplinary team management. These resources are especially important if the patient is at significant risk for experiencing acute decom­ pensated right HF from uncontrolled precapillary PH that could require extracorporeal membrane oxygenation.6 The use of venoarterial extracorpo­ real membrane oxygenation as the mechanical sup­ port device of choice for PH-induced right HF, and avoidance of an RV assist device, is also supported by a previous AHA scientific statement.19

3 PH with a severe precapillary component is defined as

mean PA pressure >40 mm Hg, pulmonary vascular resistance >5 Wood units, or evidence of significant RV morphologic alterations by echocardiography (eg, RV-to-LV diastolic diameter ratio >0.8 or RV dysfunc­ tion that is graded as moderate or severe). Patients with severe PH have a high risk for death at base­ line18 and have a higher risk for perioperative compli­ cations than those with mild or moderate disease. In a retrospective analysis of 1276 adult patients under­ going NCS with general anesthesia between 1991 and 2003, 145 patients with PAH (World Symposium on PH Groups 1, 3, or 4) displayed a mean RV sys­ tolic pressure of 68±21 mm Hg on echocardiogra­ phy. Of these, perioperative complications occurred in 60 patients (42%), where NYHA functional class II or higher, RV systolic pressure-to-systemic SBP ratio ≥0.66, and intraoperative use of vasopressors were each associated with postoperative mortality.5 Placement of a central venous catheter is based on determination of intermediate or high risk during risk

Recommendations for Pulmonary Hypertension (Continued) COR LOE Recommendations

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assessment and the need for central venous pres­ sure monitoring and anticipation of vasoactive medi­ cation use.20 Although there are diagnostic benefits to using a PA catheter in the operating room or in the intensive care unit after NCS, incorrect interpretation of information and recognized risks to placement may temper routine use.4

4 The presence of isolated precapillary PH (PH attrib­

uted to the pulmonary arterial tree without the pres­ ence of pulmonary venous occlusive disease or left-heart disease) may include those with Groups 1, 3, 4, or 5 from the World Symposium on PH classifica­ tion.17 The continuous delivery of inhaled pulmonaryselective vasodilators (eg, nitric oxide, prostacyclins) in NCS has been studied mainly in obstetric patients with Group 1 disease21 or lung transplant recipients at risk for PH-induced right HF22 and precapillary PH contributing to primary lung-allograft dysfunction.23 Importantly, MACE has not been evaluated as an outcome. Unlike oral or intravenous vasodilators, the use of these inhaled medications with short half-lives has the added advantage of immediately lowering RV afterload without adversely impacting systemic BP.6 Thus, the potential benefits of selectively lowering RV afterload to avoid acute decompensated right HF may outweigh any minor theoretical risks related to nitric oxide or prostacyclins.6 During preoperative right heart catheterization, typically for Group 1 disease, pulmo­ nary vasodilator administration may be performed to determine vasoreactivity response (responder versus nonresponder)17 and could help guide perioperative use as pulmonary vasodilators may not be helpful in a known nonresponder. Furthermore, these agents may only be available at specialized PH centers that can better care for patients at higher risk for peri­ operative MACE through the ability to provide cali­ brated devices and practice protocols to deliver these inhaled therapeutics.

6.3.3 Adult Congenital Heart Disease

Recommendation for Adult Congenital Heart Disease Referenced studies that support the recommendation are summarized in the Online Data Supplement. COR LOE Recommendation

1 B-NR 1 In patients with intermediate- to elevated-risk

congenital heart disease (CHD) lesions (Table 10) undergoing elective NCS, preoperative con­ sultation with an adult congenital heart disease (ACHD) specialist is recommended before the surgery.*1–4

*Modified from the “2018 AHA/ACC Guideline for Management of ACHD.”5

Table 10.  Adult Congenital Heart Disease Risk Stratification Before Noncardiac Surgery Risk Anatomy Functional/Hemodynamic Status Low Risk Patients with isolated small CHD lesions

Patients with repaired CHD lesion with no residual shunt Patients with bicuspid aortic valve disease and aortopathy NYHA class I functional status, normal exercise capacity

No chamber enlargement on imaging No residual shunt No PAH No arrhythmias

Intermediate risk Unrepaired moderate-large shunts (ASD, VSD, PDA, AVSD)

Repaired CHD with moderate to large residual shunt (ASD, VSD, PDA, AVSD) Obstructive left-sided lesions (congenital mitral stenosis, subaortic stenosis, supravalvular aortic stenosis, coarctation of aorta) except the ones described as low risk Obstructive right-sided lesion (pulmonary stenosis, branch pulmonary stenosis, repaired tetralogy of Fallot) Ebstein anomaly (disease spectrum includes mild, moderate, and severe variations) Anomalous coronary artery arising from the pulmonary artery Anomalous aortic origin of a coronary artery from the opposite sinus, especially with an interarterial or intramural course NYHA class II-IV functional status

Limited exercise capacity Presence of residual shunt Presence of PAH Presence of cardiac chamber enlargement Significant valvular dysfunction (more than mild in severity) Arrhythmias requiring treatment Presence of HF

Elevated risk Single-ventricle patients (palliated or status post Fontan procedure), unrepaired or palliated cyanotic CHD, double outlet right ventricle, pulmonary atresia, truncus arteriosus, TGA (classic or d-TGA; CCTGA or l-TGA), interrupted aortic arch NYHA class II-IV functional status

Limited exercise capacity Significant valvular dysfunction (more than mild in severity) Arrhythmias requiring treatment Presence of PAH Presence of HF

Adapted with permission from Stout et al.5 Copyright 2019 American Heart Association Inc., and American College of Cardiology Foundation. ASD indicates atrial septal defect; AVSD, atrioventricular septal defect; CCTGA, congenitally corrected transposition of the great arteries; CHD, congenital heart disease; d-TGA, dextro-transposition of the great arteries; HF, heart failure; L-TGA, levo-transposition of the great arteries; NYHA, New York Heart Association; PAH, pulmonary arterial hypertension; PDA, patent ductus arteriosus; TGA, transposition of the great arteries; and VSD, ventricular septal defect.

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Synopsis As the population with ACHD grows and ages across the world, these patients increasingly represent a larg­ er proportion of patients undergoing NCS. Patients with ACHD are at increased risk of in-hospital mortality and longer hospitalization and are at higher risk of re­ admission at 30 days after high-risk NCS.6–8 Although the risk may depend on the type and severity of ACHD, surgical procedure, and urgency of surgery, these pa­ tients present unique physiological challenges in peri­ operative care related to fluid balance, BP, and shunt management. Thus, preoperative consultation with an ACHD cardiovascular specialist is advised.5 Increased intra-abdominal pressure, hypothermia, hypercapnia, metabolic acidosis, and hypovolemia should be avoid­ ed in patients with Eisenmenger syndrome or with a prior Fontan procedure to maintain optimal pulmonary vascular resistance.2 If possible, NCS in patients with ACHD should be performed in a health care facility with an established ACHD program and with experi­ ence and expertise in perioperative management of patients with ACHD.

Recommendation-Specific Supportive Text

1 In a patient with ACHD, preoperative assessment

starts with the establishment of baseline risk, which is further determined by the complexity and severity of the disease. Native anatomy, surgical repair, success of the repair and current physiol­ ogy, as well as presence of HF, moderate to large residual shunt, PH, arrhythmia, hypoxemia, damage to other organs, and endocarditis can help define the baseline risk for these patients. The “2018 AHA/ACC Guideline for the Management of of Adults With Congenital Heart Disease”5 describes the ACHD anatomic and physiological classifica­ tion that is used to risk stratify this patient popula­ tion. Modified from this risk classification scheme, Table 10 describes patients with ACHD with low-, intermediate-, and high-risk CHD lesions.5 An analysis of multiple administrative databases showed that NCS carries a greater risk in patients with ACHD compared with patients without ACHD.2,3,7,9,10 Table 11 describes the issues to be considered in the assessment and management of patients with ACHD undergoing NCS.

6.3.4 Left Ventricular Assist Devices

Recommendation for Left Ventricular Assist Devices COR LOE Recommendation

1 C-EO 1.	 In patients with a left ventricular assist device (LVAD),

coordination with the LVAD care team on the appro­ priate timing and perioperative considerations of elective NCS is recommended to mitigate the risk of perioperative MACE.

Synopsis LVADs implanted in the setting of advanced HF pose challenges for perioperative care among patients under­ going NCS. Patients with an LVAD require therapeutic anticoagulation to mitigate the risk of pump thrombosis and stroke and are at risk for bleeding and other major adverse events, such as major infection, right HF, car­ diac arrhythmias, respiratory failure, renal dysfunction, and hepatic dysfunction.1,2 Moreover, patients with an LVAD undergoing NCS are at greater risk of periop­ erative MACE, including inpatient mortality and several perioperative complications that include acute kidney injury, stroke, and gastrointestinal bleeding, compared with patients without an LVAD.3–6 Despite extensive lit­ erature on known complications associated with LVAD recipients, there are limited data to define the optimal timing of elective NCS after LVAD placement. General

Table 11.  Adult Congenital Heart Disease Patient Management for Noncardiac Surgery Clarify the ACHD diagnosis and review cardiac anatomy Clarify prior procedures, residua, sequelae, and current functional status Identify factors associated with increased risk of perioperative morbidity and mortality Cyanosis HF Poor functional capacity Pulmonary hypertension Intermediate- to high-risk CHD lesions Urgent/emergency procedures Operations of the respiratory and nervous systems Multidisciplinary team discussion to develop management strategies to mini­ mize risk and optimize outcomes Issues to consider Endocarditis prophylaxis Prevention of venous thrombosis Monitoring of renal and liver function and appropriate drug dosing Complications related to underlying hemodynamics Need for hemodynamic monitoring Periprocedural anticoagulation Abnormal venous and/or arterial anatomy affecting venous and arterial access Meticulous line care, including air filters for intravenous lines to reduce risk of paradoxical embolus in patients who are cyanotic because of right-to-left shunts Arrhythmias, including bradyarrhythmias Erythrocytosis Pulmonary vascular disease Adjustment of anticoagulant volume in tubes for some blood work in cyanotic patients Adapted with permission from Stout et al.5 Copyright 2019 American Heart Association Inc., and American College of Cardiology Foundation. ACHD indicates adult congenital heart disease; CHD, congenital heart dis­ ease; and HF, heart failure.

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recommendations on perioperative management of pa­ tients with an LVAD are addressed in mechanical circu­ latory support (MCS) guidelines.7 Coordination with the LVAD care team on the appropriate timing of NCS and other perioperative considerations is recommended to help weigh the personalized benefits of NCS after LVAD placement against the risks of perioperative MACE and the risks associated with delaying elective NCS.

Recommendation-Specific Supportive Text

1 There are limited data on the timing of elective

NCS among patients with an LVAD, and much of what is known about perioperative MACE is based on evidence collected before the contemporary generation of LVADs. The potential perioperative risks of MACE in patients with an LVAD undergo­ ing NCS are numerous, potentially devastating, and challenging to predict. Therefore, personal­ ized surgical benefits must be weighed along with the risk of MACE in the timing of elective NCS in patients with an LVAD. The odds of certain periop­ erative MACE have been shown to be greater in elective NCS <6 months versus ≥6 months after LVAD implantation5; however, these data reflect the timing of NCS before the contemporary era of LVAD management and the inclusion of the newer devices in registry data.8 Coordination with the multidisciplinary LVAD team on the ideal timing of elective NCS and other considerations, including but not limited to the individual patient’s recovery from initial LVAD implantation, implant strategy (eg, bridge to transplantation or destination therapy), and prior history of MACE, is recommended to help optimize the benefits and mitigate perioperative complications. To provide future recommendations with higher levels of evidence for the optimal timing of NCS after LVAD implantation, more contempo­ rary data are needed.

6.3.5 Heart Transplantation Recipients

Synopsis In 2022, 3668 adult heart transplants were performed in the United States, with an estimated 1-year survival of >90%, 3-year survival of >85%, and 5-year survival of >80%.1 Patients with a history of heart transplanta­ tion have unique challenges that can increase the risks of perioperative complications, such as infection, woundhealing complications, and acute kidney injury. Acute re­ jection and immunosuppression-related complications, such as infection, steroid-induced hyperglycemia, and leukopenia, are more commonly encountered issues in the first year after heart transplantation.2 The effects of chronic immune suppression and chronic rejection are more commonly seen after the first year, including cardi­ ac allograft vasculopathy, malignancy, and chronic kidney disease (CKD).3 Perioperative considerations for heart transplant recipients may include changes to the immu­ nosuppression regimen if a prolonged period of oral fast­ ing is anticipated, or if wound-healing complications might be minimized by modifying the regimen. Additional fac­ tors to consider when managing heart transplant patients include cardiac denervation of the transplanted heart, interactions between anesthetic medication and immuno­ suppressive agents, and transfusion decisions that mini­ mize the risk of human leukocyte antigen allosensitization and cytomegalovirus infection.3 Given the complexity of the perioperative management of patients with a history of heart transplantation, guidelines from the International Society for Heart and Lung Transplantation recommend preoperative assessment be performed in collaboration with the transplant team, especially for major procedures requiring general or regional anesthesia.3

6.4 Valvular Heart Disease

For the complete set of recommendations and specific definitions for disease severity, please refer to the “2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease.”1

6.4.1 Aortic Stenosis

Recommendations for Aortic Stenosis COR LOE Recommendations

1 C-LD 1 Patients with severe AS should be evaluated for the

need for aortic valve intervention before elective NCS to reduce perioperative risk.*1,2

1 C-EO 2 In patients with suspected moderate or severe AS

who are undergoing elevated-risk NCS, preoperative echocardiography is recommended before elective NCS to guide perioperative management.*

2a C-LD 3 In asymptomatic patients with moderate or severe

AS and normal LV systolic function as assessed by echocardiography within the past year, it is reason­ able to proceed with elective low-risk NCS.3–5

*Modified from the “2020 ACC/AHA Guideline for the Management of Pa­ tients With Valvular Heart Disease.”6

Synopsis Severe AS, as defined by current valvular heart dis­ ease (VHD) and echocardiography guidelines,6,7 and including low-flow, low-gradient AS, is associated with increased risk for adverse cardiovascular outcomes in patients undergoing NCS.5,8,9 When feasible, periop­ erative management of patients with severe AS should be conducted in collaboration with a multidisciplinary heart valve team (Figure 2). Perioperative risk is higher in symptomatic versus asymptomatic patients, in those with reduced LV systolic function, in those with more se­ vere AS, concomitant PH, and in the setting of urgent/ emergency versus elective NCS.6,10 Echocardiography is

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recommended within 1 year of elevated-risk NCS to facilitate perioperative management by defining AS se­ verity, quantifying LV systolic and diastolic function, iden­ tifying other valvular lesions, and evaluating RV function and PA pressure.6 In patients with severe AS who meet criteria for intervention, transcatheter or surgical aortic valve replacement (AVR) before elective NCS reduces perioperative risk.1,2 In patients with severe AS who re­ quire urgent elevated-risk NCS, balloon aortic valvulo­ plasty may be considered as a bridging strategy.3,11–13 Patients with asymptomatic severe AS and normal LV function can safely undergo elective low-risk NCS, espe­ cially in the absence of severe CAD, but patients should be monitored closely to avoid hypotension, excessive hypertension, and tachycardia.6 Shared decision-making with the patient and family is appropriate in high-risk or otherwise challenging settings.

Recommendation-Specific Supportive Text

1 Limited data are available on the use of AVR

for severe AS performed immediately before

Figure 2. Management of Patients With Severe Aortic Stenosis Requiring Elective or Time-Sensitive Noncardiac Surgery. *Severe aortic stenosis: aortic valve area <1.0 cm2, mean aortic valve gradient ≥40 mm Hg, or peak aortic valve velocity Vmax ≥4.0 m/s. †Symptoms of exertional dyspnea, angina, heart failure, syncope, or presyncope. ‡Including elevated risk for hemodynamic instability, large volume shifts, or major bleeding. AVR indicates aortic valve replacement; BAV, balloon aortic valvuloplasty; LVEF, left ventricular ejection fraction; NCS, noncardiac surgery; SAVR, surgical aortic valve replacement; and TAVI, transcatheter aortic valve implantation. Colors correspond to Class of Recommendation in Table 3. Modified from Sorrentino et al.15 Copyright 2022 BMJ Publishing Group. Limited by permission from BMJ Publishing Group Limited.

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moderate- or high-risk NCS.12 However, patients with severe AS who have previously undergone AVR have reduced risk for MACE after elective NCS. In 1 study, there were no perioperative deaths among 161 patients with severe AS who under­ went AVR before NCS. In contrast, the 30-day mortality was 4.3% in 187 patients with untreated severe AS (P=0.008).2 In another study of 491 patients with severe AS undergoing elective NCS, those with prior AVR (n=203) had fewer periop­ erative MACE compared to those with untreated AS (5.4% versus 20.5%, P<0.001).1 In both stud­ ies, patients with symptomatic untreated AS had the worst outcomes, suggesting that AVR before elective NCS may be beneficial in these patients. Several small series have examined the utility of balloon aortic valvuloplasty before NCS.3,6,9,11 Although the procedure can be performed safely, data are conflicting regarding the effect of balloon aortic valvuloplasty on clinical outcomes.6,14 Due to the high risk associated with severe AS in patients undergoing elevated-risk NCS, such patients are best managed at centers capable of performing aortic valve interventions. 2.	 Severe AS has long been recognized as an inde­ pendent risk factor for adverse cardiac events and death after NCS.5,8,9 Although more recent studies suggest that the perioperative mortality risk asso­ ciated with AS has declined, AS remains a strong predictor of nonfatal cardiac events in the periop­ erative period.4 Patients with suspected moderate or severe AS who have not had an echocardiogram within 12 months before planned NCS should undergo TTE to aid in perioperative decisionmaking. Additional factors that should be consid­ ered in perioperative planning include the severity of AS, presence of significant CAD or other valvular pathology (especially MR), LV and RV function, PA pressure, type of surgery, and other factors associ­ ated with increased perioperative risk.6 If the echo­ cardiogram reveals severe AS, consultation with a heart valve team, if available, should be obtained. 3.	 Patients with asymptomatic severe AS undergo­

ing NCS are at increased risk for perioperative cardiac complications, but the risk is lower than in symptomatic patients.5,8,9 AVR before NCS could potentially reduce perioperative risk but may lead to a delay in indicated surgery (especially with sur­ gical AVR), and it is also associated with poten­ tial complications. The available evidence, while limited, favors proceeding with low-risk NCS in patients with asymptomatic AS and preserved LVEF ≥50%, especially in the absence of severe CAD.6 Preoperative evaluation for severe CAD may be considered in select patients.6 Patients with asymptomatic severe AS undergoing high-risk NCS may benefit from additional preoperative evaluation (Figure 2). All patients with severe AS should be monitored closely throughout surgery and the early postoperative period to minimize the risk of hypotension, excessive hypertension, and tachycardia, as well as to avoid dehydration or volume overload.12 Such monitoring may include invasive hemodynamic monitoring and/or intraop­ erative TEE. Consultation with a multidisciplinary heart team is appropriate, particularly if hemody­ namic instability, large volume shifts, or high risk for bleeding is anticipated in the perioperative period.6

6.4.2 Mitral Stenosis

Recommendations for Mitral Stenosis Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 B-NR 1 Patients with severe mitral stenosis (MS) should be

evaluated for the need for mitral valve (MV) interven­ tion before elective NCS.1–17

2a C-EO 2 In patients with severe MS who cannot undergo

MV intervention before NCS, perioperative invasive hemodynamic monitoring is reasonable to guide management to reduce the risk of cardiovascular complications.

2b C-LD 3 In patients with severe MS who cannot undergo MV

intervention before NCS, perioperative heart-rate control (eg, beta blockers, calcium channel blockers [CCBs], ivabradine, digoxin) may be considered to prolong diastolic filling time and decrease periopera­ tive cardiovascular complications.18–21

Synopsis Patients with moderate to severe MS are at increased risk of perioperative adverse cardiovascular events. Sus­ pected MS can be evaluated by echocardiography, and patients with severe MS may benefit from a multidisci­ plinary team approach at centers experienced with this higher-risk population. There is a paucity of data guid­ ing the management of patients with MS undergoing NCS, and much has been extrapolated from pregnancy literature.22–25 Patients with MS who meet criteria for MV intervention should receive treatment before elec­ tive NCS.26 Criteria for MV intervention include patients with severe rheumatic MS who are symptomatic (NYHA class ≥II) or asymptomatic with elevated pulmonary pres­ sures (PA systolic pressure >50 mm Hg). In cases where MV intervention cannot be performed before surgery (eg, emergency or urgent surgery), perioperative goals include maintaining a low-normal heart rate, a high-normal sys­ temic vascular resistance, ensuring adequate preload, and, when applicable, a rhythm control strategy to main­ tain sinus rhythm. Tachycardia decreases diastolic time and increases transvalvular MV gradients, which can lead to increased left atrial pressures, elevated pulmonary pressures, pul­ monary edema, and systemic hypotension. Intensive

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monitoring could improve detection and management of tachycardia and hypotension and may reduce cardiovas­ cular events. Recovery in the intensive care unit or longer monitoring periods in the postanesthesia care unit may be appropriate. For other recommendations regarding VHD and MS, including thresholds for intervention, please refer to Section 6 in the “2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease.”26

Recommendation-Specific Supportive Text

1 In patients with symptomatic severe MS or asymp­

tomatic severe MS with elevated pulmonary pres­ sures or new AF, MV intervention may reduce morbidity and mortality rates.1–17 In patients with severe MS with an indication for valve intervention in whom intervention can be successfully performed, elevated-risk elective NCS should be delayed until MS has been addressed. There may be lower-risk surgeries where clinicians may favor MV interven­ tion before elective NCS, especially if percutaneous mitral balloon commissurotomy could be performed without delaying surgery. The decision to inter­ vene before elective NCS should be contextualized according to the proposed MV intervention (percu­ taneous mitral balloon commissurotomy versus a surgical approach) and the risk of the NCS. 2.	 Patients with MS are at higher risk of pulmonary edema, hypotension, and arrhythmia. PH has been associated with adverse perioperative events,27 and changes in pulmonary hemodynamics may increase cardiovascular risk in patients with MS. Perioperative conditions (eg, hypoxia, hypercap­ nia/hypercarbia28) that could worsen PH should be avoided. Longer durations of observation in the postanesthesia/recovery care unit may allow for earlier detection and intervention of complications. In settings where there may be significant intravas­ cular fluid shifts, earlier detection and treatment of clinically significant hemodynamic changes may be possible with invasive hemodynamic monitor­ ing, providing real-time measures to guide therapy. Invasive monitoring could include Swan-Ganz cath­ eters, arterial lines, and TEE, but the intensity and level of monitoring should be commensurate to the risk of surgery and anesthesia technique. 3.	 RCTs have demonstrated that heart rate control

improves patient symptoms and exercise dura­ tion.18–21 These studies have focused on stable symptomatic outpatients with MS. There have been no RCTs examining the benefit of perioperative heart rate control in patients with MS. Heart rate control may improve symptoms in the perioperative period by increasing diastolic time and forward flow, thereby decreasing left atrial pressures and ensur­ ing adequate cardiac output. Heart rate–controlling medications may be considered for procedures where elevated heart rates or tachycardia are anticipated.

6.4.3 Chronic Aortic and Mitral Regurgitation

Recommendations for Chronic Aortic and Mitral Regurgitation COR LOE Recommendations

1 C-EO 1 In patients with suspected moderate or severe val­

vular regurgitation, preoperative echocardiography is recommended before elective NCS to guide periop­ erative management.*

1 C-EO 2 In patients with VHD who meet indications for

valvular intervention based on clinical presentation and severity of regurgitation, the need for valvular intervention should be considered before elective elevated-risk NCS to reduce perioperative risk.*1–3

2a C-LD 3 In asymptomatic patients with moderate or severe

MR, normal LV systolic function, and estimated PA systolic pressure <50 mm Hg, it is reasonable to perform elective NCS.*45

2a C-LD 4 In asymptomatic patients with moderate or severe aor­

tic regurgitation and normal LV systolic function (LVEF >55%), it is reasonable to perform elective NCS.*6

*Modified from the “2020 ACC/AHA Guideline for the Management of Pa­ tients With Valvular Heart Disease.”3

Synopsis Aortic and mitral valvular regurgitation are common, par­ ticularly in older adults, and may be detected during pre­ operative assessment for NCS.6 Patients with valvular regurgitation can have symptoms of increasing exercise intolerance, dyspnea, paroxysmal nocturnal dyspnea, or or­ thopnea.7,8 Echocardiography is the primary imaging tool to determine the presence and severity of regurgitant aortic valves and MVs.9 In asymptomatic patients with normal LV systolic function, NCS may be safely performed in the set­ ting of severe aortic regurgitation (AR) or MR.2 Exercise testing can be used to confirm the lack of symptoms.10 Valvular regurgitation is broadly classified as either primary or secondary.11 Secondary MR results from diseases that primarily affect the LV or the left atrium, causing impaired function of the MV apparatus. It is important to understand the etiology, severity, and hemodynamic consequences of valvular regurgitation before NCS. Although there is limit­ ed evidence available, decreased LVEF and AF contribute to increased perioperative risks in patients with valvular re­ gurgitation. Since the publication of the 2020 ACC/AHA VHD guideline,3 no major new evidence has warranted re­ visions to the existing guideline recommendations.

Recommendation-Specific Supportive Text

1 Patients evaluated for NCS with known or sus­

pected moderate or severe valvular regurgita­ tion should undergo a comprehensive history and physical examination, 12-lead ECG, and TTE.12 Echocardiography is important to assess the sever­ ity of valvular regurgitation, estimate right and left

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ventricular systolic and diastolic function, quantify chamber sizes, and assess PA systolic pressures.12 An echocardiogram performed within the prior 12 months may be acceptable for preoperative evalu­ ation if the patient’s functional status and symp­ toms are unchanged since the previous study.13 Preoperative recognition of the diagnosis and severity of regurgitant VHD is critical to guide peri­ operative management and decisions regarding the timing of surgery. 2.	 Although regurgitant VHD is generally better toler­

ated than valvular stenosis, aortic and mitral valvular regurgitation increase the cardiovascular risks dur­ ing NCS.3 Patients with MR or AR who are planned for elective elevated-risk NCS and who meet stan­ dard indications for intervention should have mitral or aortic valve surgery (repair or replacement) per­ formed before NCS, when feasible.3 In patients with MR with indications for repair who are not candidates for MV surgery, minimally invasive MV transcatheter edge-to-edge repair (TEER) of the MV can also be considered before NCS.1,14

3 Patients with moderate-severe MR undergoing NCS

have increased risks of perioperative HF and MI than matched patients without MR undergoing NCS.4 Risk factors for adverse perioperative outcomes in the setting of MR include lower EF and preexist­ ing AF. Asymptomatic individuals with moderate or severe MR, normal LV systolic function, and a PA systolic pressure <50 mm Hg, can be considered for NCS without preoperative valve intervention.13 In selected patients, exercise testing can be considered to confirm asymptomatic status, assessed as a nor­ mal functional capacity without dyspnea. In patients with untreated MR who undergo NCS, perioperative hemodynamic and anesthetic management strate­ gies should include avoiding increased afterload and bradycardia. General anesthesia or, alternatively, combinations of neuraxial local anesthetics and opi­ oids, cause vasodilation, lower systemic vascular resistance, and are generally favorable for patients with MR. Although vasodilation can be advantageous for MR, preload should be maintained.3,15 Invasive hemodynamic and/or intraoperative TEE may permit continuous optimization of LV filling pressures in the perioperative period. Intensive monitoring should be considered for up to 24 to 72 hours after surgery.3 In all patients with MR, careful attention to afterload and volume status is critical. In patients with asymp­ tomatic secondary MR, perioperative considerations should also include management of the underlying heart disease. 4.	 Patients with severe AR undergoing NCS are at

risk for hypotension, arrhythmias, HF, and death because of increased ventricular volumes and myo­ cardial wall stress. In an analysis of patients with moderate-severe or severe AR versus those without moderate-severe or severe AR undergoing NCS, patients with AR had more perioperative hemody­ namic instability, excess morbidity from pulmonary edema and prolonged endotracheal intubation, and higher in-hospital mortality than matched controls. LV systolic dysfunction, serum creatinine >2 mg/dL, and intermediate- or high-risk NCS were associ­ ated with excess risks of mortality in patients with AR.6 Careful attention to volume status is critical in patients with AR. To minimize the adverse hemody­ namic effects of AR, bradycardia should be avoided in the perioperative period to minimize diastolic fill­ ing times. Invasive systemic arterial and venous catheters and/or TEE may help guide perioperative management.3,13 Intensive monitoring is appropriate in the immediate postoperative period.

6.4.4. Previous Transcatheter Aortic Valve Implantation or Mitral Valve Transcatheter Edge-to-Edge Repair Recommendations for Patients With Previous Transcatheter Aortic Valve Implantation or Mitral Valve Transcatheter Edge-to-Edge Repair Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2a B-NR 1 For patients who undergo successful transcatheter

aortic valve implantation (TAVI), it is reasonable to perform NCS early* as clinically indicated.1–3

2a C-EO 2 For patients who undergo MV TEER, it is reasonable

to perform NCS after the successful MV intervention as clinically indicated.4

*Evidence supports the safety of NCS within 30 days of TAVI, if indicated.

Synopsis With an increasing number of TAVI procedures being performed in the United States and globally, NCS in pa­ tients with previous TAVI is being encountered in clinical practice with increasing frequency. Available evidence on the safety of NCS after TAVI is limited to small case series1,2 and 1 prospective TAVI registry of patients at the tertiary care University Hospital in Bern, Switzerland.3 The available evidence suggests that NCS may be per­ formed early after successful TAVI with acceptable out­ comes. In general, lifelong single antiplatelet therapy is recommended after TAVI, and DAPT with aspirin and clopidogrel for up to 6 months is commonly used in pa­ tients with sinus rhythm after MV TEER; however, there are no evidence-based recommendations for antiplate­ let/anticoagulant therapy after the TEER procedure.5–8

Recommendation-Specific Supportive Text

1 NCS may be performed safely early after success­

ful TAVI as defined by the 2020 ACC/AHA VHD guideline.8 In a cohort study of 300 patients under­ going NCS after TAVI, suboptimal performance,

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such as prosthesis-patient mismatch and paraval­ vular regurgitation, was associated with increased risk of adverse outcomes after NCS.3 Twenty-one percent of patients underwent surgery within 30 days of TAVI, with no excess risk of adverse out­ comes in this cohort compared with longer delays to surgery. Based on these data, surgery early (eg, within 30 days) after successful TAVI appears to have acceptable perioperative outcomes. Aspirin therapy should ideally be continued in the periop­ erative period of NCS in patients with prior TAVI to reduce thrombotic risks.7

2 Clinical studies have demonstrated reductions in

the severity of primary MR, LV and left atrial vol­ umes, and improved exercise capacity and QOL in patients treated with MV TEER.4,9 Although there is a lack of data on timing and safety of NCS after MV TEER, NCS may be performed early (eg, within 30 days) after a successful valve intervention if residual MR is no longer severe. Please refer to the 2020 ACC/AHA VHD guideline for the definition of a successful MV TEER procedure.8 The TRAMI (Transcatheter Mitral Valve Interventions) regis­ try was the largest real-world cohort of patients treated with TEER and confirmed lasting clini­ cal improvements and low intervention rates. The strongest predictor of long-term mortality in the TRAMI registry was a history of prior TAVI; other predictors of mortality were NYHA class IV HF, prior HF decompensation, CKD, and LVEF <30%.4

6.5 Atrial Fibrillation

Recommendations for Atrial Fibrillation COR LOE Recommendations Perioperative

2a C-LD 1 In patients with rapid AF identified in the setting of

NCS, it is reasonable to treat potential underlying triggers contributing to AF and rapid ventricular response (eg, sepsis, anemia, pain).*1–5

2a C-LD 2 In patients with new-onset AF identified in the set­

ting of NCS, initiation of postoperative anticoagula­ tion therapy can be beneficial after considering the competing risks associated with thromboembolism and perioperative bleeding.*4,6

Postdischarge

1 C-LD 3 In patients with new-onset AF identified in the set­

ting of NCS, outpatient follow-up for thromboembolic risk stratification and AF surveillance are recom­ mended given a high risk of AF recurrence.*7–11

*Adapted from the “2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation.”12

Synopsis AF is the most common arrhythmia, with an estimated prevalence of undiagnosed AF in 2009 of approximately 13% of the US population.13,14 Patients with preexisting AF undergoing NCS have higher risks of all-cause mor­ tality, HF, and ischemic stroke within 30 days of surgery than patients without preexisting AF.15 If hemodynamically stable, patients with AF who are planned for NCS gener­ ally do not require any changes in medical management other than interruption of oral anticoagulation (OAC) (Section 7.6, “Oral Anticoagulation”).16 According to the “2023 ACC/AHA/ACCP/HRS Guideline for the Diag­ nosis and Management of Atrial Fibrillation,” patients with preoperative AF and poor rate control should have medi­ cal management optimized before surgery.12 New-onset perioperative/postoperative AF (POAF) in the setting of NCS is also common, with an incidence that varies widely depending on the type of surgery and patient popula­ tion.17,18 POAF can be asymptomatic or can lead to he­ modynamic instability. Management of new-onset POAF requires identifying and treating known triggers (eg, pain, sepsis, anemia) and consideration of rate and/or rhythm control strategies to optimize patient hemodynamics. POAF is associated with increased risk of short- and longterm stroke and mortality, and anticoagulation should be considered to reduce thromboembolic risks.5,18,19 Patients with paroxysmal POAF have a high risk of recurrent AF after discharge. Future studies are needed to address op­ timal surveillance and long-term management of POAF after NCS.20 For additional information on AF and associ­ ated recommendations, please refer to the 2023 ACC/ AHA/ACCP/HRS AF guideline.12

Recommendation-Specific Supportive Text 1.	 The postoperative development of pain, anemia,

electrolyte imbalance, fluid shifts, and sepsis in NCS patients can contribute to new-onset POAF and a rapid ventricular response. Aggressive management of these underlying triggers is an essential com­ ponent of POAF management. Hemodynamically stable patients with POAF may require specific therapy to achieve an optimal heart rate (<110 bpm). Medications that block atrioventricular nodal conduction, such as beta blockers or CCBs, can be used for ventricular rate control, and digoxin can be considered as an adjunct or if other agents are con­ traindicated.21–24 Among patients with AF refractory to rate control with atrioventricular nodal blockers, rhythm control with synchronized electrical direct current cardioversion or pharmacological cardiover­ sion with antiarrhythmic drugs can be considered. Exclusion of left atrial appendage thrombus before implementing rhythm control may be indicated in patients with a prolonged duration (>48 hours) of AF or in patients at high risk for thromboembo­ lism. Synchronized direct current cardioversion is recommended for hemodynamically unstable AF with a rapid ventricular response associated with hypotension.

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2 New-onset POAF after NCS is associated with

thromboembolic risks comparable to those in nonsurgical patients with AF.6,19 In a meta-analysis of 2 458 010 patients, POAF was associated with a 62% increased risk of early stroke and a 44% increased risk of early mortality within 30 days of surgery versus patients without POAF.6 POAF was also associated with a 37% increased risk of long-term stroke and a 37% increased risk of long-term mortality.6 In subgroup analy­ ses, POAF was more strongly associated with stroke in patients undergoing NCS (hazard ratio [HR], 2.00 [95% CI, 1.70-2.35]) than in patients undergoing cardiac surgery (HR, 1.20 [95% CI 1.07-1.34]).6 It is unclear whether stroke mecha­ nisms are the same in patients with POAF com­ pared with those with nonsurgical AF. In patients with POAF after NCS, anticoagulation should be considered based on a patient’s thrombo­ embolic stroke risk (eg, CHA2DS2-VASc score) and bleeding risk. In a Danish registry analysis of patients with AF after NCS, use of OAC initi­ ated within 30 days postdischarge was associ­ ated with a 48% reduced risk of thromboembolic events compared with no anticoagulation ther­ apy.4 The use of oral nonvitamin K anticoagulant or no anticoagulation in patients with new-onset AF in the postoperative period after NCS is being tested in ASPIRE-AF (Anticoagulation for Stroke Prevention in Patients with Recurrent Episodes of Perioperative AF after NCS), an ongoing RCT.19

3 In a longitudinal database of 10 723 patients with

newly diagnosed AF (age 68±10 years, 41% women), 15% developed POAF after NCS. POAF after NCS was associated with a 39% risk of AF recurrence at 5 years, with an increased risk of HF and death.20 Given these findings, POAF after NCS warrants timely outpatient follow-up to coordinate AF surveillance, determine the need for anticoagulation, optimize risk factors, titrate medications for rate control, and consider rhythm control. More intensive monitoring, such as with 1- to 2-week ambulatory electrocardiographic monitoring, 30-day electrocardiographic event monitoring, or implantable cardiac monitoring in selected patients, may be warranted. In cardiac surgery patients, continuous monitoring postsur­ gery is associated with a higher detection of AF.7–9 This is consistent with previous studies showing higher sensitivity of AF detection with longer-term monitoring.10,11 Although the optimal frequency, duration, and type of rhythm monitoring with post­ operative AF remains unclear, outpatient followup within 3 to 6 months of NCS to evaluate the incidence of AF after NCS is recommended.25 6.6 Cardiovascular Implantable Electronic

Devices Recommendations for Preoperative Management of Patients With Cardiovascular Implantable Electronic Devices Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 B-NR 1 Patients with cardiovascular implantable electronic

devices (CIED) having elective NCS should have a management plan developed before surgery if elec­ tromagnetic interference (EMI) is anticipated, includ­ ing identification of the type of CIED (eg, pacemaker, implantable cardioverter-defibrillator [ICD], implant­ able monitor), manufacturer, and model.1–6

1 B-NR 2 Patients who are pacemaker-dependent having

surgeries above the umbilicus with anticipated EMI should have the pacemaker reprogrammed or have a magnet placed on the generator to provide an asyn­ chronous mode to avoid pacing inhibition.1,7

1 B-NR 3 Pacemaker-dependent patients with a transvenous

ICD undergoing surgery above the umbilicus with anticipated EMI should have the device repro­ grammed*; if the patient is not pacemakerdependent, then either reprogramming or a magnet placed on the generator can be used to inhibit tachytherapies or inappropriate shocks.8,9

1 B-NR 4 Patients who have a pacemaker or ICD repro­

grammed to asynchronous pacing or have tachy­ therapies programmed off before surgery should have device functioning restored in the postoperative period before hospital discharge.10

1 C-LD 5 Patients with leadless pacemakers who are

pacemaker-dependent having surgeries with antici­ pated EMI above the umbilicus should have their pace­ makers reprogrammed to an asynchronous mode.11

2a C-LD 6 For patients with subcutaneous ICD having noncardiac

or nonthoracic surgery with anticipated EMI above the groin, it is reasonable to reprogram the device or use a magnet to temporarily disable tachytherapies.12

*For pacemaker-dependent patients with an ICD, tachytherapies should be disabled and the device should be reprogrammed to an asynchronous mode to avoid pacing inhibition.

Synopsis A CIED may be identified by history and physical ex­ amination, review of records, and chest radiography. The closer the electrosurgery unit (ESU) is to the pulse generator or leads of the CIED, the more likely EMI will occur.9 The risk of EMI dissipates with distance away from the CIED.9 An ESU below the umbilicus is unlikely to cause EMI with transvenous devices.2,13,14 Failure to identify a CIED can lead to adverse outcomes from EMI, inhibition of pacing, inappropriate tachycardia detection, inappropriate shocks, and damage to the device.1,2 Use of intermittent, irregular bursts of monopolar ESU at the lowest feasible energy can limit EMI. Bipolar ESU and ul­ trasonic scalpels are unlikely to cause EMI.14 Even if EMI is not anticipated, there may be circumstances when pa­ tient movement from an CIED shock is undesirable, such as during intracranial, intraspinal, or intraocular surgeries. EMI may obscure pacing spikes and QRS complexes on

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the ECG. Magnets should not be relied on without pre­ operative confirmation of their effects on CIEDs.1 Some devices have programmable magnet responses that have effects other than forcing asynchronous pacing. It is im­ portant to ensure the CIED is functioning properly before surgery.15 Patients with CIED frequently have cardiac diseases that are equally important to evaluate, such as arrhythmias, structural or congenital heart disease, isch­ emic and nonischemic cardiomyopathies, and HF. For emergencies with anticipated EMI, a magnet should be used, and the CIED type, manufacturer, and programmed parameters should be identified as soon as possible. A magnet will not force asynchronous pacing in an ICD.

Recommendation-Specific Supportive Text

1 The type of CIED, the manufacturer, the model, pri­

mary indication for placement, pacing dependency, effects of a magnet, and proper functioning of the CIED must be determined.1,5 Information is obtained from medical records, patient identification cards, the CIED management team, interrogation reports, or a preoperative interrogation.3 Clinicians should confirm battery status through recommended inter­ rogations (every 12 months for a pacemaker, every 6 months for an ICD).1 A plan for reprogramming or use of a magnet should be developed before beginning procedures, with input from the CIED professionals, anesthesiologists, and surgeons. Institutions should have a CIED protocol in place (Figures 3 and 4).5,16 Management plans should incorporate the procedure details, patient position­ ing (eg, prone), and the type of anticipated EMI. Recommendations should state specific program­ ming changes if needed, response to a magnet, patient pacemaker dependency, battery life, and history of serious arrhythmias.1,5 Recommendations and changes need to be included in the medi­ cal record and accessible to all perioperative clinicians.1–5

2 Magnet pacing rates vary by manufacturer and bat­

tery status. With ample battery supply, devices pace

Figure 3. Patients With Transvenous CIEDs. *EMI is considered a significant risk when the source is <15 cm from the CIED generator. External pacing and/or defibrillation must be available. Clinicians must confirm device magnet capabilities are enabled and individual magnet responses are known. Consider consulting a CIED team for cardiac resynchronization therapy devices. Colors correspond to Class of Recommendation in Table 3. CIED indicates cardiovascular implantable electronic device; EMI, electromagnetic interference; and ICD, implantable cardioverter-defibrillator.

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at 85 to 100 bpm.15 Magnet rates decrease with battery depletion. It is important to confirm asyn­ chronous (VOO or DOO) pacing at the expected rate with magnet use. Magnet use with some pace­ makers only forces asynchronous pacing for 10 beats and then reverts to programmed settings.17 These devices must be reprogrammed to avoid EMI. Magnets may not be effective in obese or prone patients, or if continuous generator contact cannot be ensured.1,12 EMI from ESU, monitors, bone saws, or patient movement can trigger rate-responsive functions, resulting in undesirable tachycardia that may cause unwanted hemodynamic effects or may be misinterpreted.7 Deactivating the rate adaptive function is recommended during lithotripsy or elec­ troconvulsive therapy. Monopolar ESU require a dispersive electrode to divert current away from the CIED to avoid damage. EMI is more common with monopolar than bipolar ESU and with coagulation versus cutting mode.13,14 The dispersive electrode is positioned as far as possible from the generator and the heart. The current path should not cross the generator or the leads.9 There is a risk of EMI even with ESU below the umbilicus with underbody dispersive electrodes, and practitioners need to use a magnet or reprogram the CIED.9,18

3 ICDs need to be programmed to asynchronous

pacing in pacemaker-dependent patients. ICDs will misinterpret EMI as a tachyarrhythmia, thus trig­ gering tachytherapies. Antitachyarrhythmia func­ tions are disabled to avoid inappropriate therapies. Removal of a magnet rapidly restores tachythera­ pies if needed.8 Some, but not all, devices emit a tone with application of a magnet. Comments regarding ESU and dispersive electrodes noted previously for pacemakers apply to ICDs. 4.	 If external cardioversion or defibrillation is not an

option during a procedure, transcutaneous pac­ ing or defibrillator pads should be on the patient when CIED functions are disabled. When ICDs

Figure 4. Patients With Nontransvenous Devices. *For patients with a leadless pacemaker, a magnet will not force asynchronous pacing. †A subcutaneous ICD does not currently provide pacing. A magnet, if used, should be secured with adhesive tape. If the patient is in a position other than supine, or extensive EMI is anticipated when performing the surgery above the diaphragm, consider reprogramming. A magnet placed over the subcutaneous ICD will emit an R wave synchronous beep, indicating that the magnet is correctly positioned. If the tone is not audible, reprogramming is necessary. Colors correspond to Class of Recommendation in Table 3. EMI indicates electromagnetic interference; and ICD, implantable cardioverter-defibrillator.

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have been reprogrammed, the devices need to be interrogated and reprogrammed to their original or recommended settings before the patient is dis­ charged to an unmonitored setting or to home.10 Patients with sudden death have been reported to registries after failure to reactivate tachythera­ pies.10 Patients with CIED can play a role in safe care and appropriate CIED functionality by sending a remote transmission upon discharge. 5.	 Leadless pacemakers are miniaturized, fully selfcontained devices that are nonsurgically implanted in the RV via a catheter.11,19 The pacemaker may or may not be magnet responsive and is manufacturer specific. Identification of the correct placement of a magnet can be difficult given that these devices are fully intracardiac. 6.	 Subcutaneous ICDs are more susceptible to ESU

above the groin, likely due to their large surface area and location along the left chest wall.12

6.7 Previous Stroke or Transient Ischemic

Attack Recommendation for Previous Stroke or Transient Ischemic Attack Referenced studies that support the recommendation are summarized in the Online Data Supplement. COR LOE Recommendation

2a B-NR 1 In patients with a history of stroke or transient isch­

emic attack, it is reasonable to delay elective NCS for ≥3 months after the most recent cerebrovascular event to reduce the incidence of recurrent stroke, MACE, or both.1,2

Synopsis Patients with prior stroke or transient ischemic attack are at higher perioperative risk of a recurrent stroke or worsening of neurological deficits.3 This increased risk appears to diminish over time, with reduction of inflam­ mation, decreased hemorrhage risk, and reestablishment of cerebral autoregulation.4 However, there is limited ob­ servational evidence that determines the optimal time interval to delay elective NCS after a stroke. Prior stud­ ies compared elective noncardiac surgical patients with and without prior stroke, rather than prior stroke with and without NCS; patients with prior stroke have a baseline 5-year risk of recurrence of 12%.5 For management of stroke risk, please refer to the 2021 AHA/ASA stroke prevention guideline.5

Recommendation-Specific Supportive Text 1.	 When compared with patients without prior stroke,

an analysis from a large Danish registry found an increased risk of recurrent stroke, MI, and cardiovas­ cular death in patients with recent stroke, particularly <3 months after the event (OR, 14.23), compared with 3 to 6 months (OR, 4.85), 6 to 11 months (OR, 3.04), or ≥12 months of the index event (OR, 2.47).2 The odds of a postoperative ischemic stroke within the first 3 months of a prior stroke were high. However, over the ensuing months, this marked elevated risk waned and plateaued at 9 months but did not approach baseline risk, even at 12 months postinfarction (OR, 8.2). A more recent analysis of a Medicare database of ∼6 million patients undergo­ ing elective noncardiac and non-neurological surgery found a far lower overall rate of secondary strokes compared with those with no prior stroke for opera­ tions performed <30 days or performed between 61 and 90 days after prior stroke (OR, 8.0 [95% CI, 6.37-10.10] and OR, 5.0 [95% CI, 4.0-6.29], respec­ tively).1 Importantly, there was only a very small dec­ rement in risk between 61 and 90 days and 6 and 12 months (OR, 4.76 [95% CI, 4.26-5.26]). Based on this new evidence, delaying NCS for ≥6 months does not appear to provide additional protection against the occurrence of recurrent stroke.

6.8 Obstructive Sleep Apnea

Recommendation for Obstructive Sleep Apnea Referenced studies that support the recommendation are summarized in the Online Data Supplement. COR LOE Recommendation

2a B-NR 1 In patients scheduled for NCS, obstructive sleep

apnea (OSA) screening using validated question­ naires is reasonable to assess the risk of periopera­ tive complications.1–3

Synopsis The pathophysiology of OSA is complex, multifactorial, and associated with several cardiovascular complica­ tions, including hypertension, AF, HF, CAD, stroke, PH, metabolic syndrome, diabetes, and cardiovascular mor­ tality.4,5 Approximately 34% of men and 17% of women between the ages of 40 and 60 years meet the diag­ nostic criteria for OSA.4 In a recent meta-analysis of 22 studies evaluating outcomes of NCS in patients with (n=184 968) and without OSA (n=2 848 846),6 a preoperative diagnosis of OSA was associated with an increased incidence of a composite of postoperative car­ diac and cerebrovascular complications. In comparison to patients without OSA, patients with OSA had a 2.5-fold greater risk of developing postoperative pulmonary com­ plications. A diagnosis of OSA was also associated with an increased incidence of perioperative MI and AF but not HF. In a separate meta-analysis of 46 studies, OSA was associated with risks of postoperative pulmonary complications and cardiac complications that increased with greater OSA severity. Specifically, OSA was associ­ ated with an increased incidence of MI, AF, and HF but not an increased incidence of stroke.7 Among patients

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with a diagnosis of OSA who require the use of noninva­ sive positive airway pressure ventilation before surgery, positive airway pressure should be restarted postopera­ tively as early as possible.8–10 In patients with OSA under­ going NCS, regional anesthesia is reasonable to reduce the use of systemic opioids, sedatives, and the risk of pulmonary complications.2,10

Recommendation-Specific Supportive Text

1 A prospective multicenter study analyzed the pre­

operative sleep study results of 1218 patients with­ out a prior diagnosis of OSA who were scheduled for major NCS.3 Among these patients, 67.6% were assigned a new diagnosis of previously recognized OSA, 30.5% had at least moderate OSA, and 11.2% had severe OSA. For those patients with severe OSA, there was an increased risk of the compos­ ite outcome of myocardial injury, cardiac death, HF, thromboembolism, AF, and stroke within 30 days of surgery.3 In a prospective study of 2877 adults who completed OSA risk screening questionnaires dur­ ing preoperative assessment before NCS,11 23.7% were identified as high risk for OSA. Few patients identified as high risk had a prior OSA diagnosis, and among 207 who elected to undergo a home sleep study, 170 (82.1%) were found to have OSA (mild, n=97; moderate, n=40; severe, n=33).11 Another prospective study enrolled 245 adults with ≥2 risk factors for OSA scheduled for NCS. All patients were screened with the STOP-Bang questionnaire, and among them 182 patients underwent a preoperative level III polysomnogram.1,12 Seventy patients (38%) were diagnosed with OSA, including 11 patients (6%) with moderate to severe OSA. Although pro­ spective evidence to support routine OSA screening before surgery is lacking, the increased prevalence of OSA in surgical patients with CVD and potential for benefit with OSA treatment provide a reasonable rationale for OSA screening before NCS.

7 PERIOPERATIVE MEDICAL THERAPY

7.1 Statins

Recommendations for Statins Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 B-NR 1 In patients currently on statins and scheduled for

NCS, continuation of statin therapy is recommended to reduce the risk of MACE.1–3

1 B-R 2 In statin-naïve adult patients who meet criteria for

statin use based on ASCVD history or 10-year risk assessment and are scheduled for NCS, periopera­ tive initiation of statin is recommended with intention of long-term use.4,5 Synopsis

The use of long-term lipid-lowering therapies for primary and secondary prevention of atherosclerotic cardiovas­ cular events is well established. Hydroxymethyl gluta­ ryl coenzyme A reductase inhibitors (statins) reduce atherogenic low-density lipoprotein-cholesterol, confer pleiotropic anti-inflammatory effects, and may confer benefits to patients in the perioperative period and be­ yond. Multiple small RCTs, observational cohorts, and meta-analyses demonstrate that perioperative statin use is safe and may reduce cardiovascular outcomes, par­ ticularly in patients undergoing major vascular surgery. However, the benefit of routine preoperative administra­ tion of statins remains uncertain in patients undergoing nonvascular surgery, as compelling observational data and meta-analyses are counterbalanced by a small but more scientifically rigorous RCT in which statin use did not confer benefit.2,3,6–10 The LOAD (Lowering the Risk of Operative Complications using Atorvastatin Loading Dose) trial, the largest RCT to date, randomly assigned 648 statin-naïve patients to atorvastatin 80 mg loading (within 18 hours preoperatively) followed by 40 mg daily for 7 days versus placebo and evaluated the compos­ ite of all-cause mortality, nonfatal MI, and stroke at 30 days.10 There was no difference in short-term periop­ erative MACE; long-term benefits of therapy were not evaluated in this study. Future large RCTs are needed to elucidate the role of perioperative statin initiation on outcomes in lower-risk patients or procedures, as well as the ideal timing and dosing regimens (eg, reloading), before routine statin initiation can be recommended. Of note, the measurement of low-density lipoproteincholesterol concentrations to guide initiation of statin therapy in patients with appropriate indications, should not delay surgery; however, the NCS setting is an excel­ lent opportunity to initiate therapies with the objective to improve long-term outcomes.

Recommendation-Specific Supportive Text

1 Among patients receiving statin therapy who are

planned for NCS, large cohorts report safety and possible reductions in cardiovascular complica­ tions associated with continued use of lipid low­ ering throughout the perioperative period.1 In a large US cohort (n=780 591), 9.9% of patients receiving perioperative lipid-lowering therapy had lower surgical mortality overall and after propen­ sity matching than those who did not receive lipid-lowering therapy.1 Although these data favor continuation of home-dose statins, the benefits of statin reloading or intensification before surgery are uncertain. One study randomly assigned 500 consecutive patients who were receiving statins and were admitted for urgent or emergent NCS to either reloading of atorvastatin or continuation

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of home statin.11 In this study, statin reloading was associated with a 5.6% absolute risk reduction in perioperative MACE at 30 days, as well as reduc­ tions in AF and length of stay. Additional RCTs are needed to determine the benefits of statin inten­ sification, reloading, or both in the perioperative period of NCS. 2.	 In a single-center RCT, 100 patients planned to

undergo vascular surgery were randomly assigned to atorvastatin 20 mg daily for 45 days or placebo. Vascular surgery was performed an average of 30 days after statin initiation, and statins were con­ tinued long term in patients in whom low-density lipoprotein-cholesterol was ≥100 mg/dL. The primary endpoint, the composite of death from cardiac causes, nonfatal MI, stroke, and unstable angina at 6 months, occurred in 4 patients (8.0%) assigned to atorvastatin and 13 patients (26%) assigned to placebo (P=0.031).4 Furthermore, in a 2018 systematic review and meta-analysis, statin therapy appeared to reduce perioperative MACE and improve survival after vascular sur­ gery.5 Long-term use of statin therapy is important to reduce primary and secondary atherosclerotic events in at-risk patients.12 Evaluation practices outlined in the AHA/ACC guidelines may help to identify patients whose long-term cardiac outcomes would be improved by adherence to GDMT. However, given the lack of benefit in the LOAD trial, short-term use to lower perioperative risk requires further evaluation. As such, NCS should not be delayed if low-density lipoproteincholesterol is not already available.10

7.2 Renin-Angiotensin-Aldosterone System

Inhibitors Recommendations for Perioperative Renin-Angiotensin-Aldosterone System Inhibitors Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2b B-R 1 In select* patients on chronic renin-angiotensin-

aldosterone system inhibitors (RAASi) for hypertension undergoing elevated-risk NCS, omission 24 hours before surgery may be beneficial to limit intraoperative hypotension.1–6

2a C-EO 2.	 In patients on chronic RAASi for HFrEF, periopera­

tive continuation is reasonable.†1,2

*Patients with controlled BP and undergoing elevated-risk surgical procedures. †Modified from the “2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure.”7

Synopsis ACEi and ARBs are widely used for their antihyperten­ sive and cardiac benefits; therefore, the safety and effi­ cacy of the perioperative use of RAASi is of importance. RCTs comparing omission to continuation of RAASi have enrolled a variety of low- to intermediate-risk patients undergoing major NCS. In these studies, intraoperative hypotension (MAP <60 mm Hg) occurred more com­ monly when these agents were continued; however, continuation compared with omission did not result in worse clinical outcomes (eg, myocardial injury after NCS [MINS]). Of note, patients with high (SBP >160 mm Hg) or low (SBP <105 mm Hg) BP are often excluded from RCTs, and there has been limited enrollment of high-risk patients including those with HFrEF. No data currently exist regarding the perioperative role (harm or benefit) of the angiotensin receptor/neprilysin inhibitor, sacubitril/ valsartan. Given the important role of RAASi in prevent­ ing MI, stroke, HF, and decline in kidney function, larger RCTs are still needed before recommending routine in­ terruption of RAASi in all patients before planned sur­ gery; thus, an individualized approach to perioperative management of ACEi or ARBs is warranted.

Recommendation-Specific Supportive Text

1 Intraoperative hypotension, particularly prolonged

episodes, may increase postoperative myocar­ dial injury and mortality.8 However, while omitting RAASi before surgery has been shown to reduce intraoperative hypotension, RCTs have failed to prove this strategy improves clinical outcomes.1,2,9 The PREOP-ACEI (Prospective Randomized Evaluation of Perioperative Angiotensin- Converting Enzyme Inhibition) study for patients stable on ACEi for at least 6 weeks before planned major noncardiac nonvascular surgery observed that fewer episodes of intraoperative hypotension (SBP <80 mm Hg) occurred in patients random­ ized to omit the final preoperative ACEi dose compared with patients continuing use. Major adverse cardiovascular endpoints were not dif­ ferent, nor was postanesthesia unit recovery time or length of stay.1 These findings are corrobo­ rated by the meta-analysis of earlier studies that included data from 6022 patients in whom ACEi or ARB was omitted or continued before planned NCS.2 Although intraoperative hypotension was more common in patients who continued ACEi/ ARB, there was no difference in MACE. Ongoing studies, including STOPorNOT (Impact of RAASi Continuation on Outcome after Major Surgery), will seek to answer questions about the clini­ cal impact of continuation or omission of RAASi before planned surgery.10,11 Recently published results from POISE-3 demonstrated no differ­ ence in major vascular events (MINS, vascular death, stroke, or cardiac arrest at 30 days) in nearly 7500 patients with vascular disease or risk factors randomized to hypotension-avoidance or

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hypertension-avoidance perioperative BP strate­ gies.12 In this study, antihypertensive agents were either withheld or continued based on the BP management strategy. Notably, 72% of patients in both groups were taking an ACEi/ARB at the time of randomization, with no excess adverse events in the group randomly assigned to continue their home BP regimen on the morning of surgery.12

2 The role of RAASi in HFrEF, HF with mildly reduced

ejection fraction, and HF with preserved ejection fraction is supported by clinical guidelines.7 RAASi confer a significant reduction in mortality and even dose-dependent reduction in outcomes such as hospitalizations for HF, particularly in patients with LVEF <40%.7 The complexity of HF medication regimens and goals of care warrant careful con­ sideration and ideally, minimal interruption. In our review of existing data, RCTs of perioperative omis­ sion of RAASi have largely excluded patients with moderate to severe HF or had limited inclusion.1 Further, a meta-analysis in 2018 found only 1 study reporting the influence of RAASi interruption on HF outcomes.2

7.3 Calcium Channel Blockers

Synopsis CCBs comprise a heterogenous class of medica­ tions that can be subdivided into nondihydropyridine (verapamil, diltiazem) and dihydropyridine agents (eg, amlodipine, felodipine, nifedipine extended release). Dihydropyridines are largely used to manage hyper­ tension, while nondihydropyridines are important for management of cardiac dysrhythmias, and both play a role in symptom relief in patients with chronic stable angina. Perioperative CCB administration has been explored in small RCTs. In 2003, a meta-analysis of 11 RCTs encompassing 1007 patients evaluated the benefit of perioperative CCBs versus placebo on perioperative MACE.1 Most trials tested perioperative intravenous diltiazem or intravenous verapamil. Initia­ tion of CCBs failed to reduce perioperative mortality or perioperative MI, although they were associated with re­ ductions in the composite of MI and death, as well as postoperative supraventricular tachycardia. Significant hypotension and bradycardia were observed in individual studies but not in the overall pooled analysis, possibly owing to the varying medication and dosage regimens chosen. A more recent meta-analysis evaluated CCBs (largely dihydropyridines), compared with other antihy­ pertensive agents, to treat postoperative hypertension.2 Of the 14 studies included, no significant differences in postoperative hemodynamics were noted.2 Although these data do not support the benefit of perioperative CCB initiation, continuation may be reasonable with rec­ ognition of the potential for intraoperative hypotension (for dihydropyridines) and/or bradycardia (for nondihy­ dropyridines).3

7.4 Alpha-2 Receptor Agonists

Recommendation for Perioperative Alpha-2 Receptor Agonists Management Referenced studies that support the recommendation are summarized in the Online Data Supplement.

COR LOE Recommendation

3: No benefit B-R 1 In patients undergoing NCS, initiation of low-dose

clonidine perioperatively is not recommended to reduce cardiovascular risk.1

Synopsis A single large, well-designed RCT showed no benefit of initiation of clonidine to prevent perioperative MACE. This same trial raised concerns regarding the safety of this approach. New administration is thus not recom­ mended; however, perioperative continuation of chronic therapy has not been addressed in RCTs. Chronic use of clonidine, and other alpha-2 receptor agonists, is re­ served for patients with severe resistant hypertension or special populations (eg, CKD, impulse control disorders). Abrupt discontinuation can lead to norepinephrine surge and resultant rebound hypertension.2 Short-term inter­ ruption for surgery has not been studied.

Recommendation-Specific Supportive Text

1 The POISE-2 trial was a blinded RCT of 10 010

patients undergoing major NCS, randomized to lowdose clonidine or placebo 2 to 4 hours before sur­ gery, to evaluate the impact on 30-day risk of death or nonfatal MI and included patients were ≥45 years old and at high risk of cardiovascular complications (history of ASCVD event or ≥3 traditional risk fac­ tors).1 If baseline SBP was ≥105 mm Hg and heart rate was ≥55 bpm, patients received 0.2 mg of clonidine orally and application of a transdermal 0.2 mg per day clonidine patch or placebo for 72 hours. At 30 days, no difference was seen in the primary outcome, composite of death or nonfatal MI, or key secondary endpoints. Patients treated with clonidine were significantly more likely to experience nonfatal cardiac arrest and clinically significant bradycardia or hypotension. Results of POISE-2, as well as 23 additional RCTs in NCS, were included in a 2018 meta-analysis that reported nonsignificant differ­ ences in all-cause mortality, cardiac mortality, and MI.3 There was, however, moderate-to-high quality evidence to demonstrate significant increased risk of hypotension and bradycardia. Importantly, in addi­ tion to clonidine, these studies included dexmedeto­ midine and mivaserol, which were never approved in the United States.3

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7.5 Antiplatelet Therapy and Timing of

Noncardiac Surgery in Patients With Coronary Artery Disease Recommendations for Antiplatelet Therapy and Timing of Noncardiac Surgery in Patients With Coronary Artery Disease Referenced studies that support the recommendations are summarized in the Online Data Supplement.

COR LOE Recommendations

1 B-NR 1.	 For patients with CAD undergoing elective NCS,

management of perioperative antiplatelet therapy and timing of surgery should be determined by a multidisciplinary team with shared decision-making to weigh the risks of bleeding, thrombosis, and con­ sequences of delayed surgery.1–7

Timing of NCS After PCI

1 C-LD 2 In patients with recent coronary artery balloon

angioplasty without stent placement, elective NCS should be delayed for a minimum of 14 days to minimize perioperative MACE.8,9

1 B-NR 3 In patients with DES-PCI placed for ACS who

require elective NCS with interruption of ≥1 anti­ platelet agents, surgery should ideally be delayed ≥12 months to minimize perioperative MACE.5,10–15

2a B-NR 4 In patients with DES-PCI placed for CCD who

require elective NCS with interruption of ≥1 anti­ platelet agents, it is reasonable to delay surgery for ≥6 months after PCI to minimize perioperative MACE.16–24

2b B-NR 5 In patients with DES-PCI who require time-sensitive

NCS with interruption of ≥1 antiplatelet agents, NCS may be considered ≥3 months after PCI if the risk of delaying surgery outweighs the risk of MACE.5,23,24

3: Harm B-NR 6 In patients with a recent (≤30 days) bare-metal

stent (BMS) or DES-PCI, elective NCS requiring interruption of ≥1 antiplatelet agents is potentially harmful due to a high risk of stent thrombosis and ischemic complications.6,9,22,25,26

Perioperative Antiplatelet Management Post PCI

1 B-R 7 In patients with prior PCI undergoing NCS, it is

recommended to continue aspirin* (75-100 mg), if possible, to reduce the risk of cardiac events.27–30

1 B-NR 8 In patients with CAD who require time-sensitive

NCS within 30 days of PCI with BMS or <3 months of PCI with DES, DAPT should be con­ tinued unless the risk of bleeding outweighs the benefit of the prevention of stent thrombosis.23,31

1 B-NR 9 In patients with prior PCI in whom OAC monotherapy

must be discontinued before NCS, aspirin should be substituted when feasible in the perioperative period until OAC can be safely reinitiated.27–29

2b B-NR 10 In select patients after PCI who have a high throm­

botic risk, perioperative bridging with intravenous antiplatelet therapy may be considered <6 months after DES or <30 days after BMS if NCS cannot be deferred.32,33

Perioperative Antiplatelet Management in Patients Without Prior PCI

2b B-R 11 In patients with CCD without prior PCI undergoing

elective NCS, it may be reasonable to continue aspirin in selected patients when the risk of cardiac events outweighs the risk of bleeding.27,34,35 3: No benefit B-R 12 In patients with CAD but without prior PCI who are

undergoing elective noncarotid NCS, routine initiation of aspirin is not beneficial.27,36

*Platelet adenosine diphosphate receptor (P2Y12) monotherapy may be con­ sidered if surgical bleeding risks are acceptable or if aspirin is not tolerated.

Synopsis Management of antiplatelet therapy in the perioperative period of NCS is complex, particularly for patients with CAD and prior PCI, as the timing of antiplatelet interrup­ tion must be balanced against competing risks of throm­ botic complications (Table 12 and Figure 5). The risk of perioperative stent thrombosis is greatest in the first 4 to 6 weeks post-PCI, with excess risks that decline over time but persist to 6 months. For most patients with CCD, DAPT is recommended for 6 months, followed by single antiplatelet therapy (either with aspirin or P2Y12 inhibi­ tor).37–39 Selected patients may be eligible for shorter du­

rations of DAPT (28-31 days or 90 days) post-PCI based on recent data,40–42 but the safety of this approach in pa­ tients planned for NCS requires further study. Patients with PCI performed for MI have nearly 3-fold higher risks of postoperative MACE versus those with CCD as the in­ dication for PCI.16,17 Ideally, NCS should be postponed ≥1 year after PCI for ACS, although NCS can be considered ≥6 months after DES placement for CCD12,15 and after 3 months for time-sensitive NCS if the benefits of surgery outweigh the risk of MACE. If a patient requires urgent NCS requiring interruption of DAPT, balloon angioplasty without stents may be considered, with NCS delayed for a minimum of 14 days due to higher perioperative MACE risk very early after PCI.15,43

Recommendation-Specific Supportive Text

1 The decision to perform NCS in a patient with CAD

should involve the patient, the surgeon, the anes­ thesiologist, and the cardiologist managing the

Recommendations for Antiplatelet Therapy and Timing of Noncardiac Surgery in Patients With Coronary Artery Disease (Continued)

COR LOE Recommendations

Table 12.  Duration of Antiplatelet Therapy Effect

Antiplatelet Agent Minimum Time From Drug Interruption to Restoration of Platelet Function Aspirin 4 d Clopidogrel 5-7 d Prasugrel 7-10 d Ticagrelor 3-5 d Minimum times from drug interruption to noncardiac surgery should be guided by pharmacokinetic data, restoration of platelet function after drug withdrawal, and drug-specific FDA-prescribing information.67–71

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patient’s antiplatelet therapy and ischemic risk.5–7,44 Antiplatelet therapy is frequently indicated for the prevention of ischemic cardiac events in patients with CAD. Temporary discontinuation of antiplatelet therapy can be safe depending on the timing of NCS relative to any prior PCI and time-independent indications for the procedure. The risk of antiplate­ let therapy interruption should be individualized to balance MACE risks with optimal surgical timing.7 Decisions for continuation or cessation of aspirin, P2Y12 inhibitor, or both in the perioperative period of NCS should be undertaken by multidisciplinary team members and should involve the patient and their family.44 The use of aspirin for primary pre­ vention has decreased based on evidence that it does not reduce cardiovascular risks, and multi­ disciplinary team consensus may not be required for perioperative interruption of aspirin when it is prescribed for primary cardiovascular preven­ tion.45 Multidisciplinary input may be considered in those receiving aspirin or other antiplatelet therapy for secondary prevention or noncardiovascular indications. 2.	 Elective NCS after balloon angioplasty alone with­

out placement of a stent can proceed after ≥14 days of uninterrupted DAPT; however, high-quality data to inform management of these patients are limited.8,9 3 In patients with prior DES-PCI, the optimal timing

of elective NCS requiring interruption of antiplate­ let therapy requires careful consideration. Multiple studies have identified a continuum of declining perioperative MACE risk after PCI.12 However, a large retrospective analysis of >20 000 patients corroborated smaller studies identifying that prior PCI remains a risk factor for perioperative MACE and bleeding to 1 year.14,15 A small retrospective cohort identified that perioperative cardiac events still occur 6 months after DES-PCI.13 Perioperative risks of NCS are particularly high within the first year after PCI when coronary stent placement occurs for the treatment of acute MI.11,16,17 In patients with DES-PCI performed for ACS, elective NCS should be delayed ≥12 months after PCI. A 12-month delay between PCI and NCS may also be appropriate for patients undergoing complex DES-PCI (eg, bifurcation stents, long stent lengths, multivessel PCI) or when details regarding prior DES-PCI are unavailable.17

4 In a matched cohort study from US Department

of Veterans Affairs hospitals, perioperative MACE events were highest during the first 6 months after PCI and stabilized thereafter at 1%.16 A ret­ rospective analysis of 221 379 hospital admis­ sions for NCS found high rates of perioperative MI (4.7%), bleeding (32%), and mortality (4.4%)

Figure 5. Optimal Timing of Elective or Time-Sensitive NCS for Prior PCI Requiring Management of DAPT. Colors correspond to Class of Recommendation in Table 3. ACS indicates acute coronary syndrome; BMS, bare-metal stent; CCD, chronic coronary disease; DAPT, dual antiplatelet therapy; DES, drug-eluting stent; NCS, noncardiac surgery; and PCI, percutaneous coronary intervention.

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within 6 months of PCI.5 Stent type (BMS versus DES) was not associated with perioperative MACE at 6 months in a large cohort study.12 Similarly, another registry showed no significant differences in perioperative MACE between those patients with BMS or DES, only identifying PCI for ACS as an independent MACE risk factor.11 However, a multicenter prospective registry (approximately 40 000 patients) identified stent type as a risk fac­ tor for MACE events, with older-generation DES associated with higher risk of events at any time point compared with BMS.21 In a Canadian study (approximately 8000 patients), the incidence of MACE associated with major elective NCS per­ formed >6 months after DES-PCI was 1.2%, with risk approaching that of intermediate-risk surgical patients without prior PCI.6 The variation seen in these analyses emphasizes that stent type, time from PCI, and indication for PCI represent impor­ tant factors in shared decision-making regarding consideration of surgery at 6 months post-PCI. 5.	 In patients with prior PCI and a time-sensitive indi­ cation for NCS (eg, resection of malignancy), a risk assessment balancing the potential delay of surgery against perioperative MACE should be performed. Risks of perioperative MACE after NCS appear highest when surgery is performed within the first 3 months after PCI.17 A previous study found lower incidence of MACE when NCS was performed >3 months (2.8%) compared with <30 days (10.5%) after BMS-PCI.8 The incidence of perioperative MACE after NCS was also lowest if surgery was performed >3 months after DES-PCI.46 In a pro­ spective study evaluating perioperative MACE and bleeding, event rates were high in the first 30 days after PCI, with time from stent implantation to sur­ gery <3 month as an independent risk factor for bleeding.24 Finally, in a large pooled analysis of nonsurgical patients post-PCI, DAPT discontinua­ tion at >3 months was not associated with excess stent thrombosis.47 Taken together, these data sug­ gest that, in selected patients, it may be reasonable to undergo NCS ≥3 months post-PCI if the benefit of surgery outweighs the risk of MACE. 6.	 Elective NCS should not be performed <30 days

of PCI. Early case series reported a high incidence of bleeding and MACE after NCS scheduled within 30 days of PCI.48 Larger studies subsequently con­ firmed excess risk of perioperative MACE within this timeframe post-PCI.5,8,9,23,49 Catastrophic outcomes of NCS within 30 days of PCI have been reported, with risks of MI, stent thrombosis, bleeding, and mortality.8,48,49 Surgical trauma leads to catechol­ amine surges, inflammatory cytokines, activation of the clotting cascade, enhanced platelet activation, and decreased fibrinolysis, all of which contribute to the thrombotic milieu, and consequently surgery should be delayed after PCI.22 A prospective study of patients post-PCI found that those undergoing NCS at <35 days from PCI had a 2-fold higher risk of complications compared with those under­ going surgery >90 days after PCI.26 Another study found that NCS <1 month post-PCI had a higher incidence of MI (7.2% versus 0.5%), cardiac death (5% versus 0.4%), and all-cause mortality (9% ver­ sus 2.1%) than those undergoing surgery within the first 12 months after PCI.23 Elective NCS after PCI with BMS can proceed after ≥30 days of unin­ terrupted DAPT, although BMS are rarely placed in the contemporary era.8,9

7 In patients with prior PCI with coronary stent place­

ment undergoing NCS, aspirin use was associated with lower rates of death and nonfatal MI (abso­ lute risk reduction, 5.5%), with comparable major and life-threatening bleeding.29 Although the risks of bleeding with DAPT are higher than those with aspirin alone,25,48,50–53 in a meta-analysis of 46 studies including >30 000 patients undergoing NCS, both single and double antiplatelet therapy were associated with a modest increased risk of bleeding without additional thrombotic risk com­ pared with placebo or interruption of antiplatelet therapy.54 A systematic review found limited data to support either continuation or discontinua­ tion of DAPT before NCS as a strategy to reduce thrombotic risk, bleeding, or mortality.35 In patients planned for NCS that requires interruption of DAPT, aspirin monotherapy should be continued whenever possible. 8.	 The risk of stent thrombosis is highest in the first 4 to 6 weeks after PCI with BMS and in the first 3 months after DES implantation.6,9–12,25,48,52,55–58 In a Danish national registry from 2005 to 2012, NCS within 1 month of PCI-DES was associated with a 13-fold higher risk of cardiac death and a 4-fold higher risk of all-cause mortality.23 When timesensitive NCS is necessary within 30 days of BMS- PCI or within 3 months of DES-PCI, DAPT should be continued in the perioperative period, if feasible, from a surgical bleeding perspective. 9.	 In patients with prior PCI in whom oral anticoagu­ lation monotherapy is planned to be interrupted before NCS, initiation of aspirin monotherapy is reasonable to reduce risks of stent thrombosis and ischemic complications. After NCS, aspirin may be discontinued, and oral anticoagulation monother­ apy may be reinitiated as surgical bleeding risks permit. 10.	 In patients who are within 1 to 6 months of PCI and

continue to need DAPT, use of intravenous anti­ platelet therapy as a bridge for nondeferrable sur­ gery has been inadequately studied.4 The BRIDGE

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(Bridging Antiplatelet Therapy With Cangrelor in Patients Undergoing Cardiac Surgery) trial stud­ ied oral P2Y12 inhibitor discontinuation and sub­ sequent use of cangrelor versus placebo.59 This study of patients undergoing CABG demonstrated greater platelet inhibition with cangrelor without excessive risk of major bleeding. The MONET BRIDGE (Maintenance of Antiplatelet Therapy in Patients with Coronary Stenting Undergoing Surgery) trial is currently underway for evaluating cangrelor as a bridging strategy in patients under­ going NCS within 12 months of PCI.60 There are no established data on the use of glycoprotein IIB/ IIIA inhibitors as a bridging strategy.61,62

11 In observational studies of patients undergoing

NCS, aspirin continuation was associated with a 1.5-fold greater risk of nonserious bleeding events.34 Withdrawal of aspirin preceded up to 10% of perioperative acute cardiovascular syndromes.34 In a small RCT of 220 patients undergoing NCS, perioperative aspirin was associated with a 7.2% absolute risk reduction for postoperative MACE.63 In a meta-analysis of >30 000 patients with and with­ out prior PCI undergoing NCS, antiplatelet therapy was associated with minimal bleeding risk and no increase in thrombotic complications.54 In the pre­ specified stratum of POISE-2 (n=4382) trial, aspi­ rin continuation did not reduce death or nonfatal MI compared with aspirin interruption (7.7% versus 7.8%; HR, 1.00 [95% CI, 0.81-1.23]).27 Although aspirin should not be routinely continued in the perioperative period of NCS, continuation may be reasonable in selected patients after consideration of individualized thrombotic and bleeding risks.35

12 The POISE-2 trial randomly assigned 10 010

patients planned for NCS and at risk for cardiovas­ cular complications to perioperative aspirin versus placebo.27 Administration of aspirin before surgery and for 30 days postoperatively did not reduce the composite of death or nonfatal MI (7.0% versus 7.1%; HR, 0.99 [95% CI, 0.86-1.15]; P=0.92) but was associated with a 23% increased hazard for major bleeding. Findings were consistent regard­ less of aspirin use before trial enrollment.27 Among patients in POISE-2 undergoing vascular surgery, perioperative withdrawal of chronic aspirin therapy was not associated with increased cardiovascular events.64 In the POISE-3 trial, among patients undergoing NCS, the incidence of the composite bleeding outcome was significantly lower with tranexamic acid than with placebo.65 The net clinical benefit of tranexamic acid appears patient-specific; that is, it is worthwhile for those at increased risk for bleeding outcomes but harmful for those at increased risk for adverse cardiovascular events.66 7.6 Oral Anticoagulants

Recommendations for Oral Anticoagulants Management Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations OAC Management

1 B-NR 1 For patients with CVD receiving OAC who require

elective NCS, a multidisciplinary team-based approach to time-based* interruption is recom­ mended to balance the competing risks of thromboembolism and perioperative bleeding (Tables 13 and 14).1–7

OAC Bridging

2a C-LD 2 In patients with CVD and high thrombotic risk (Table

14) undergoing NCS where interruption of vitamin K antagonist (VKA) is required, preoperative bridging with parenteral heparin can be effective to reduce thromboembolic risk.8–10

3: Harm C-LD 3 In most patients with CVD who are undergoing

elective NCS where OAC interruption is warranted, routine periprocedural bridging is not recommended due to increased bleeding risk.8,11

OAC Resumption

2a C-LD 4.	 In patients with preoperative OAC interruption,

resumption of OAC is reasonable after hemostasis is achieved.9

*Timing of preoperative interruption is based on patient-specific factors (eg, thrombotic risk, age, sex, body weight, renal clearance), surgical bleeding risk, and drug factors (eg, pharmacokinetics, dosing, drug interactions).

Synopsis Both major bleeding and thrombosis (eg, stroke and ve­ nous thromboembolism) are important surgical outcomes and key contributors to death in NCS.12 Balancing these perioperative risks is particularly challenging in patients receiving chronic OAC, including VKA and direct oral anti­ coagulants (DOAC). Development of a perioperative plan for elective NCS should include evaluation of patientspecific factors (eg, age, thrombotic risk, renal func­ tion, history of bleeding), procedural factors (eg, timing of surgery, bleeding risk), and drug properties (eg, dos­ ing, drug interaction, onset/offset).12,13 Whenever fea­ sible, multidisciplinary assessments (eg, OAC prescriber, cardiologist, vascular specialist, hematologist, surgeon, anesthesiologist) should be performed to better under­ stand patient characteristics and surgical risk. Such ap­ proaches, applied as part of a standardized preoperative screening process, may greatly improve patient safety.14 Finally, guidance on monitoring for residual drug effects and hemostasis as well as approaches to OAC reversal is highlighted, particularly when surgical interventions must occur urgently.

Recommendation-Specific Supportive Text

1 It is generally safe to perform surgeries with mini­

mal bleeding risk without interrupting OAC therapy (Tables 13 and 14).1–3,15–17 For NCS with greater

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bleeding risks, time-based interruption (“time reversal”) of OAC is advised.5,18–20 A DOAC inter­ ruption protocol tested in 3007 patients with AF in the PAUSE (Perioperative Anticoagulation Use for Surgery Evaluation) study7 resulted in low rates of major bleeding or thromboembolism (Table 13). Findings were similar in the prospective, observa­ tional, EMIT-AF/VTE (Edoxaban Management in Diagnostic and Therapeutic Procedures) study.6 In select patients with recent thromboses

and high residual thrombotic risk, delaying elec­ tive NCS may permit safer interruption of OAC. Time reversal of OAC is always preferred, but this may not be feasible for urgent or emergency procedures with moderate or high bleeding risk.21 The measurement of coagulation parameters, drug levels, or both may identify ongoing drug effects. In the absence of altered coagulation parameters or detectable drug levels, OAC reversal agents may not be necessary.22–24 Otherwise, rapid reversal of OAC can be achieved with prothrombin com­ plex concentrates,25,26 andexanet alfa for factor Xa inhibitors (rivaroxaban, apixaban, or edoxaban), or idarucizumab for dabigatran (Table 15).27,28

Procedures with higher bleeding risks (eg, neur­

axial anesthesia) should be performed with com­ plete interruption of OAC.29 When minimal drug effect is desired, anticoagulants should be held

Table 13.  Perioperative Management of Direct Oral Anticoagulants and Vitamin K Antagonists Preoperative DOAC Schedule

Procedure Bleeding Risk Preoperative Interruption Surgery/ Procedure Postoperative Resumption

Day -6 Day -5 Day -4 Day -3 Day -2 Day -1 Day 0 Day +1 Day +2 Day +3 Day +4

Apixaban, edoxaban, rivaroxaban High * * * * † † † † † * *

Low/Moderate * * * * * † † * * * * Minimal * * * * * * * * * * *

Apixaban, edoxaban, rivaroxaban with renal impairment (CrCl <30 mL/min) High * * * † † † † † † * *

Low/Moderate * * * * † † † * * * * Minimal * * * * * * * * * * *

Dabigatran CrCl ≥50 mL/min High * * * * † † † † † * *

Low/Moderate * * * * * † † * * * * Minimal * * * * * * * * * * *

Dabigatran CrCl <50 mL/min High * * † † † † † † † * *

Low/Moderate * * * * † † † * * * * Minimal * * * * * * * * * * *

VKA Schedule

Procedure Bleeding Risk Preoperative Interruption Surgery/ Procedure Postoperative Resumption

Day -6 Day -5 Day -4 Day -3 Day -2 Day -1 Day 0 Day +1 Day +2 Day +3 Day +4

Warfarin in low/moderate thrombotic risk High * † † † † † † * * * *

Low/ Moderate * † † † † † † * * * * Minimal * * * * * * * * * * *

Warfarin in high thrombotic risk High * † † ‡ ‡ ‡ † * * *# *#

Low/ Moderate * † † ‡ ‡ ‡ † * *# *# *# Minimal * * * * * * * * * * *

Management for perioperative bleeding risk and DOAC or VKA schedule should incorporate team-based decision-making, especially in high thrombotic risk patients or when undergoing procedures with higher risks of adverse outcome, should bleeding occur (eg, neuraxial anesthesia). Minimal bleeding risk = 30-day risk of major bleeding 0% (eg, cataract surgery, minor dental/dermatological procedures). Low/moderate bleeding risk = 30-day risk of major bleeding <2% (eg, complex dental, gastrointestinal, breast surgery, procedures using large-bore needles). High bleeding risk = 30-day risk of major bleeding ≥2%. *Administer DOAC or VKA. †Withhold DOAC or VKA. ‡While withholding VKA in select very high thrombotic risk patients, preoperative bridging with parenteral heparin once INR is less than desired therapeutic range. #Resuming postoperative LMWH bridge at either full dose or prophylaxis dose until INR is within therapeutic range is a team-based decision that weighs the risks and benefits. CrCl indicates creatinine clearance; DOAC, direct oral anticoagulants; INR, international normalized ratio; LMWH, low-molecular-weight heparin; and VKA, vitamin K antagonist.

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for ≥5 half-lives (Table 13), ≥3 days for factor Xa inhibitors (rivaroxaban, apixaban, edoxaban), and ≥4 days for dabigatran (5-6 days, if creatinine clearance <50 mL/min).30

2 In high thrombotic risk patients who are receiv­

ing VKA (Table 13), bridging with paren­ teral anticoagulation is a common practice; however, data supporting efficacy (ie, prevention of thromboembolism) or safety (ie, bleeding) are not available. A meta-analysis of patients with venous thromboembolism reported the incidence of recurrent thromboembolism to be low, regard­ less of perioperative management strategy or baseline thromboembolic risk, and that bridging increased the incidence of bleeding.8 A systematic review and meta-analysis of NCS perioperative

Table 14.  Thromboembolic Risk for Common Oral Anticoagulant Indications

Risk Category Venous Thromboembolism Atrial Fibrillation Mechanical Valve Other Anticoagulation Indications Low VTE >12 mo CHA2DS2-VASc 1-4 (without prior history of stroke) Bileaflet mechanical AVR without major risk factors for stroke* Moderate VTE ≤3-12 mo

Recurrent VTE CHA2DS2-VASc 5-6 Bileaflet mechanical AVR with major risk factors for stroke* Nonsevere coagulopathy (heterozygous factor V Leiden or prothrombin gene G20210A mutation)

Active cancer

High Recent VTE (<1 mo or <3 mo) CHA2DS2-VASc ≥7 (or 5-6 with recent stroke or TIA)

AF with rheumatic valvular heart disease Mechanical mitral valve

Caged ball or tilting-disk valve Mechanical heart valve in any position with recent stroke or TIA (<3 mo) Recent cardioembolic stroke (<3 mo)†

Active cancer associated with high VTE risk LV thrombus (within past 3 mo) Severe thrombophilia† Antiphospholipid antibodies

Adapted from Douketis et al.15 Copyright 2022 Elsevier, with permission from Elsevier. *Major risk factors for stroke include AF, multiple prior strokes/TIAs (≥3 months), prior perioperative stroke, or prior valve thrombosis. †Deficiency of protein C, protein S, or antithrombin; homozygous factor V Leiden or prothrombin gene G20210A mutation or double heterozygous for each mutation, multiple thrombophilias. AF indicated atrial fibrillation; AVR, aortic valve replacement; CHA2DS2-VASc, congestive heart failure, hypertension, age ≥75 (doubled), diabetes mellitus, prior stroke or transient ischemic attack or thromboembolism (doubled), vascular disease, age 65 to 74 years, sex category; LV, left ventricular; OAC, oral anticoagulant; TIA, transient ischemic attack; and VTE, venous thromboembolism.

Table 15.  Pharmacokinetic Characteristics, Monitoring, and Reversal of Vitamin K Antagonist and Direct Oral Anticoagulants

Warfarin Apixaban Rivaroxaban Edoxaban Dabigatran

Mechanism of action VKORC1 (vitamin Kdependent factors) Factor Xa inhibitor Factor Xa inhibitor Factor Xa inhibitor Factor IIa inhibitor (direct thrombin inhibitor) Bioavailability >95% 50% 100% (66% without food) 62% 3%-7% Time to Cmax 2-6 h 3-4 h 2-4 h 1-2 h 1.25-3 h Plasma half-life (t1/2) 36-48 h 9-14 h 6-9 h (11-13 h in older persons) 10-14 h 12-15 h Duration of action ∼5 d (beyond normalization of INR) 24 h 24 h 24 h 24 h Renal clearance (%) 0 27 33 37-59 85

(partially dialyzable)

Drug interaction CYP p450 3A4, p-glycoprotein CYP 450 3A4/2J2, p-glycoprotein CYP 450 3A4 (<5%), p-glycoprotein p-glycoprotein Altered anticoagulation parameters PT, aPTT, ACT PT, aPTT, ACT PT, aPTT, ACT aPTT, ACT, PT/INR, DTT Monitor for presence of drug effect PT/INR Anti-Xa*

(DOAC) Anti-Xa*

(DOAC) Anti-Xa*

(DOAC) ECT (DOAC)

Antidote/reversal34 Vitamin K, 4F-PCC, FFP 4F-PCC, andexanet alfa 4F-PCC, andexanet alfa 4F-PCC, andexanet alfa 4F-PCC, idarucizumab *Quantitative assessment requires drug-specific calibrators. With no therapeutic levels, use can indicate ongoing drug effect. 4F-PCC indicates 4-factor prothrombin complex concentrate; ACT, activated clotting time; Anti-Xa, assay to measure anticoagulation activity; aPTT, activated partial thromboplastin time; CYP, cytochrome; DOAC, direct oral anticoagulant; DTT, diluted thrombin time; ECT, ecarin clotting time; FFP, fresh frozen plasma; INR, international normalized ratio; and PT, prothrombin.

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bridging in patients with mechanical heart valves (35.8% of patients with mechanical mitral valves) identified 15 studies with 2453 bridging episodes and found that bridging increased overall bleeding, with near significant differences in major bleeding, and without the benefit of lowering thromboem­ bolism; however, both noted the majority of results were based on poor-quality cohorts overall.10 The PERIOP-2 (Postoperative Low Molecular Weight Heparin Bridging Treatment for Patients at High Risk of Arterial Thromboembolism) study enrolled 1471 patients on VKA requiring NCS (79% AF, 14% mechanical heart valve, 7% with both).9 All patients had warfarin held 5 days before NCS and received low-molecular-weight heparin for 3 days preoperatively followed by postoperative random­ ization to placebo or low-molecular-weight heparin at either a prophylactic or full dose based on pro­ cedural bleeding risk. Thromboembolism was simi­ lar across all patient populations, and secondary outcomes of bleeding were increased with post­ operative bridging. Although further RCTs are war­ ranted, available data support limiting the use of bridging to very high thrombotic risk (eg, mechani­ cal mitral valves) patients on VKA, with careful consideration of bleeding risk (eg, HAS-BLED,31 previous personal bleeding history, and periopera­ tive bleeding risk) to determine an individualized strategy. 3.	 The BRIDGE trial enrolled 1844 patients with AF

on VKA and randomized them to low-molecularweight heparin bridge therapy or placebo starting 3 days preoperatively and continued 5 days postop­ eratively. All patients had warfarin held from preop­ erative day 5 through postoperative day 1. Bridging anticoagulation was noninferior to placebo for prevention of thromboembolism, but bridging increased the risk of major bleeding.11 Subsequent analysis showed bridge therapy, along with history of renal disease and procedures with high bleeding risk, to be a baseline predictor of major bleeding.32 The pharmacokinetic properties of DOAC therapy allow for a more rapid onset and offset of anti­ coagulant effects and thus shorter perioperative interruptions. A simple DOAC interruption strategy without heparin bridging results in minimal time off DOAC, low bleeding, and low thromboembolic risk in patients with AF.7 Data from phase 3 AF studies support these findings. Some patients who required procedures in these studies (approximately 11% of DOAC-treated patients) received unfractionated heparin or low- molecular-weight heparin bridging, which resulted in increased risk of bleeding with­ out reduction in thromboembolic risk.18–20 Based on these studies, most patients with AF will not benefit from bridging anticoagulation. 4 When restarting VKA after interruption, it can take

several days to achieve full anticoagulant effect. Therefore, once hemostasis is achieved after a low or moderate bleeding risk procedure, it is rea­ sonable to restart VKA as early as 12 to 24 hours postoperatively. It is suggested to resume VKA at the previous therapeutic dose, bearing in mind that additional monitoring may be required because concomitant medications (eg, antibiotics, nonste­ roidal anti-inflammatory drugs, acetaminophen), nutrition, and drug clearance may be altered during the perioperative period. After initiation of DOAC, in most patients, peak levels and a therapeutic anti­ coagulation effect are achieved in ∼2 to 3 hours. Therefore, DOACs should be resumed when full anticoagulation is clinically appropriate, which may be as early as 6 hours postoperatively if hemosta­ sis has occurred. In the PAUSE trial, DOACs were resumed 48 to 72 hours after high bleeding risk procedures, with overall low bleeding and throm­ botic events.7,33

7.7 Perioperative Beta Blockers

Recommendations for Perioperative Beta Blockers Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 B-NR 1 In patients on stable doses of beta blockers under­

going NCS, beta blockers should be continued through the perioperative period as appropriate based on the clinical circumstances.1,2

2b B-NR 2 In patients scheduled for elective NCS who have a

new indication for beta blockade, beta blockers may be initiated far enough before surgery (optimally >7 days) to permit assessments of tolerability and drug titration if needed.3

3: Harm B-R 3 In patients undergoing NCS and with no immediate

need for beta blockers, beta blockers should not be initiated on the day of surgery due to increased risk for postoperative mortality.4

Synopsis Initial optimism regarding the efficacy of perioperative beta blockers on ischemia and subsequent major car­ diac events was significantly tempered by large RCTs, suggesting that their moderate benefit of reducing isch­ emic cardiac events and atrial arrhythmias was offset by harm (eg, stroke) and was associated with increased all-cause mortality. As a result, the practice of periop­ erative beta blockers to reduce perioperative risk is not advised.3,5 There are no large RCTs of adequate size or power to determine the optimal timing of beta-blocker initiation in the perioperative period, an approach to dose titration pre- or postoperatively, whether specific patient subgroups benefit (eg, based on RCRI), or whether sur­ gery alone is an indication for beta-blockade outside of

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acceptable indications (eg, HF, history of CAD). Absent this evidence, an optimal strategy should restrict the use of beta blockers in patients with clear long-term or acute indications, initiating beta blockers at least 1 week before surgery, managing chronic beta blockers as ap­ propriate to patients’ perioperative hemodynamics, and ensuring they are continued at discharge.

Recommendation-Specific Supportive Text

1 Early studies of beta-blockade suggesting benefit

may have produced their results by withdrawing beta blockers in patients who had been on them long term.6 Acutely discontinuing beta blockers for long-term indications is harmful1,2,7 and should be avoided. Clinical judgment should be used to titrate beta blockers as appropriate during the periopera­ tive period, with a focus on ensuring the medica­ tion is continued through the hospital stay and at discharge unless clear contraindications arise. 2.	 Results from POISE indicate that initiating beta blockers on the day of surgery is harmful, particu­ larly if the medication is started at higher doses.8 Contemporaneous studies focused on initiating beta-blockade weeks in advance and titrated to physiological effect showed clinical benefit, but these results have since been called into question.9 A large observational study of beta-blocker initia­ tion before NCS suggested higher risks of death if beta blockers were initiated <7 days before sur­ gery3 compared with patients who initiated beta blockers >31 days earlier. Patients who initiated beta blockers between 8 and 30 days did not have excess mortality, nor did they show any periopera­ tive benefits. Thus, if a patient requires initiation of beta blockers before surgery, the medication should be initiated ≥7 days before the surgery. 3.	 Initial evidence for perioperative beta blockers was

derived from several relatively underpowered RCTs and a large observational study suggesting ben­ efit from perioperative beta blockers. These were followed by the large multicenter POISE study,8 which demonstrated mixed benefits (eg, moderate reduction in MACE) balanced by harms (eg, hypo­ tension, stroke, with a net increase in all-cause mortality) when high-dose beta blockers were administered to beta blocker–naïve patients imme­ diately before surgery and maintained throughout the perioperative period.9,10 Similar to the system­ atic review for the “2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery,”11 this guideline excludes a group of peri­ operative beta-blocker trials from consideration because of concern for unreliable data leading to spurious results. Evidence from 3 meta-analyses was concordant regarding potential harms of perioperative beta-blocker administration; how­ ever, the results of each of these studies were heavily influenced by the large POISE-1 sample size.4,11,12 Although large observational studies have suggested higher potential benefit of betablockade in patients at increased risk as defined by the RCRI, these results have not been repli­ cated in clinical trials.13,14

7.8 Perioperative Management of Blood

Glucose Recommendations for Perioperative Management of Blood Glucose Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2a B-NR 1 In patients with or at risk for diabetes who are

scheduled for elective NCS, preoperative hemoglobin A1c (HbA1C) testing is reasonable if it has not been performed in ≤3 months.1–4

1 C-LD 2 In patients scheduled for NCS, SGLT2i should be

discontinued 3 to 4 days* days before surgery to reduce the risk of perioperative metabolic acidosis.5–7

2a C-LD 3 In patients with diabetes or impaired glucose toler­

ance, continuation of metformin during the periop­ erative period is reasonable to maintain glycemic control.8–12

*Canagliflozin, dapagliflozin, and empagliflozin should be stopped ≥3 days and ertugliflozin ≥4 days before scheduled surgery.13

Synopsis In the United States, 34.1 million adults have diabetes, representing 13% of the population.14,15 Additionally, undiagnosed diabetes is present in 7.3 million adults, or 2.8% of the population.14 It is estimated that up to 20% of general surgery patients have diabetes, and 23% to 60% have prediabetes or undiagnosed diabetes.5 Patients with diabetes have an increased prevalence of ASCVD, including CAD, CKD, and HF. Diabetes confers increased risks of perioperative cardiovascular events and surgical site infections. The finely regulated bal­ ance between hepatic glucose production and glucose utilization in peripheral tissue is altered by the stress of anesthesia and surgery, thereby affecting regulatory hormones and inflammatory cytokines.15,16 Thus, man­ agement of perioperative hyperglycemia is imperative; however, the optimal blood glucose targets for intraop­ erative glycemic control are not well-defined.17 Emerging data suggest that glucagon-like polypeptide-1 (GLP-1) agonists, increasingly used for the management of diabetes, can cause clinically sig­ nificant gastroparesis and delayed gastric emptying.18 A recent consensus statement from the ASA recommends that weekly formulations of GLP-1 agonists be held >1 week before elective NCS for weekly dosed GLP-1 ago­ nists and the day before for daily dosed GLP-1 agonists to reduce the risk of pulmonary aspiration of gastric con­ tents at the time of surgery.

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Recommendation-Specific Supportive Text

1 If not obtained within 3 months of NCS, it is rea­

sonable to check the preoperative hemoglobin A1c before surgery.5,15,19 Multiple studies have assessed hemoglobin A1c and surgical outcomes, but it remains controversial whether elevated levels are linked to poor postoperative outcomes or are just a marker of poor perioperative glucose control.1–4 At this time, there is no evidence that deferring sur­ gery to achieve better glycemic control improves cardiovascular outcomes. Although there are no validated hemoglobin A1c risk thresholds, it may be reasonable to postpone an elective surgery if hemoglobin A1c is higher than 8%.1 Emergent or time-sensitive procedures should not be delayed to achieve a target hemoglobin A1c; instead, the focus should be on optimizing perioperative glucose con­ trol. A retrospective study of preoperative blood glucose levels in patients undergoing noncardiac and nonvascular surgery found glucose concentra­ tions ≥200 mg/dL to be associated with a >2-fold higher all-cause mortality rate and a >4-fold car­ diovascular mortality rate compared with patients with normal blood glucose levels.20 This study also demonstrated that preoperative patients undergo­ ing treatment for diabetes had lower all-cause and cardiovascular mortality.20,21

2 SGLT2i, noninsulin glucose–lowering agents that

facilitate glycemic control by inhibiting renal glu­ cose reabsorption and thus promoting glycosuria, must be discontinued 3 to 4 days before surgery.5 A rare complication of these agents is euglycemic diabetic ketoacidosis, which is a serious postopera­ tive complication defined as normoglycemia (blood glucose <250 mg/dL) in the presence of meta­ bolic acidosis (pH <7.3), total decreased serum bicarbonate (<18 mEq/L), and elevated serum and urine ketones.5–7,22 There are no clear guidelines regarding restarting SGLT2i after surgery. Ideally, they should not be recommended until the patient is clinically stable and has resumed a normal diet. 3.	 Prior recommendations to discontinue metformin

in the perioperative period stemmed from the con­ cern that lactic acidosis could be precipitated in the setting of physical stressors; however, more recent data suggest that metformin is not associated with lactic acidosis. A population-based cohort of >10 600 patients with type 2 diabetes identified 163 patients who had been hospitalized with lac­ tic acidosis. When compared with sex- and agematched controls, current use of metformin was not associated with a risk of lactic acidosis.9 There have been several studies demonstrat­

ing cardiovascular risk reduction in nonopera­ tive patients taking metformin.8,10–12 The UKPDS (United Kingdom Prospective Diabetes Study) showed that, in addition to lowering blood glu­ cose, metformin reduced cardiovascular mortality in patients with obesity and type 2 diabetes. The prespecified subgroup analysis showed risk reduc­ tions of 32% for any diabetes-related endpoint, 42% for diabetes-related death, and 36% for all-cause mortality.23 These findings were further supported by a 10-year follow-up that showed sig­ nificant risk reduction persisted in the metformin group for any diabetes-related endpoint (21%), MI (33%), and death from any cause (27%).24

8 ANESTHETIC CONSIDERATIONS AND

INTRAOPERATIVE MANAGEMENT

8.1 Choice of Anesthetic Technique and Agent

Recommendations for Choice of Anesthetic Technique and Agent Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2a A 1 In patients undergoing NCS, use of a volatile-based

anesthetic agent or total intravenous anesthesia is reasonable for general anesthesia with no apparent difference in associated cardiovascular events (eg, MI, ischemia).1–3

2a B-R 2 In patients undergoing NCS where neuraxial is

feasible, either neuraxial or general anesthesia is reasonable with no apparent difference in associated cardiovascular events.4–6

Synopsis Broadly, there are 4 major classes of anesthesia: local anesthesia, regional anesthesia (eg, neuraxial blockade and peripheral nerve block), monitored anesthesia care (sedation with or without local anesthesia), and general anesthesia (either volatile or intravenous anesthesia). A combination of anesthetic class agents is frequently used. Neuraxial anesthesia can be performed as a pri­ mary anesthetic technique alone or with sedation or as a supplement to general anesthesia. An evaluation of risk factors (other than cardiac), including type and duration of surgical procedure, comorbidities, patient preference, and coagulation status, is crucial for determining the risk versus the benefits of each type of anesthetic technique. The concentration of oxygen administered has also been studied in the perioperative period. Several studies investigated the impact of 30% versus 80% of fraction of inspired oxygen on myocardial injury and infarc­ tion during surgery. Two separate RCTs independently reported that oxygen concentration was not associ­ ated with increased risk of myocardial injury within 3 days or postoperative release of NT-proBNP.7,8 These results confirm those of a previously published retro­ spective analysis including 1617 surgical patients that

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demonstrated no association between increased oxygen concentration and incidence of myocardial injury, cardiac arrest, and 30-day mortality.9

Recommendation-Specific Supportive Text

1 Over the past few decades, several studies have

indicated a possible myocardial protective benefit of volatile anesthetic agents over total intravenous anesthesia, most commonly propofol, in surgical patients undergoing cardiac surgery. In 2009, a meta-analysis including >6000 surgical patients undergoing NCS failed to demonstrate a differ­ ence in rates of MI among patients who received anesthesia with sevoflurane or propofol.10 Several subsequent studies, including 4 RCTs, failed to identify any significant advantage to inhaled versus intravenous anesthesia.1–13,11 In 2011, 88 patients were randomized to sevoflurane versus propofol, with no difference in detectable cardiac troponin I elevation or in median peak release of cardiac troponin I.11 In 2012, 385 surgical patients at car­ diovascular risk undergoing major NCS were ran­ domized to sevoflurane or propofol.2 The incidence of myocardial ischemia, postoperative release of NT-proBNP, MACE, or delirium was not decreased with the use of sevoflurane. In 2013, 193 surgi­ cal patients scheduled for elective abdominal aortic surgery were randomized to either sevoflurane or propofol/remifentanil.1 Again, sevoflurane did not decrease postoperative release of cardiac troponin T, postoperative complications, nonfatal coronary events, or mortality when compared with propofol and remifentanil. In 2017, another trial randomized 120 older patients with established CAD to sevo­ flurane versus propofol/remifentanil, with no differ­ ence observed in release of cardiac troponin T or BNP 8 or 24 hours after surgery.3

2 A large nationwide retrospective cohort study in

Denmark was performed in surgical patients undergoing first-time open inguinal and infrain­ guinal arterial reconstruction procedures.4 A sig­ nificant benefit in terms of reduction of mortality and cardiac morbidity (MI, HF, dysrhythmias) was observed with regional anesthesia (includ­ ing neuraxial and peripheral anesthesia) when compared with patients under general anesthe­ sia.4 In contrast, another retrospective analysis examined a large dataset of patients undergoing above knee amputation.6 After propensity match­ ing, there was no observed difference in either 30-day mortality or any secondary outcomes, including cardiac complications.6 In a recent ran­ domized trial of 1600 surgical patients receiv­ ing spinal or general anesthesia for surgical management of hip fracture,5 no difference was reported between groups in primary outcome, a composite of death, or an inability to walk 10 feet independently or with a walker or cane approxi­ mately 60 days after surgery. Other outcomes were examined, including MI, nonfatal cardiac arrest, and stroke, but no significant difference between groups was detected.5 These results are in accordance with a previous meta-analysis in patients after hip fracture that reported no 30-day mortality benefit.12 Evidence related to neuraxial anesthesia for postoperative pain con­ trol is discussed in Section 8.2 (“Perioperative Pain Management”).

8.2 Perioperative Pain Management

Recommendations for Perioperative Pain Management Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2a B-R 1.	 For patients undergoing major abdominal surgery,

the use of epidural analgesia for postoperative pain relief is reasonable to decrease the incidence of perioperative cardiac events.1,2

2b B-R 2 For patients with a hip fracture waiting for surgi­

cal repair, epidural analgesia may be considered to decrease the incidence of preoperative cardiac events.3

Synopsis Pain is a common experience after surgery, and physi­ ological manifestations, such as tachyarrhythmias and hypertension, can have serious consequences in pa­ tients with preexisting cardiac disease. In patients with CAD, increased myocardial oxygen demand from sym­ pathetic effects of acute pain could lead to the develop­ ment of type 2 MI (supply-demand imbalance without acute atherothrombotic plaque disruption).4 Intravenous or regional administration of analgesics are the main­ stay of pain control in the postoperative period. Epidural analgesia and catheter-based regional anesthetics al­ low for medication administration for acute pain relief up to several days after surgery. Thoracic epidural an­ algesia (TEA) is preferred for most abdominal incisions, while lumbar epidural analgesia is commonly used for hip fractures and lower extremity orthopedic injuries. The benefits of TEA for the prevention of postoperative MI after abdominal surgery have been demonstrated.1,2 Enhanced recovery after NCS protocols are increasingly using TEA as part of a multimodal pain management strategy to reduce both intravenous and oral administra­ tion of opioid-based analgesics.5 The use of gabapentin or pregabalin as adjunct medications has been less suc­ cessful in promoting an opioid-sparing technique, with adverse effects that include visual disturbances, dizzi­ ness, respiratory depression,6,7 and postoperative de­ lirium in patients ≥65 years of age.8

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Recommendation-Specific Supportive Text

1 TEA remains a cornerstone for anesthetic tech­

nique in major abdominal surgery to treat pain in the perioperative period. An updated 2016 Cochrane review in patients undergoing abdominal aortic surgery concluded there was a decreased incidence of MI associated with epi­ dural analgesia compared with intravenous sys­ temic opioid-based pain management.1 A recent RCT of patients undergoing abdominal surgery (gastrectomy, Whipple, distal esophagectomy) comparing TEA (n=60) with intravenous analge­ sia (n=60) demonstrated a lower rate of postop­ erative myocardial injury (8.33% versus 36.67%) and supraventricular tachyarrhythmia (11.66% versus 36.67%) in the TEA cohort.2 A large, ret­ rospective NSQIP database analysis of >8000 patients demonstrated the benefit of epidural analgesia compared with intravenous analgesia in open abdominal surgery for preventing cardio­ pulmonary complications (OR, 0.58). However, there is a lack of high-quality evidence from RCTs comparing TEA with intravenous analgesia within enhanced recovery after NCS protocols, making it difficult to assess primarily for perioperative MI and other MACE after major abdominal surgery. 2.	 In patients with hip fractures, lumbar epidural

analgesia for pain control appears to decrease the incidence of perioperative MACE. A sys­ tematic review and meta-analysis from 2022 that included 4 RCTs published between 2000 and 2014 (n=221 patients) supported the use of epidural analgesia for the prevention of peri­ operative MACE (to include combined events of cardiac death, MI, unstable angina, HF, or newonset AF).3

8.3 Intraoperative Monitoring Techniques

8.3.1 Echocardiography

Recommendations for Echocardiography Referenced studies that support the recommendations are summarized in the Online Data Supplement.

2a C-LD 1 In patients with unexplained hemodynamic instability

undergoing NCS, the emergency use of periopera­ tive TEE or FoCUS is reasonable to determine the cause if expertise is readily available.1–4

3: No benefit C-LD 2 In patients undergoing NCS without risk factors or

procedural risks for significant hemodynamic com­ promise, the routine use of intraoperative TEE is not recommended to screen for cardiac abnormalities or to monitor for myocardial ischemia.5–8

Synopsis Echocardiography has the capacity to assess biven­ tricular and valvular function, intracardiac structures, the pericardial space, and the thoracic aorta.9–11 Different echocardiographic modalities (eg, TTE, TEE) are used during NCS, mostly as diagnostic tools in the setting of persistent, unexplained hemodynamic instability that oc­ curs more frequently in the intraoperative or postopera­ tive period.1,2,11–13 However, TEE has been increasingly used as an intraoperative monitoring tool in patients with high-risk factors or undergoing high-risk noncardiac pro­ cedures.7,8,14–17 In addition, TEE is widely used in cardiac surgery and lung transplantation.8 Although TEE is a low-risk procedure overall, complications may still occur; therefore, the benefits and risks must be considered.18,19 FoCUS using TTE is an evolving field in perioperative medicine3,4,12,13,20,21 that comprises limited, standard car­ diac views and is used to coarsely identify pathology in the setting of hemodynamic instability. If additional echocardiographic information is needed to rule out a cardiac-related cause, a comprehensive examination should be performed.20,21 The choice of the echocardio­ graphic modality used depends on the circumstances, the availability of equipment and expertise, and the indi­ cation for the examination (eg, the left atrial appendage and the thoracic aorta are better evaluated with TEE).

Recommendation-Specific Supportive Text

1 The emergency use of perioperative TEE to deter­

mine the cause of unexplained, severe hemody­ namic instability that persists despite attempted corrective therapy is appropriate where avail­ able.1,2,11,16,22 Clinical practice guidelines for the appropriate use of TEE have been developed by the American Society of Anesthesiologists, the Society of Cardiovascular Anesthesiologists, and the American Society of Echocardiography.10,11,22 A systematic review showed that intraoperative FoCUS with TTE may be a useful, noninvasive tool to diagnose the cause of unexplained hypoten­ sion and to guide treatment.3 The evidence was of low quality, most likely reflecting the challenges in designing high-quality studies such as RCTs involv­ ing situations of unpredictable hemodynamic insta­ bility.4 Recommendations suggest appropriately trained practitioners perform the TEE or FoCUS examinations.10–13,22

2 Limited evaluation data exist on the effective­

ness of routine use of intraoperative TEE during noncardiac procedures, in screening for regional myocardial function and its association with peri­ operative cardiovascular outcomes.5,6 In addition, the data to recommend routine TEE monitoring are insufficient in terms of predictive accuracy, costeffectiveness, or safety. However, TEE is used routinely as a monitoring tool in cardiac and lung transplantation cases and is also more commonly used in other procedures with high risk for hemo­ dynamic instability.7,8

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8.3.2 Body Temperature

Recommendation for Body Temperature Referenced studies that support the recommendation are summarized in the Online Data Supplement. COR LOE Recommendation

2a B-R 1 In patients with CVD undergoing NCS, maintenance

of normothermia is reasonable to avoid perioperative complications overall.1–5

Synopsis Hypothermia has been associated with several periop­ erative complications, including wound infection, MACE, immune dysfunction, coagulopathy, increased blood loss, death, and transfusion requirements.1,6–14 Emerg­ ing literature suggests that mild intraoperative hypo­ thermia (35.5°C)2 is not correlated with postoperative cardiac events.1,2 Likewise, mild intraoperative hypother­ mia (>35.5°C) in nonobese patients with preserved re­ nal function is not correlated with postoperative cardiac events.2 Hypothermia has been reported to be proar­ rhythmogenic by increasing sympathetic nervous system activity. Hypothermia can also induce shivering, which can lead to perioperative cardiac injury due to an imbal­ ance of oxygen supply and demand.6,15–17

Recommendation-Specific Supportive Text

1 A multicenter trial in 2010 that randomized 1000

patients with subarachnoid hemorrhage to either normothermia (36.7°C±0.5°C) or hypothermia (33.3°C±0.8°C) demonstrated no increased inci­ dence of perioperative cardiovascular events in the hypothermia group.3 In a prospective study of 8841 patients undergoing orthopedic surgery, a body temperature of ≥36°C was associated with signifi­ cantly lower risks for cardiac or cerebral events, or both, in the arthroplasty subgroup but not in the general orthopedic surgery cohort.4 In 2022, a mul­ ticenter, superiority trial randomized 5056 patients to be warmed to a core temperature of 37°C or to receive routine management to a temperature of 35.5°C. The incidence in 30-day composite of major cardiovascular outcomes did not significantly differ between the 2 groups.2

8.3.3 Temporary Mechanical Circulatory Support

Recommendation for Temporary Mechanical Circulatory Support COR LOE Recommendation

2b C-LD 1 In patients with acute, severe hemodynamic instabil­

ity and cardiopulmonary dysfunction undergoing urgent or emergency NCS, temporary MCS devices may be used preemptively or as rescue therapy.1–5

Synopsis Temporary MCS devices may be used to help main­ tain adequate organ perfusion during procedures that would otherwise be hemodynamically challenging.3,5,6 Another use of temporary MCS is to allow time for diagnostic evaluation, treatment, and patient participa­ tion in the management decision-making process.6,7 Currently, no high-quality evidence exists to support the routine use of MCS in patients at risk for cardio­ genic shock undergoing NCS. The emergency use of MCS has increased in recent years,1–4 calling renewed attention to this rare and challenging perioperative clinical scenario.8,9

Recommendation-Specific Supportive Text

1 Case reports have described the prophylactic

use of temporary MCS devices in high-risk car­ diac patients before urgent NCS, the intention being to show the benefit of using these devices to hemodynamically support patients when their cardiac condition could not be corrected before surgery.10–15 A retrospective study showed no increase in mortality in patients requiring the use of temporary MCS before heart transplanta­ tion compared with patients who did not require temporary MCS.16 Emergency use of temporary MCS devices, including intra-aortic balloon pump counterpulsation, extracorporeal membrane oxy­ genation, and percutaneous ventricular assist devices, has been described as a rescue treat­ ment for unexpected cardiogenic shock when pharmacological treatment fails.4,8,9,17–19 This allows time for diagnosis and treatment or recov­ ery while also providing hemodynamic support.6 Several series have reported outcomes in patients with MCS undergoing noncardiac procedures.20–26 A multidisciplinary approach that includes expert guidance on anticoagulation strategies, MCS man­ agement, hemodynamic monitoring, and infection prevention strategies is essential to the periop­ erative management of these patients. Specific recommendations are addressed in the American Association for Thoracic Surgery/International Society for Heart and Lung Transplantation clini­ cal practice guidelines for MCS.22,26

8.3.4 Pulmonary Artery Catheters

Recommendations for Pulmonary Artery Catheters Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2b C-LD 1 In patients with CVD undergoing NCS, the use of

PA catheterization may be considered when under­ lying medical conditions that significantly affect hemodynamics (eg, decompensated HF, severe valvular disease, combined shock states, PH) cannot be corrected before surgery.1,2

3: No benefit A 2 In patients with CVD undergoing NCS, routine use

of PA catheterization is not recommended to reduce morbidity or mortality.3

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Synopsis The theoretical basis for better outcomes with the routine use of PA catheterization in NCS is derived from an im­ proved understanding of perioperative hemodynamics by clinicians.4 However, there are no large RCTs proving its use improves patient outcomes,3,4 and pulmonary cath­ eter placement is an invasive and costly procedure. Some have argued that the PA catheter is a monitoring device and, thus, patient outcomes should be based on the ap­ propriate interpretation of the data provided as well as the therapeutic protocols implemented.5 Despite a decline in its use over the past years, PA catheterization remains the preferred method for monitoring hemodynamically unstable patients. In severely injured trauma patients with severe shock, advanced age, or acute HF, PA catheteriza­ tion was associated with a survival benefit.1,2

Recommendation-Specific Supportive Text

1 A retrospective data analysis of 53 312 patients

admitted to intensive care units found that severely injured patients in shock, with advanced age, or with acute HF benefited from PA-guided management.1 Another prospective, observational multicenter cohort study reported that appropriate use of PA catheters decreased mortality in patients in acute HF, especially in hypotensive patients or those receiving inotropes.1

2 Clinical trial data regarding the benefit of routine

use of PA catheterization in NCS are sparse. One trial randomly allocated patients at high surgical risk, defined by an ASA risk score of III or IV, to medical management with or without the use of PA cathe­ ters.6 There were no differences found in mortality or morbidity, except for an increase in pulmonary embo­ lism noted in the pulmonary artery catheter arm.6 In 2013, a systematic review and meta-analysis of 5 studies (n=2395) concluded the preoperative opti­ mization and hemodynamic management guided by a PA catheter did not alter patient perioperative outcomes when compared with central venous pres­ sure catherization.3 The types of surgeries included vascular,7,8 abdominal, thoracic, orthopedic,6 abdomi­ nal reconstructive surgeries,9 as well as high-risk surgical patients.10 Similar results were reported in an additional study involving patients undergoing aortic reconstruction surgery.11

8.4 Perioperative Anemia Management

Recommendations for Perioperative Anemia Management Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

2a A 1.	 In patients having NCS with expected blood loss,

tranexamic acid is reasonable to reduce intraoperative blood loss, reduce transfusions, and avoid anemia.1–3 2a B-R 2 In patients with iron deficiency anemia having elec­

tive NCS, iron therapy (either oral or intravenous) administered preoperatively is reasonable to reduce blood transfusions and to increase hemoglobin.4–18

Synopsis Even mild preoperative anemia is an independent risk factor for postoperative morbidity and mortality, including respiratory, urinary, wound, septic, and thromboembolic complications.10,19–22 Patients with CKD, diabetes, CVD, and HF have a high prevalence of anemia.23–26 Limited tis­ sue oxygen delivery is a common mechanism of adverse outcomes in patients with anemia.27 Anemia may contrib­ ute to myocardial ischemia, particularly in patients with CAD.20 Postoperative hemoglobin is associated with myo­ cardial injury, type 2 MI, and mortality.20,28 The World Health Organization defines anemia as a hemoglobin concentra­ tion <13 g/dL in men and <12 g/dL in women. Up to 64% of surgical patients have anemia,19,29 more than half of which is moderate to severe.30 Iron deficiency is respon­ sible in 40% to 50% of cases.15,29–31 A ferritin concen­ tration <100 ng/mL, transferrin saturation <20%, and/or microcytic hypochromic red cells (mean corpuscular vol­ ume <80 fL, mean corpuscular hemoglobin concentration <27 g/dL) are indicative of iron deficiency. A screening system in which anemia automatically triggers evaluation for iron deficiency using previously collected blood identi­ fies iron-deficiency anemia far better than clinicians using normal procedures.31 Most anemias are correctable within 2 to 4 weeks. Anemia management programs decrease the rate of transfusions, complications, and mortality.9

Recommendation-Specific Supportive Text

1 Bleeding is associated with mortality.32 Preoperative

and intraoperative anemia is associated with stroke, MI, and acute kidney injury that is proportional to the lowest preoperative and intraoperative hemoglobin concentration.10,33,34 Higher rates of pulmonary, sep­ tic, wound, thromboembolic complications, as well as acute kidney injury, longer length of stay, and infections are associated with receiving a transfu­ sion compared with not receiving a transfusion.7,35–38 Intraoperative transfusions are associated with an increased risk of death.36,37,39 A restrictive transfu­ sion threshold of 8 g/dL for orthopedic surgery patients and those with CVD is recommended by the Association for the Advancement of Blood & Biotherapies. A transfusion threshold of 7 g/dL is likely comparable to 8 g/dL, but evidence is lack­ ing.7 A meta-analysis of patients with ACS found no differences in mortality, MACE, recurrent ACS, HF at 30 days, or reductions in transfusions and costs using transfusion thresholds of hemoglobin

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≤8 g/dL compared with ≤10 g/dL.22 Tranexamic acid is an orally, intravenously, or topically admin­ istered synthetic lysine antifibrinolytic analog that impedes the binding of plasminogen to fibrin, thus safely decreasing intraoperative bleeding.1–3 Even in high-risk patients undergoing lower extremity arthroplasty with a history of venous thromboem­ bolism, MI, seizures, ischemic stroke, transient isch­ emic attack, renal disease, and AF, tranexamic acid was associated with fewer transfusions and was not associated with venous thromboembolism, MI, seizures, strokes, or transient ischemic attack.2

2 Iron supplementation is underused in the preopera­

tive period.30 The use of intravenous iron in patients with iron deficiency is safe and efficacious to reverse anemia.8,12,14,30,40,41 Oral iron therapy is minimally effective if administered only 1 to 2 weeks preopera­ tively and therefore is not adequate for rapid preop­ erative treatment of iron deficiency anemia due to its low bioavailability, lack of tolerance, and long duration of treatment. Intravenous iron, even in a single dose, is more effective than oral iron to increase hemoglo­ bin concentrations and iron stores and reduce trans­ fusion and readmission rates.4,11,12,16–18,40 With an anemia management approach for patients under­ going NCS, the number-needed-to-treat to prevent 1 complication is only 6 and to prevent 1 complicationrelated death is 25.6 Postoperative intravenous iron to treat iron deficiency anemia improves hemoglobin and reduces postoperative transfusions, infections, and length of stay.5,14,16 Ferric carboxymaltose, ferric derisomaltose, and ferumoxytol consist of iron sur­ rounded by a carbohydrate shell, which allows for a slower release of the iron, and higher doses can be administered in a single infusion. Iron sucrose is less stable and is administered in lower doses, with a maximum dose of 200 to 300 mg per infusion.

9 PERIOPERATIVE SURVEILLANCE AND

MANAGEMENT OF MYOCARDIAL INJURY AND INFARCTION

9.1 Myocardial Injury After Noncardiac Surgery

Surveillance and Management Recommendations for Myocardial Injury After Noncardiac Surgery Surveillance and Management Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations MINS Surveillance

2b B-NR 1.	 In patients with known CVD, symptoms of CVD,

or age ≥65 years with cardiovascular risk factors undergoing elevated-risk NCS, it may be reasonable to measure cTn at 24 and 48 hours after surgery to identify myocardial injury.1–4 3: No benefit B-NR 2 In patients undergoing low-risk NCS, routine post­

operative screening with cTn levels is not indicated without signs or symptoms suggestive of myocardial ischemia or MI.5,6

MINS Management

2a B-NR 3 In patients who develop MINS, especially in those

not previously known to have excess cardiovascular risk, outpatient follow-up is reasonable for optimiza­ tion of cardiovascular risk factors.4,7–10

2b C-LD 4 In patients who develop MINS, antithrombotic ther­

apy may be considered to reduce thromboembolic events.4,11

Synopsis Perioperative myocardial injury occurs in approxi­ mately 20% of patients undergoing NCS and spans a spectrum of clinical presentations from asymptomatic myocardial injury to overt postoperative MI, defined by ischemic symptoms or electrocardiographic changes, pathologic Q-waves, or evidence on imaging of a loss of viable myocardium (Figure 6).1,4,12–14 MINS encompasses both type 1 and type 2 MI, including asymptomatic myo­ cardial injury, because surgical patients may be unable to report symptoms due to anesthesia, analgesia, or dis­ tracting pain at the surgical site.4,14 A diagnosis of MINS requires >1 elevated cTn (>99th percentile of the upper reference limit) of presumed ischemic origin (excluding nonischemic etiologies such as pulmonary embolism, stroke, and sepsis) and is associated with adverse shortand long-term outcomes.1,12,14–17 Overall, 30-day mortal­ ity associated with MINS is high (approximately 10%),9 with risks proportional to the peak cTn concentration (17% in the highest quartile versus 1% in the lowest)15 and a 34% population attributable risk of 30-day post­ operative mortality.1,16 Even among the 80% to 90% of patients with MINS without ischemic signs or symptoms, 30-day mortality is substantial.1,4,14 Predictors of MINS include cardiovascular risk factors and disease, kidney disease, and urgent or emergent surgery.9,16,17 Although mechanisms of MINS may be heterogeneous, athero­ sclerotic CAD is the presumed etiology in most cases and medical therapy may be warranted in patients with MINS to mitigate postoperative cardiovascular risks. For additional details, see the AHA scientific statement “Di­ agnosis and Management of Patients With Myocardial Injury After Noncardiac Surgery.”12

Recommendation-Specific Supportive Text

1 Troponin surveillance may be reasonable in patients

with known CVD, cardiovascular risk factors, and in individuals undergoing high-risk surgery to identify patients at elevated risk of postoperative events.14 In a prospective cohort study of 21 842 patients

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Figure 6. Evaluation of an Abnormal Troponin Obtained for Postoperative Surveillance. *Presumes a rise and fall of troponin consistent with acute myocardial injury. Troponin may be measured using a conventional fourth-generation or a high-sensitivity assay. †Nonischemic myocardial injury encompasses pulmonary embolism, sepsis, acute decompensated heart failure, or acute stroke. Colors correspond to Class of Recommendation in Table 3. ECG indicates electrocardiogram/electrocardiographic GDMT, guidelinedirected management and therapy; MI, myocardial infarction; MINS, myocardial injury after noncardiac surgery; NCS, noncardiac surgery; NSTEMI, non–ST-segment-elevation myocardial infarction; STEMI, ST-segment-elevation myocardial infarction; and URL, upper reference limit.

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aged ≥45 years undergoing high-sensitivity tropo­ nin T surveillance after NCS, elevated postoperative cTn without an ischemic feature was independently associated with a 3-fold greater hazard of 30-day mortality, while an elevated postoperative cTn with an ischemic feature was associated with a 5-fold greater hazard of 30-day mortality compared to patients without MINS.1,15 Evaluating elevated-risk patients for MINS with serial troponin is recom­ mended in the Fourth Universal Definition of MI and suggested in a recent AHA scientific state­ ment.12,13,18 To properly interpret elevated post­ operative troponin concentrations, a baseline preoperative value, or serial postoperative mea­ sures, are useful to determine whether myocar­ dial injury is acute or chronic. Based on availability, conventional fourth-generation or high-sensitivity cTn assays may be used for perioperative surveil­ lance. Although surveillance of cTn is effective at identifying patients at >20% risk of cardiac events, the optimal management of patients with MINS remains uncertain and requires further study.19 In elevated-risk patients with established ASCVD who are already receiving maximal GDMT for CAD, it is unclear whether a diagnosis of MINS will change the clinical management. A well-defined manage­ ment strategy is urgently needed to inform effective approaches to postoperative cTn surveillance. 2.	 Data on troponin surveillance after NCS in low-risk populations are limited.5,6 Given the low likelihood of perioperative cardiovascular events, troponin surveillance in asymptomatic individuals undergo­ ing low-risk NCS is unlikely to identify myocardial injury or confer clinical benefit. Therefore, surveil­ lance in low-risk populations should not be rou­ tinely performed. 3.	 Although the optimal management to reduce

adverse cardiovascular events in patients with a diagnosis of MINS is uncertain, the prognostic impact is clear. Elevated postoperative cTn con­ centrations consistently identify surgical patients at increased risk for short- and long-term mortal­ ity. A single-center study of approximately 5000 patients found that patients with MINS who received cardiology consultation or transfer to a cardiology department had lower mortality in the first 30 days.7 Another study identified early refer­ ral for cardiology consultation after a diagnosis of MINS to be associated with a significant reduction in early death.8 Patients should be made aware of the MINS diagnosis during their surgical encoun­ ter. The optimal medical therapy for MINS is uncer­ tain. In a small observational study of patients with MINS, intensification of cardiovascular medical therapy was associated with lower MACE at 1 year.20 Data to support the use of antiplatelets and statins for presumed CAD in patients with MINS are based solely on observational cohorts. A post hoc analysis of the POISE study reported that among patients with perioperative MI, the use of aspirin and statins was associated with reduced 30-day mortality.9 In another observational study (n=5109), postoperative statin use was associated with lower mortality at 1 year.10 A role for statins in MINS may also be extrapolated from trials of nonsurgical patients with CVD and spontaneous MI.21,22 In a prospective study, less than one-third of patients with MINS had intensification of GDMT for CVD.14 Establishing the optimal medical ther­ apy for MINS is an important evidence gap that requires further investigation. 4.	 Postoperative administration of DOACs may

decrease the risk of long-term cardiovascular events. The MANAGE (Management of Myocardial Injury After Noncardiac Surgery) trial, the only RCT evaluating medical therapy for MINS, randomly assigned 1754 postsurgical patients to antico­ agulation with dabigatran 110 mg twice daily ver­ sus placebo within 35 days of MINS. In this trial, dabigatran significantly decreased the composite of major vascular events without increasing major bleeding but was associated with excess minor and gastrointestinal bleeding. Furthermore, nearly one-half of all patients in both arms discontin­ ued the study drug before study termination, and there was a post hoc change in the primary study outcomes due to slow enrollment and a reduced sample size. In a propensity-matched retrospective observational analysis of patients with MINS, anti­ platelet therapy at hospital discharge was asso­ ciated with a reduced risk of 1-year mortality.11 Because increased preoperative expression of platelet- and coagulation-related genes has been identified as a risk factor for subsequent MINS, there is a plausible mechanistic hypothesis for the role played by antithrombotic agents.23 Further investigation is needed to understand the patho­ physiological mechanisms of MINS and to confirm the role of postoperative antithrombotic therapy in these patients.

9.2 Management of Postoperative STEMI/

NSTEMI Recommendations for Management of Postoperative STEMI/NSTEMI Referenced studies that support the recommendations are summarized in the Online Data Supplement. COR LOE Recommendations

1 B-NR 1 Patients who develop STEMI after NCS should be

considered for GDMT, including consideration of ICA, balancing bleeding and thrombotic risks with the severity of the clinical presentation.1–3

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1 C-EO 2 Patients who develop NSTEMI after NCS should

receive medical therapy as recommended for patients with spontaneous MI but after consideration of postoperative bleeding risks and hemodynamic status.

2a C-LD 3 Patients who develop NSTEMI after NCS can be

considered for ICA, balancing bleeding and throm­ botic risks with the severity of clinical presentation.2,3

Synopsis The incidence of perioperative MI ranges widely from 0.9% to 15% depending on the definitions, patient risk factors, and surgical type.2,4–8 Patients presenting with perioperative MI after NCS are more likely to present with type 2 MI due to supply-demand mismatch com­ pared with type 1 MI (eg, acute plaque rupture).1,9,10 Recognition of MI may be difficult in the perioperative period because sedation and analgesia can limit pa­ tients’ symptoms, the ability to report them, or both.11 Patients with perioperative STEMI and NSTEMI have a substantial mortality risk, with nearly one-third of patients either dying or being readmitted at 30 days.4,6,11–16 Risk factors for mortality include the peak cTn concentration, bleeding events, and the presence of peripheral artery disease.13 Ideally, management of perioperative type 1 MI should include medical therapy as recommended for patients with spontaneous MI due to ASCVD. In patients with suspected type 2 MI, management should address the underlying cause of supply-demand mismatch (eg, hypertension, hypotension, tachycardia, anemia). Cardi­ ac troponin elevation may also occur due to nonischemic causes, such as HF, sepsis, or pulmonary embolism. ICA may be indicated when acute coronary occlusion is sus­ pected, after individualized risk stratification that ac­ counts for factors including residual bleeding risk, type of surgery, and time since surgery. See Figure 6 for an algorithm depicting the diagnosis and management of patients with myocardial injury or infarction after NCS.

Recommendation-Specific Supportive Text

1 Perioperative STEMI due to acute plaque rupture

occurs in a minority of patients with perioperative MI but is associated with in-hospital mortality of 30% to 35%.1,2,11 GDMT for patients with periop­ erative STEMI should be promptly initiated, balanc­ ing the postoperative risks, which include bleeding and hypotension. Emergent ICA should be strongly considered, weighing bleeding and thrombotic risks with the severity of the clinical presentation. Patients with perioperative STEMI should have management decisions made in a team-based manner, including the surgeon, anesthesiologist, and cardiologist. 2 Patients with perioperative NSTEMI should receive

GDMT as recommended for nonsurgical patients with spontaneous MI. In some cases, GMDT may need to be tailored based on hemodynamic status and bleeding risks. Medical therapy should include at least 1 antiplatelet, provided the benefits out­ weigh the bleeding risks, and initiation of a highintensity statin. In patients whose hemodynamic status permits, beta blockers, ACEi, and nitrates may be considered for both symptomatic relief from angina and long-term cardiovascular risk reduction. 3.	 ICA may be appropriate in selected perioperative

patients with postoperative NSTEMI. In retrospec­ tive observational analyses, invasive management of MI was associated with lower in-hospital mor­ tality compared with conservative management.2 However, given the potential need for systemic anti­ coagulation and longer-term antiplatelet therapies after PCI, the decision to pursue invasive treatment should be balanced with the risk of residual postop­ erative bleeding, type of surgery, and time since sur­ gery. The severity of clinical presentation, peak cTn concentration, presence of ischemic electrocardio­ graphic changes, and other patient-specific factors should also be considered.3 Individuals with ongo­ ing symptoms not responsive to GDMT, evidence of hemodynamic instability, persistent biomarker elevation, or imaging evidence of new regional wall motion abnormalities or reduced ventricular func­ tion may derive the greatest benefit from urgent ICA in the perioperative period. Decisions to pursue invasive management of MI after NCS should be undertaken in a team-based manner, involving the surgeon, anesthesiologist, and cardiologist.

10 SPECIAL POPULATIONS

10.1 Preoperative Evaluation Before Liver and

Kidney Transplantation Synopsis Patients with end-stage kidney or liver disease have a higher prevalence of cardiovascular risk factors and CAD than the general population1–6 and are at risk for other cardiovascular conditions, such as HF and PH.7 Recent studies suggest that a targeted approach to preoperative screening for CAD before kidney trans­ plantation appears to be associated with similar post­ operative outcomes than with routine preoperative testing for CAD. Data from the US Renal Data System and Medicare claims reported that more frequent inva­ sive or noninvasive CAD testing in the year before kid­ ney transplantation was not associated with lower rates of 30-day posttransplant death or acute MI.8 In the ISCHEMIA-CKD (International Study of Compara­ tive Health Effectiveness With Medical and Invasive

Recommendations for Management of Postoperative STEMI/NSTEMI (Continued) COR LOE Recommendations

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Approaches–Chronic Kidney Disease) trial, which en­ rolled nonsurgical adults with advanced CKD, CCD, and moderate to severe ischemia on stress testing, an initial invasive approach of coronary angiography with revas­ cularization plus medical therapy did not reduce the risk of death or MI versus initial medical therapy alone at a median follow-up of 2.2 years.9 The 2022 AHA scien­ tific statement “Emerging Evidence on Coronary Heart Disease Screening in Kidney and Liver Transplantation Candidates”1 summarizes the contemporary data and de­ fines approaches to screening and management of CAD in candidates for kidney and liver transplantation.

10.2 Obesity and Bariatric Surgery

Synopsis Obesity is a growing global epidemic and affects more than one-third of the US adult population.1–3 Bariatric sur­ gery is the most effective and long-lasting weight loss intervention for patients with body mass index ≥35 kg/ m2, resulting in significant weight loss and the improve­ ment or resolution of obesity-related diseases, including type 2 diabetes, hypertension, and dyslipidemia.4–6 In a population-based retrospective cohort study (n=2638), bariatric surgery was associated with a lower incidence of MACE in patients with CVD and obesity over a me­ dian 4.6-year follow-up.7 Bariatric surgery patients tend to be young and may be selected for lower-risk features; however, bariatric surgery is not without risks. In large meta-analyses, perioperative MI was identified in 0.37% of bariatric surgeries, and the all-cause mortality rate was reported in 0.08%.7–9 In a retrospective, multicenter study (n=494 611) of patients who underwent Roux-en-Y gas­ tric bypass or sleeve gastrectomy,10 prior cardiac history was associated with greater risks of perioperative cardiac arrest and 30-day mortality. In this study, sleeve gastrec­ tomy was associated with fewer adverse events than Roux-en-Y. Another observational study of patients with obesity undergoing bariatric surgery reported that a his­ tory of ACS or HF was associated with increased risks of perioperative cardiovascular complications.11 Thus, care­ ful attention to history and risk factors during preopera­ tive assessments is essential. Patients with obesity are increasingly prescribed GLP-1 receptor agonists to achieve weight loss. Considerations regarding the discontinuation of these drugs before NCS are addressed in Section 7.8 (“Perioperative Management of Blood Glucose”).

11 COST–VALUE CONSIDERATIONS

11.1 Cost–Value Considerations

Health economics seeks to assess the value (eg, cost versus health benefit) associated with use of medical technology. For medical therapies, the relationship be­ tween technology use and value is direct; however, for diagnostic tests, the relationship is indirect and contin­ gent. This is because diagnostic tests produce data that must be used by clinicians to create value.1 The value of a diagnostic test may be substantially affected by varia­ tions in the clinical context of patient and surgical risk levels in which the medical test is performed. In some contexts, clinicians can use the medical test results to improve patient health. Here, value is driven by tradeoffs between the cost of the medical test and the resulting improvements in patient health (ie, cost-effectiveness). In other contexts, a clinician’s knowledge of the test result does not lead to improvements in patient health, and in this instance, value may be created by not performing the test. Last, there are contexts in which administration of the diagnostic test may lead to patient harm (eg, inci­ dental findings leading to additional testing, which may expose patients to additional risk or delays in treatment). These are also contexts in which value may be created by not performing the test. Thus, the key cost–value con­ siderations for diagnostic tests are the cost of the medi­ cal test, the context of administration, and the extent to which clinicians can use the test results to improve pa­ tient health.

11.1.1 Cost–Value Considerations for Biomarkers

B-Type Natriuretic Peptide and N-Terminal Pro B-Type Natriuretic Peptide Preoperative BNP or NT-proBNP levels can be used to evaluate perioperative risk for patients undergoing elevated-risk NCS with known CVD, CVD symptoms, or age ≥65 years with cardiovascular risk factors. However, there have been no studies that evaluated whether this information can be used by clinicians to improve patient outcomes and impact health care costs.1 For this reason, the use of preoperative BNP or NT-proBNP for these patients has uncertain value (ie, relationship between medical cost and health benefit cannot be determined). Similarly, there is no evidence that measuring preopera­ tive BNP or NT-proBNP levels for patients without CVD or cardiovascular risk factors scheduled for low-risk NCS will improve patient outcomes and impact health care costs. Besides the immediate cost savings, eliminating low-value BNP or NT-proBNP testing will eliminate the cascade of subsequent diagnostic testing. Cardiac Troponin Preoperative cTn levels can be used to evaluate periop­ erative risk for patients undergoing elevated-risk NCS with known CVD, CVD symptoms, or age ≥65 years with cardiovascular risk factors. However, there have been no studies that evaluated whether this information can be used by clinicians to improve patient outcomes and im­ pact health care costs. For this reason, the use of preop­ erative cTn testing for patients undergoing elevated-risk NCS has uncertain value (ie, relationship between medi­ cal cost and health benefit cannot be determined).

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11.1.2. Cost–Value Considerations for 12-Lead ECG The 12-lead ECG is an inexpensive diagnostic tool ($14.57 per 2022 Medicare reimbursement), and its use is considered cost-effective if it leads to modest improvements in patient health.1 For patients under­ going elevated-risk NCS with active CVD symptoms or increased risk of MACE, the preoperative ECG is predictive of short-term mortality and MACE.2–6 However, the value of ECGs in these situations is de­ termined by whether it adds incremental risk assess­ ment beyond the history and physical and whether clinicians are able to use electrocardiographic results to improve patient health. Although 1 study of 2967 patients undergoing NCS reported that the ECG did not improve postoperative death and MI predic­ tion beyond risk factor information in the patient his­ tory, no studies have reported whether knowledge of electrocardiographic results in improved physician decision-making or leads to improvements in longterm patient clinical and economic outcomes.4 For these reasons, the use of preoperative ECG for pa­ tients undergoing elevated-risk NCS has uncertain value (ie, relationship between medical cost and health benefit cannot be determined). In contrast, many stud­ ies agree that a routine preoperative ECG in low-risk patients undergoing low-risk NCS has little effect on patient outcomes and its elimination would be costsaving.7–10 Besides the immediate cost savings, a cascade of care is eliminated when a preoperative 12-lead ECG is not performed.11,12 11.1.3. Cost–Value Considerations for Coronary Computed Tomography Angiography Although CCTA offers anatomic information for assess­ ing myocardial ischemia, it has been associated with in­ creased interventional coronary angiography and greater health care costs versus functional stress testing.1 The PROMISE (A Randomized Comparison of Anatomic versus Functional Diagnostic Testing Strategies in Symptomatic Patients with Suspected Coronary Artery Disease) trial evaluated CCTA versus functional test­ ing in symptomatic patients with suspected CAD and reported that CCTA did not improve clinical outcomes versus functional testing over a median of 2 years followup.2 Average diagnostic testing costs were: exercise electrocardiography, $174; CCTA, $404; stress echo­ cardiography: pharmacological, $501, exercise, $514; and nuclear testing: exercise, $946, and stress, $1132.3 At 90 days, average costs were similar (CCTA, $2494 versus functional testing, $2240; difference, $254; 95% CI, −$634, $906), with CCTA resulting in more interventional cardiac procedures. Cumulative 3-year costs were also similar (CCTA, $7213; functional test­ ing, $6586; difference, $627; 95% CI, −$463, $1609). A Markov microsimulation model study using PROM­ ISE trial patient data compared CCTA supplemented with noninvasive functional flow reserve with functional testing and reported that CCTA with functional flow re­ serve was more efficient in ICA selection.4 Over a pa­ tient’s lifetime, CCTA with functional flow reserve versus functional testing provided greater quality-adjusted life years (25.15 versus 24.68; difference, 0.46; 95% CI, 0.44-0.49) and lower costs ($7222 versus $7989; dif­ ference, −$767; 95% CI, −$805 to −$729). Although important insights are provided by the PROMISE data, the study did not enroll patients undergoing evaluation before NCS, and caution must be used when extrapolat­ ing these findings to testing performed before NCS.

11.1.4. Cost–Value Considerations for Stress Testing Although stress echocardiography has greater accura­ cy than electrocardiographic exercise testing (exercise ECG), it also costs more per use.1 An RCT of diagnostic testing modalities in stable patients with suspected an­ gina (not limited to NCS) with similar pretest CAD prob­ abilities reported significant differences in test results. Exercise electrocardiographic results were 55.7% nega­ tive, 7.2% positive, and 37.1% inconclusive, whereas stress echocardiography results were 94.8% negative, 4.7% positive, and 0.5% inconclusive.2 Stress echocar­ diography was associated with fewer clinic and emer­ gency visits, less coronary angiography (6.3% versus 13.4%; P=0.02), lower mean costs (P=0.04), and no difference in the composite of death, MI, unplanned re­ vascularization, and hospitalization for chest pain (3.7% versus 3.2%; P=0.38) at 3 years.3 Patients with good functional capacity and stable symptoms as well as lowrisk patients undergoing low-risk NCS do not benefit from preoperative stress testing.4,5 The PROMISE Mini­ mal Risk Tool has been used to identify low-risk patients for diagnostic test deferral.6,7 Simulated results dem­ onstrate that deferral of diagnostic testing in low-risk patients may be associated with greater patient health benefits and lower costs.7 Cost savings were −$749 (95% CI, –$1647 to −$158) in the PROMISE patients with 10% lowest risk and −$677 (95% CI, −$1333 to –$71) in the patients with 20% lowest risk. Although PROMISE data provide important insights, the study did not enroll patients undergoing evaluation before NCS, and caution must be used when extrapolating these find­ ings to testing performed before NCS.

12 EVIDENCE GAPS AND FUTURE

RESEARCH DIRECTIONS

Since the 2014 guideline was published, there have been numerous advancements in the perioperative man­ agement of patients undergoing NCS. However, a num­ ber of key questions in perioperative medicine remain, and knowledge gaps that should serve as areas of future research are described below.

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Approaches to Perioperative Care Delivery and Assessment of Risk •	 Few multidisciplinary care delivery models have been rigorously studied to assess the impact on perioperative testing (eg, appropriate use of noninvasive stress testing) or cardiovascular outcomes. Specifically, further study is required regarding the use of remote visits/telemedi­ cine for preoperative assessments and for the coordination of specialty care for higher-risk patients. •	 Evidence is lacking to support the use of one peri­ operative risk index over another. Additional data are needed to determine how risk scores may be best used to guide perioperative management and reduce postoperative MACE. Perioperative Management •	 Optimal approaches to BP assessment, thresholds, and measurement frequency most appropriate to guide perioperative care have not been estab­ lished. High-quality RCTs are needed to identify specific perioperative BP thresholds associated with a reduced incidence of adverse cardiovascular outcomes. •	 There are no RCTs evaluating perioperative rate versus rhythm control strategies in patients with new-onset AF undergoing NCS. Additional studies are needed to address the optimal surveillance and management of postoperative AF. •	 There is limited evidence to support coronary revascularization before NCS in stable patients, nor are there RCTs documenting improved outcomes in high-risk patients undergoing revascularization before major NCS. •	 Limited data are available to guide the optimal tim­ ing of NCS after LVAD implantation. •	 In patients with recent stroke, the optimal time delay before elective NCS is uncertain. The excess cardiovascular and cerebrovascular risks imposed by NCS in patients with recent stroke are not well-defined.

Preoperative Evaluation •	 In the absence of indications beyond an isolated preoperative elevation in troponin concentra­ tion, there is no evidence that further testing (eg, stress test or coronary artery catheterization) is beneficial. •	 No studies have reported whether knowledge of electrocardiographic results improve clinician deci­ sion-making or lead to improvements in long-term patient clinical and economic outcomes. •	 Data are lacking to support routine preopera­ tive assessment of LV function (eg, routine use of FoCUS, echocardiography) in stable patients undergoing NCS.

Perioperative Medical Therapy •	 There are limited high-quality data regarding DAPT management for patients who have had elective NCS after balloon angioplasty alone without place­ ment of a stent, after TAVI, or after TEER. •	 The efficacy and safety of shorter durations of DAPT after PCI in patients undergoing NCS requires further study. •	 Large RCTs are needed to elucidate the role of perioperative statin initiation on long-term out­ comes, in lower-risk patients or procedures, and to define the ideal timing, medication, and dosing regimens (eg, reloading). •	 No data currently exist regarding the perioperative role (harm or benefit) of the angiotensin receptor/ neprilysin inhibitor, sacubitril/valsartan. Given the important role of RAASi in preventing MI, stroke, HF, and declines in kidney function, large RCTs are needed to determine preoperative management of RAASi for patients planned for NCS. •	 Large RCTs are needed to evaluate both the risk and benefits of omission, continuation, or initiation of CCBs in the perioperative patient. •	 Perioperative continuation of chronic alpha-2 receptor agonists therapy has not been addressed in RCTs. •	 There are no established data for the use of glyco­ protein IIB/IIIA inhibitors as a bridging strategy in patients undergoing NCS. •	 The optimal approach to beta-blocker initiation in the perioperative period remains unknown, includ­ ing the identification of patient subgroups who may derive the greatest benefit, medication selection, the timing of beta-blocker initiation with respect to surgery, and the safety of preoperative dose titration. •	 Challenges in the perioperative care of patients with diabetes mellitus include assessing markers of glucose control that predict postoperative out­ comes, selection of methods to control periopera­ tive glucose, and the perioperative management of old and new diabetic agents as few studies address optimal perioperative blood glucose levels or timing of reinitiation of SGLT2i after surgery. •	 Further research is needed, but advisories sug­ gest GLP-1 agonists should be held for 1 dose before elective NCS to reduce the risk of pulmo­ nary aspiration of gastric contents at the time of surgery.

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Intraoperative Management •	 Data supporting the effectiveness of routine use of intraoperative TEE during noncardiac procedures is limited. •	 Currently, there is no high-quality evidence to sup­ port the routine use of MCS in patients at risk for cardiogenic shock undergoing NCS. •	 There are no large RCTs demonstrating that PA catheters improve patient outcomes or are cost effective.

Perioperative Surveillance •	 MINS is an underrecognized clinical dilemma requiring further investigation to understand its underlying pathophysiological mechanisms. There are limited data regarding optimal therapy for risk mitigation after the diagnosis of MINS, including the use of antiplatelet agents and statins.

PEER REVIEW COMMITTEE MEMBERS

Jacqueline E. Tamis-Holland, MD, FACC, FAHA, Chair; Marietta Ambrose, MD, MPH, MSEd, FACC; Danielle Blais, PharmD; Jeanna Blitz, MD; Renee Bullock-Palmer, MD, FACC, FAHA; Shea E. Hogan, MD, MSCS, FACC; Michelle M. Kittleson, MD, PhD, FACC, FAHA; Clauden Louis, MD, MPH, MS, FACC; Elizabeth Magnuson, ScD; Kanae Mukai, MD, FACC, FSCMR*; Grant Reed, MD, FACC; Jennifer Rymer, MD, MBA, FACC, FAHA†

AHA/ACC JOINT COMMITTEE ON CLINICAL PRACTICE GUIDELINES

Joshua A. Beckman, MD, MS, FAHA, FACC, Chair; Cath­ erine M. Otto, MD, FACC, FAHA Chair-Elect; Anastasia Armbruster, PharmD, FACC; Leslie L. Davis, PhD, RN, ANP-BC, FACC, FAHA; Lisa de las Fuentes, MD, MS, FAHA‡; Anita Deswal, MD, MPH, FACC, FAHA‡; Victor A. Ferrari, MD, FACC, FAHA, MSCMR; Stephen Fremes, MD, MSc, FACC; Adrian F. Hernandez, MD, MHS, FAHA‡; Hani Jneid, MD, FACC, FAHA; Heather M. Johnson, MD, MS, FACC, FAHA; W. Schuyler Jones, MD, FACC; Sadiya S. Khan, MD, MSc, FACC, FAHA; Prateeti Kha­ zanie, MD, MPH, FAHA; Michelle M. Kittleson, MD, PhD, FACC, FAHA; Venu Menon, MD, FACC, FAHA; Debabrata Mukherjee, MD, FACC, FAHA; Latha Palaniappan, MD, MS, FACC, FAHA‡; Tanveer Rab, MD, FACC‡; Garima Sharma, MD, MBBS, FACC, FAHA; Daichi Shimbo, MD; Jacqueline E. Tamis-Holland, MD, FACC, FAHA‡; Y. Jo­ seph Woo, MD, FACC, FAHA‡; Boback Ziaeian, MD, PhD, FACC, FAHA

PRESIDENTS AND STAFF

American College of Cardiology Cathleen Biga, MSN, FACC, President Cathleen C. Gates, Chief Executive Officer Richard J. Kovacs, MD, MACC, Chief Medical Adviser Mindy J. Saraco, MHA, Director, Clinical Policy and Guidelines Grace D. Ronan, Senior Production and Operations Manager, Clinical Policy Publications Leah Patterson, Associate Project Manager, Clinical

Content American College of Cardiology/American Heart Association Thomas S.D. Getchius, National Senior Director, Guidelines Abdul R. Abdullah, MD, Director, Guideline Science and

Methodology American Heart Association Joseph C. Wu, MD, PhD, FAHA, President Nancy Brown, Chief Executive Officer Mariell Jessup, MD, FAHA, Chief Science and Medical Officer Nicole Aiello Sapio, EdD, Executive Vice President, Office of Science Strategies and Operations Radhika Rajgopal Singh, PhD, Senior Vice President, Office of Science and Medicine Prashant Nedungadi, BPharm, PhD, Vice President, Science and Medicine, Clinical Guidelines Sally S. Wong, PhD, RD, CDN, FAHA, National Senior Director, Science and Medicine Jody Hundley, Senior Production and Operations

Manager, Scientific Publications

ARTICLE INFORMATION This document was approved by the American College of Cardiology Clinical Pol­ icy Approval Committee and the American Heart Association Science Advisory and Coordinating Committee in May 2024, the American College of Cardiology Science and Quality Committee in July 2024, and the American Heart Associa­ tion Executive Committee in August 2024. Supplemental materials are available with this article at https://www. ahajournals.org/doi/suppl/10.1161/CIR.0000000000001285 This article has been copublished in the Journal of the American College of Cardiology. Copies: This document is available on the websites of the American Heart Association (professional.heart.org) and the American College of Cardiology (www. acc.org). A copy of the document is also available at https://professional.heart.org/ statements by selecting the “Guidelines & Statements” button. To purchase addi­ tional reprints, call 215-356-2721 or email Meredith.Edelman@wolterskluwer.com. The expert peer review of AHA-commissioned documents (eg, scien­ tific statements, clinical practice guidelines, systematic reviews) is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit https://professional.heart.org/statements. Select

*Society for Cardiovascular Magnetic Resonance representative. †Society for Vascular Medicine representative. ‡Former AHA/ACC Joint Committee on Clinical Practice Guidelines member; current member during the writing effort.

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the “Guidelines & Statements” drop-down menu near the top of the webpage, then click “Publication Development.” Permissions: Multiple copies, modification, alteration, enhancement, and dis­ tribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at https://www.heart.org/permissions. A link to the “Copyright Permissions Request Form” appears in the second paragraph (https://www.heart.org/en/about-us/ statements-and-policies/copyright-request-form).

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cine for post-discharge surgical care: a systematic review. J Am Coll Surg. 2016;222:915–927. 12.	 Miguela Alvarez SM, Bartra Ylla A, Salvador Carreno J, et al. Telephone con­ sultation service in orthopedics during COVID-19 pandemic. Rev Esp Cir Ortop Traumatol (Engl Ed). 2021;65:167–171. 13.	 Mihalj M, Carrel T, Gregoric ID, et al. Telemedicine for preoperative assess­ ment during a COVID-19 pandemic: recommendations for clinical care. Best Pract Res Clin Anaesthesiol. 2020;34:345–351. 14.	 Asiri A, AlBishi S, AlMadani W, et al. The use of telemedicine in surgical care: a systematic review. Acta Inform Med. 2018;26:201–206. 15.	 Zhang K, Rashid-Kolvear M, Waseem R, et al. Virtual preoperative assess­ ment in surgical patients: a systematic review and meta-analysis. J Clin Anesth. 2021;75:110540. 16.	 Chorath K, Luu N, Go BC, et al. ERAS protocols for thyroid and parathy­ roid surgery: a systematic review and meta-analysis. Otolaryngol Head Neck Surg. 2022;166:425–433. 17.	 Scheib SA, Thomassee M, Kenner JL. Enhanced recovery after sur­ gery in gynecology: a review of the literature. J Minim Invasive Gynecol. 2019;26:327–343. 18.	 Zacharakis D, Diakosavvas M, Prodromidou A, et al. Enhanced recovery pro­ tocols in urogynecologic and pelvic floor reconstructive surgery: a systemat­ ic review and meta-analysis. Urogynecology (Hagerstown). 2023;29:21–32. 19.	 Puccetti F, Wijnhoven BPL, Kuppusamy M, et al. Impact of standardized clin­ ical pathways on esophagectomy: a systematic review and meta-analysis. Dis Esophagus. 2022;35:doab027. 20.	 Cohen R, Gooberman-Hill R. Staff experiences of enhanced recov­ ery after surgery: systematic review of qualitative studies. BMJ Open. 2019;9:e022259. 21.	 Inglis SC, Clark RA, Dierckx R, et al. Structured telephone support or noninvasive telemonitoring for patients with heart failure. Heart. 2017;103:255– 257. 22.	 Armstrong K, Coyte P, Semple J. The effect of mobile app follow-up care on the number of in-person visits following ambulatory surgery: a randomized control trial. Stud Health Technol Inform. 2015;216:894. 23.	 Goode PS, Johnson TM 2nd, Newman DK, et al. Perioperative mobile tele­ health program for post-prostatectomy incontinence: a randomized clinical trial. J Urol. 2022;208:379–387. 24.	 Hansen MM. Impact of complementary therapies via mobile technologies on Icelandic same day surgical patients' reports of anxiety, pain and selfefficacy in healing: a randomized controlled trial in process. Stud Health Technol Inform. 2013;192:1165. 25.	 Higgins J, Chang J, Hoit G, et al. Conventional follow-up versus mobile application home monitoring for postoperative anterior cruciate liga­ ment reconstruction patients: a randomized controlled trial. Arthroscopy. 2020;36:1906–1916. 26.	 Mangieri CW, Johnson RJ, Sweeney LB, et al. Mobile health applications en­ hance weight loss efficacy following bariatric surgery. Obes Res Clin Pract. 2019;13:176–179. 27.	 Park J, Park HJ. Development and validation of evidence-based mo­ bile application for cardiac risk stratification for noncardiac surgery. presented at: Hospital Medicine 2018; April 8-11, 2018; Orlando, FL. Accessed March 15, 2021. https://search.ebscohost.com/login. aspx?direct=true&db=cgh&AN=CN-01995322&site=ehost-live 28.	 Robinson A, Oksuz U, Slight R, et al. Digital and mobile technologies to promote physical health behavior change and provide psychological support for patients undergoing elective surgery: meta-ethnography and systematic review. JMIR Mhealth Uhealth. 2020;8:e19237. 29.	 Rodas E, Mora F, Tamariz F, et al. Low-bandwidth telemedicine for pre- and postoperative evaluation in mobile surgical services. J Telemed Telecare. 2005;11:191–193. 30.	 Mata J, Pecorelli N, Kaneva P, et al. A mobile device application (app) to improve adherence to an enhanced recovery program for colorectal surgery: a randomized controlled trial. Surg Endosc. 2020;34:742–751. 31.	 Baniasadi T, Ghazisaeedi M, Hassaniazad M, et al. Surgical patients followup by smartphone-based applications: a systematic literature review. Stud Health Technol Inform. 2020;271:85–92. 32.	 Dionisi S, Giannetta N, Di Simone E, et al. The use of mHealth in orthopedic surgery: a scoping review. Int J Environ Res Public Health. 2021;18:12549. 33.	 Eustache J, El-Kefraoui C, Ekmekjian T, et al. Do postoperative telemedicine interventions with a communication feature reduce emergency department visits and readmissions? A systematic review and meta-analysis. Surg En­ dosc. 2021;35:5889–5904. 34.	 van der Meij E, Anema JR, Otten RH, et al. The effect of periopera­

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2.2 Quality of Life 1.	 World Health Organization. WHOQOL: measuring quality of life. Accessed

October 24, 2022. https://www.who.int/tools/whoqol 2.	 Wiebe S, Guyatt G, Weaver B, et al. Comparative responsiveness of generic and specific quality-of-life instruments. J Clin Epidemiol. 2003;56:52–60. 3.	 Guyatt GH, King DR, Feeny DH, et al. Generic and specific measurement of health-related quality of life in a clinical trial of respiratory rehabilitation. J Clin Epidemiol. 1999;52:187–192. 4.	 CPOC. Shared decision making and OSIRIS. Centre for Perioperative Care. Accessed October 24, 2022. https://www.cpoc.org.uk/shared-decisionmaking-and-osiris 5.	 Sepucha KR, Vo H, Chang Y, et al. Shared decision-making is associated with better outcomes in patients with knee but not hip osteoarthritis: the DECIDE-OA randomized study. J Bone Joint Surg Am. 2022;104:62–69. 6.	 Richter HE, Redden DT, Duxbury AS, et al. Pelvic floor surgery in the older woman: enhanced compared with usual preoperative assessment. Obstet Gynecol. 2005;105:800–807. 7.	 Niburski K, Guadagno E, Abbasgholizadeh-Rahimi S, et al. Shared deci­

sion making in surgery: a meta-analysis of existing literature. Patient. 2020;13:667–681. 3.1. Cardiovascular Risk Indices 1.	 Smilowitz NR, Berger JS. Perioperative cardiovascular risk assessment and management for noncardiac surgery: a review. JAMA. 2020;324:279–290. 2.	 Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043–1049. 3.	 Cohen ME, Ko CY, Bilimoria KY, et al. Optimizing ACS NSQIP modeling for evaluation of surgical quality and risk: patient risk adjustment, procedure mix adjustment, shrinkage adjustment, and surgical focus. J Am Coll Surg. 2013;217: 336–346.e1. 4.	 Choi DY, Hayes D, Maidman SD, et al. Existing nongated CT coronary cal­ cium predicts operative risk in patients undergoing noncardiac surgeries (ENCORES). Circulation. 2023;148:1154–1164. 5.	 Gupta PK, Gupta H, Sundaram A, et al. Development and validation of a risk calculator for prediction of cardiac risk after surgery. Circulation. 2011;124:381–387. 6.	 Wilcox T, Smilowitz NR, Xia Y, et al. Cardiovascular risk scores to predict perioperative stroke in noncardiac surgery. Stroke. 2019;50:2002–2006. 7.	 Ford MK, Beattie WS, Wijeysundera DN. Systematic review: prediction of perioperative cardiac complications and mortality by the revised cardiac risk index. Ann Intern Med. 2010;152:26–35. 8.	 Bertges DJ, Goodney PP, Zhao Y, et al. The Vascular Study Group of New England Cardiac Risk Index (VSG-CRI) predicts cardiac complications more accurately than the Revised Cardiac Risk Index in vascular surgery patients. J Vasc Surg. 2010;52:674–683, 683.e1–683.e3. 9.	 Msheik A, Kaspar C, Mailhac A, et al. Performance of the AUB-HAS2 car­ diovascular risk index in vascular surgery patients. Vasc Med. 2021;26:535– 541. 10.	 Wolters U, Wolf T, Stutzer H, et al. ASA classification and perioperative vari­ ables as predictors of postoperative outcome. Br J Anaesth. 1996;77:217– 222. 11.	 Glance LG, Faden E, Dutton RP, et al. Impact of the choice of risk model for identifying low-risk patients using the 2014 American College of Cardiol­ ogy/American Heart Association Perioperative Guidelines. Anesthesiology. 2018;129:889–900. 12.	 Protopapa KL, Simpson JC, Smith NC, et al. Development and validation of the Surgical Outcome Risk Tool (SORT). Br J Surg. 2014;101:1774– 1783. 13.	 Bilimoria KY, Liu Y, Paruch JL, et al. Development and evaluation of the universal ACS NSQIP surgical risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surg. 2013;217:833– 842.e1-3. 14.	 Dakik HA, Chehab O, Eldirani M, et al. A new index for pre-operative cardio­

vascular evaluation. J Am Coll Cardiol. 2019;73:3067–3078. 15 Wilcox T, Smilowitz NR, Xia Y, et al. Cardiovascular risk factors and peri­

operative myocardial infarction after noncardiac surgery. Can J Cardiol. 2021;37:224–231. 16.	 Goldman L, Caldera DL, Nussbaum SR, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med. 1977;297:845–850. 17.	 Alrezk R, Jackson N, Al Rezk M, et al. Derivation and validation of a

geriatric-sensitive perioperative cardiac risk index. J Am Heart Assoc. 2017;6:e006648. 3.2. Functional Capacity Assessment 1.	 Reilly DF, McNeely MJ, Doerner D, et al. Self-reported exercise toler­ ance and the risk of serious perioperative complications. Arch Intern Med. 1999;159:2185–2192. 2.	 Lurati Buse GAL, Puelacher C, Gualandro DM, et al. Association between self-reported functional capacity and major adverse cardiac events in pa­ tients at elevated risk undergoing noncardiac surgery: a prospective diag­ nostic cohort study. Br J Anaesth. 2021;126:102–110. 3.	 Marsman M, van Waes JAR, Grobben RB, et al. Added value of subjective assessed functional capacity before non-cardiac surgery in predicting post­ operative myocardial injury. Eur J Prev Cardiol. 2021;28:262–269. 4.	 Gupta PK, Gupta H, Sundaram A, et al. Development and validation of a risk calculator for prediction of cardiac risk after surgery. Circulation. 2011;124:381–387. 5.	 Visnjevac O, Davari-Farid S, Lee J, et al. The effect of adding functional classification to ASA status for predicting 30-day mortality. Anesth Analg. 2015;121:110–116. 6.	 Hlatky MA, Boineau RE, Higginbotham MB, et al. A brief self-administered questionnaire to determine functional capacity (the Duke Activity Status In­ dex). Am J Cardiol. 1989;64:651–654. 7.	 Wijeysundera DN, Pearse RM, Shulman MA, et al. Assessment of functional capacity before major non-cardiac surgery: an international, prospective co­ hort study. Lancet. 2018;391:2631–2640. 8.	 Wijeysundera DN, Beattie WS, Hillis GS, et al. Integration of the Duke Activ­ ity Status Index into preoperative risk evaluation: a multicentre prospective cohort study. Br J Anaesth. 2020;124:261–270. 9.	 Lurati Buse GA, Mauermann E, Ionescu D, et al. Risk assessment for major

adverse cardiovascular events after noncardiac surgery using self-reported functional capacity: international prospective cohort study. Br J Anaesth. 2023;130:655–665.

3.3 Frailty 1.	 Siddiqui E, Banco D, Berger JS, et al. Frailty assessment and perioperative

major adverse cardiovascular events after noncardiac surgery. Am J Med. 2023;136:372–379.e375. 2.	 Hall DE, Arya S, Schmid KK, et al. Association of a frailty screening ini­ tiative with postoperative survival at 30, 180, and 365 days. JAMA Surg. 2017;152:233–240. 3.	 Birkelbach O, Morgeli R, Spies C, et al. Routine frailty assessment predicts postoperative complications in elderly patients across surgical disciplines-a retrospective observational study. BMC Anesthesiol. 2019;19:204. 4.	 Tjeertes EKM, van Fessem JMK, Mattace-Raso FUS, et al. In­ fluence of frailty on outcome in older patients undergoing noncardiac surgery-a systematic review and meta-analysis. Aging Dis. 2020;11:1276–1290. 5.	 McIsaac DI, Harris EP, Hladkowicz E, et al. Prospective comparison of pre­ operative predictive performance between 3 leading frailty instruments. Anesth Analg. 2020;131:263–272. 6.	 Collard RM, Boter H, Schoevers RA, et al. Prevalence of frailty in community-dwelling older persons: a systematic review. J Am Geriatr Soc. 2012;60:1487–1492. 7.	 Denfeld QE, Winters-Stone K, Mudd JO, et al. The prevalence of frailty in heart failure: a systematic review and meta-analysis. Int J Cardiol. 2017;236:283–289. 8.	 Uchmanowicz I, Lee CS, Vitale C, et al. Frailty and the risk of all-cause mor­ tality and hospitalization in chronic heart failure: a meta-analysis. ESC Heart Fail. 2020;7:3427–3437. 9.	 Nidadavolu LS, Ehrlich AL, Sieber FE, et al. Preoperative evaluation of the frail patient. Anesth Analg. 2020;130:1493–1503. 10.	 Norris CM, Close JCT. Prehabilitation for the frailty syndrome: improving outcomes for our most vulnerable patients. Anesth Analg. 2020;130:1524– 1533. 11.	 Charipova K, Urits I, Viswanath O, et al. Preoperative assessment and opti­

mization of cognitive dysfunction and frailty in the ambulatory surgical pa­ tient. Curr Opin Anaesthesiol. 2020;33:732–739.

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al of disability prevention in frail older patients screened in primary care: the FRASI study. Design and baseline evaluation. Aging Clin Exp Res. 2006;18:359–366. 3.4. Perioperative Biomarkers for Risk Stratification 1.	 Duceppe E, Patel A, Chan MTV, et al. Preoperative N-terminal pro-B-type natriuretic peptide and cardiovascular events after noncardiac surgery: a cohort study. Ann Intern Med. 2020;172:96–104. 2.	 Devereaux PJ, Duceppe E, Guyatt G, et al. Dabigatran in patients with myo­ cardial injury after non-cardiac surgery (MANAGE): an international, ran­ domised, placebo-controlled trial. Lancet. 2018;391:2325–2334. 3.	 Rodseth RN, Biccard BM, Le Manach Y, et al. The prognostic value of pre-operative and post-operative B-type natriuretic peptides in patients undergoing noncardiac surgery: B-type natriuretic peptide and Nterminal fragment of pro-B-type natriuretic peptide: a systematic re­ view and individual patient data meta-analysis. J Am Coll Cardiol. 2014;63:170–180. 4.	 Humble CAS, Huang S, Jammer I, et al. Prognostic performance of pre­ operative cardiac troponin and perioperative changes in cardiac tropo­ nin for the prediction of major adverse cardiac events and mortality in noncardiac surgery: a systematic review and meta-analysis. PLoS One. 2019;14:e0215094. 5.	 Vernooij LM, van Klei WA, Moons KG, et al. The comparative and added prognostic value of biomarkers to the Revised Cardiac Risk Index for pre­ operative prediction of major adverse cardiac events and all-cause mortality in patients who undergo noncardiac surgery. Cochrane Database Syst Rev. 2021;12:CD013139. 6.	 Zhao BC, Liu WF, Deng QW, et al. Meta-analysis of preoperative highsensitivity cardiac troponin measurement in non-cardiac surgical patients at risk of cardiovascular complications. Br J Surg. 2020;107:e81–e90. 7.	 Lurati Buse G, Larmann J, Gillmann HJ, et al. NT-proBNP or self-reported functional capacity in estimating risk of cardiovascular events after noncar­ diac surgery. JAMA Netw Open. 2023;6:e2342527. 8.	 Golubovic M, Jankovic R, Sokolovic D, et al. Preoperative midregional pro-

adrenomedullin and high-sensitivity troponin T predict perioperative cardio­ vascular events in noncardiac surgery. Med Princ Pract. 2018;27:278–284. 4.1. 12-Lead Electrocardiogram 1.	 Jeger RV, Probst C, Arsenic R, et al. Long-term prognostic value of the preoperative 12-lead electrocardiogram before major noncardiac surgery in coronary artery disease. Am Heart J. 2006;151:508–513. 2.	 Payne CJ, Payne AR, Gibson SC, et al. Is there still a role for preoperative 12-lead electrocardiography? World J Surg. 2011;35:2611–2616. 3.	 van Klei WA, Bryson GL, Yang H, et al. The value of routine preoperative electrocardiography in predicting myocardial infarction after noncardiac sur­ gery. Ann Surg. 2007;246:165–170. 4.	 Noordzij PG, Boersma E, Bax JJ, et al. Prognostic value of routine preopera­ tive electrocardiography in patients undergoing noncardiac surgery. Am J Cardiol. 2006;97:1103–1106. 5.	 Biteker M, Duman D, Tekkesin AI. Predictive value of preoperative electro­

cardiography for perioperative cardiovascular outcomes in patients under­ going noncardiac, nonvascular surgery. Clin Cardiol. 2012;35:494–499. 6 Knutsen R, Knutsen SF, Curb JD, et al. Predictive value of resting electro­

cardiograms for 12-year incidence of stroke in the Honolulu Heart Program. Stroke. 1988;19:555–559. 7.	 Sutherland SE, Gazes PC, Keil JE, et al. Electrocardiographic abnormalities and 30-year mortality among white and black men of the Charleston Heart Study. Circulation. 1993;88:2685–2692. 8.	 Correll DJ, Hepner DL, Chang C, et al. Preoperative electrocardiograms: pa­ tient factors predictive of abnormalities. Anesthesiology. 2009;110:1217– 1222. 9.	 Scheidt-Nave C, Barrett-Connor E, Wingard DL. Resting electrocardio­ graphic abnormalities suggestive of asymptomatic ischemic heart disease associated with non-insulin-dependent diabetes mellitus in a defined popu­ lation. Circulation. 1990;81:899–906. 10.	 De Hert SG. Preoperative electrocardiograms: obsolete or still useful? An­ esthesiology. 2009;110:1205–1206. 11.	 Sowerby RJ, Lantz Powers AG, Ghiculete D, et al. Routine preoperative electrocardiograms in patients at low risk for cardiac complications during shockwave lithotripsy: are they useful? J Endourol. 2019;33:314–318. 12.	 Prasada S, Desai MY, Saad M, et al. Preoperative atrial fibrillation and cardiovascular outcomes after noncardiac surgery. J Am Coll Cardiol. 2022;79:2471–2485. 13.	 Wogan JM, Lowenstein SR, Gordon GS. Second-degree atrioventricular block: Mobitz type II. J Emerg Med. 1993;11:47–54. 14.	 Jiang J, He M, Xu Y. Preoperative electrocardiogram and perioperative methods for predicting new-onset atrial fibrillation during lung surgery. J Cardiothorac Vasc Anesth. 2021;35:1424–1430. 15.	 Chen CL, Lin GA, Bardach NS, et al. Preoperative medical testing in Medi­

care patients undergoing cataract surgery. N Engl J Med. 2015;372:1530– 1538. 4.2.1. Left Ventricular Function 1.	 Hammill BG, Curtis LH, Bennett-Guerrero E, et al. Impact of heart fail­ ure on patients undergoing major noncardiac surgery. Anesthesiology. 2008;108:559–567. 2.	 Hernandez AF, Whellan DJ, Stroud S, et al. Outcomes in heart failure pa­ tients after major noncardiac surgery. J Am Coll Cardiol. 2004;44:1446– 1453. 3.	 Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043–1049. 4.	 Lerman BJ, Popat RA, Assimes TL, et al. Association of left ventricular ejec­ tion fraction and symptoms with mortality after elective noncardiac surgery among patients with heart failure. JAMA. 2019;321:572–579. 5.	 Chang HY, Chang WT, Liu YW. Application of transthoracic echocardiog­ raphy in patients receiving intermediate- or high-risk noncardiac surgery. PLoS One. 2019;14:e0215854. 6.	 Flu WJ, van Kuijk JP, Hoeks SE, et al. Prognostic implications of asymp­ tomatic left ventricular dysfunction in patients undergoing vascular surgery. Anesthesiology. 2010;112:1316–1324. 7.	 Healy KO, Waksmonski CA, Altman RK, et al. Perioperative outcome and long-term mortality for heart failure patients undergoing intermediate- and high-risk noncardiac surgery: impact of left ventricular ejection fraction. Congest Heart Fail. 2010;16:45–49. 8.	 van Diepen S, Bakal JA, McAlister FA, et al. Mortality and readmission of patients with heart failure, atrial fibrillation, or coronary artery disease un­ dergoing noncardiac surgery: an analysis of 38047 patients. Circulation. 2011;124:289–296. 9.	 Canty DJ, Heiberg J, Yang Y, et al. One-year results of the pilot multicentre randomised trial of preoperative focused cardiac ultrasound in hip fracture surgery. Anaesth Intensive Care. 2019;47:207–208. 10.	 Canty DJ, Royse CF, Kilpatrick D, et al. The impact of focused transthoracic echocardiography in the pre-operative clinic. Anaesthesia. 2012;67:618– 625. 11.	 Cowie B. Focused transthoracic echocardiography predicts perioperative cardiovascular morbidity. J Cardiothorac Vasc Anesth. 2012;26:989–993. 12.	 Wijeysundera DN, Beattie WS, Karkouti K, et al. Association of echocar­ diography before major elective non-cardiac surgery with postoperative survival and length of hospital stay: population based cohort study. BMJ. 2011;342:d3695. 13.	 Xu-Cai YO, Brotman DJ, Phillips CO, et al. Outcomes of patients with sta­ ble heart failure undergoing elective noncardiac surgery. Mayo Clin Proc. 2008;83:280–288. 14.	 Levitan EB, Graham LA, Valle JA, et al. Pre-operative echocardiography

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13 Eichelberger JP, Schwarz KQ, Black ER, et al. Predictive value of dobuta­

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ercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exer­ cise Testing). J Am Coll Cardiol. 1997;30:260–311. 4.4. Cardiopulmonary Exercise Testing 1.	 Moran J, Wilson F, Guinan E, et al. Role of cardiopulmonary exercise test­ ing as a risk-assessment method in patients undergoing intra-abdominal surgery: a systematic review. Br J Anaesth. 2016;116:177–191. 2.	 Steffens D, Ismail H, Denehy L, et al. Preoperative cardiopulmonary exer­ cise test associated with postoperative outcomes in patients undergoing cancer surgery: a systematic review and meta-analyses. Ann Surg Oncol. 2021;28:7120–7146. 3.	 Roxburgh BH, Cotter JD, Campbell HA, et al. Physiological relationship be­ tween cardiorespiratory fitness and fitness for surgery: a narrative review. Br J Anaesth. 2023;130:122–132. 4.	 Levett DZH, Jack S, Swart M, et al. Perioperative cardiopulmonary exercise

testing (CPET): consensus clinical guidelines on indications, organization, conduct, and physiological interpretation. Br J Anaesth. 2018;120:484– 500. 5.	 Fleisher LA, Linde-Zwirble WT. Incidence, outcome, and attributable re­

source use associated with pulmonary and cardiac complications after ma­ jor small and large bowel procedures. Perioper Med (Lond). 2014;3:7. 6.	 Wijeysundera DN, Pearse RM, Shulman MA, et al. Assessment of functional capacity before major non-cardiac surgery: an international, prospective co­ hort study. Lancet. 2018;391:2631–2640. 7.	 West MA, Asher R, Browning M, et al. Validation of preoperative cardiopul­ monary exercise testing-derived variables to predict in-hospital morbidity after major colorectal surgery. Br J Surg. 2016;103:744–752. 8.	 Otto J, Levett, DZ, Grocott, MPW. Cardiopulmonary exercise testing for preoperative evaluation: what does the future hold? Current Anesthesiology Reports. 2020;1–11. 9.	 Shulman MA, Cuthbertson BH, Wijeysundera DN, et al. Using the 6-minute

walk test to predict disability-free survival after major surgery. Br J Anaesth. 2019;122:111–119. 4.5. Coronary Computed Tomography Angiography 1.	 Sheth T, Chan M, Butler C, et al. Prognostic capabilities of coronary com­ puted tomographic angiography before non-cardiac surgery: prospective cohort study. BMJ. 2015;350:h1907. 2.	 Koshy AN, Ha FJ, Gow PJ, et al. Computed tomographic coronary angiog­ raphy in risk stratification prior to non-cardiac surgery: a systematic review and meta-analysis. Heart. 2019;105:1335–1342. 3.	 Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/ PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2012;126:e354–e471. 4.	 Hwang JW, Kim EK, Yang JH, et al. Assessment of perioperative cardiac risk of patients undergoing noncardiac surgery using coronary computed tomographic angiography. Circ Cardiovasc Imaging. 2015;8:e002582. 5.	 McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization be­ fore elective major vascular surgery. N Engl J Med. 2004;351:2795–2804. 6.	 Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/ SAEM/SCCT/SCMR guideline for the evaluation and diagnosis of chest pain: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;144:e368–e454. 7.	 Mark DB, Federspiel JJ, Cowper PA, et al. Economic outcomes with ana­

tomical versus functional diagnostic testing for coronary artery disease. Ann Intern Med. 2016;165:94–102. 4.6. Invasive Coronary Angiography 1.	 Garcia S, Moritz TE, Goldman S, et al. Perioperative complications after vas­ cular surgery are predicted by the revised cardiac risk index but are not reduced in high-risk subsets with preoperative revascularization. Circ Car­ diovasc Qual Outcomes. 2009;2:73–77. 2.	 McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization be­ fore elective major vascular surgery. N Engl J Med. 2004;351:2795–2804. 3.	 Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/ PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2012;126:e354–e471. 4.	 Cheng XS, Liu S, Han J, et al. Association of pretransplant coronary heart disease testing with early kidney transplant outcomes. JAMA Intern Med. 2023;183:134–141. 5.	 Monaco M, Stassano P, Di Tommaso L, et al. Systematic strategy of prophy­ lactic coronary angiography improves long-term outcome after major vas­ cular surgery in medium- to high-risk patients: a prospective, randomized study. J Am Coll Cardiol. 2009;54:989–996. 6.	 Illuminati G, Schneider F, Greco C, et al. Long-term results of a randomized controlled trial analyzing the role of systematic pre-operative coronary angi­ ography before elective carotid endarterectomy in patients with asymptom­ atic coronary artery disease. Eur J Vasc Endovasc Surg. 2015;49:366–374. 7.	 Maron DJ, Hochman JS, Reynolds HR, et al. Initial invasive or conservative

strategy for stable coronary disease. N Engl J Med. 2020;382:1395–1407.

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without PCI for stable coronary disease. N Engl J Med. 2007;356:1503– 1516. 14.	 Frye RL, August P, Brooks MM, et al. Bari D. Study Group. A randomized trial of therapies for type 2 diabetes and coronary artery disease. N Engl J Med. 2009;360:2503–2515. 15.	 Maron DJ, Hochman JS, Reynolds HR, et al. Initial invasive or conservative strategy for stable coronary disease. N Engl J Med. 2020;382:1395–1407. 16.	 Lawton JS, Tamis-Holland JE, Bangalore S, et al. 2021 ACC/AHA/SCAI guideline for coronary artery revascularization: a report of the American Col­ lege of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2022;145:e18–e114. 17.	 Virani SS, Newby LK, Arnold SK, et al. 2023 AHA/ACC/ACCP/ASPC/ NLA/PCNA guideline for the management of patients with chronic coro­ nary disease: a report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2023;148:e9–e119. 18.	 Stone GW, Grines CL, Cox DA, et al. Comparison of angioplasty with stent­ ing, with or without abciximab, in acute myocardial infarction. N Engl J Med. 2002;346:957–966. 19.	 Garcia S, Moritz TE, Ward HB, et al. Usefulness of revascularization of pa­ tients with multivessel coronary artery disease before elective vascular sur­ gery for abdominal aortic and peripheral occlusive disease. Am J Cardiol. 2008;102:809–813. 20.	 Monaco M, Stassano P, Di Tommaso L, et al. Systematic strategy of prophy­ lactic coronary angiography improves long-term outcome after major vas­ cular surgery in medium- to high-risk patients: a prospective, randomized study. J Am Coll Cardiol. 2009;54:989–996. 21.	 Illuminati G, Ricco JB, Greco C, et al. Systematic preoperative coronary angiography and stenting improves postoperative results of carotid end­ arterectomy in patients with asymptomatic coronary artery disease: a ran­ domised controlled trial. Eur J Vasc Endovasc Surg. 2010;39:139–145. 22.	 Garcia S, Rider JE, Moritz TE, et al. Preoperative coronary artery revascular­ ization and long-term outcomes following abdominal aortic vascular surgery in patients with abnormal myocardial perfusion scans: a subgroup analysis of the coronary artery revascularization prophylaxis trial. Catheter Cardiovasc Interv. 2011;77:134–141. 23.	 Wong EY, Lawrence HP, Wong DT. The effects of prophylactic coronary revascularization or medical management on patient outcomes after non­ cardiac surgery: a meta-analysis. Can J Anaesth. 2007;54:705–717. 24.	 Ultee KH, Rouwet EV, Hoeks SE, et al. Coronary revascularization induces a shift from cardiac toward noncardiac mortality without improving survival in vascular surgery patients. J Vasc Surg. 2015;61:1543–1549.e1. 25.	 Smith BB, Warner MA, Warner NS, et al. Cardiac risk of noncardiac surgery

after percutaneous coronary intervention with second-generation drugeluting stents. Anesth Analg. 2019;128:621–628. 6.2. Hypertension and Perioperative Blood Pressure 1.	 Abdelmalak BB, Abd-Elsayed AA, Dalton JE, et al. The association between preinduction arterial blood pressure and postoperative cardiovascular, renal, and neurologic morbidity, and in-hospital mortality in elective noncardiac surgery: an observational study. J Hypertens. 2018;36:2251–2259. 2.	 Howell SJ, Sear JW, Foex P. Hypertension, hypertensive heart disease and perioperative cardiac risk. Br J Anaesth. 2004;92:570–583. 3.	 Walsh M, Devereaux PJ, Garg AX, et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: to­ ward an empirical definition of hypotension. Anesthesiology. 2013;119:507– 515. 4.	 Salmasi V, Maheshwari K, Yang D, et al. Relationship between intraoperative hypotension, defined by either reduction from baseline or absolute thresh­ olds, and acute kidney and myocardial injury after noncardiac surgery: a retrospective cohort analysis. Anesthesiology. 2017;126:47–65. 5.	 Monk TG, Bronsert MR, Henderson WG, et al. Association between intraop­ erative hypotension and hypertension and 30-day postoperative mortality in noncardiac surgery. Anesthesiology. 2015;123:307–319. 6.	 Sessler DI, Meyhoff CS, Zimmerman NM, et al. Period-dependent associa­ tions between hypotension during and for four days after noncardiac sur­ gery and a composite of myocardial infarction and death: a substudy of the POISE-2 trial. Anesthesiology. 2018;128:317–327. 7.	 Deng C, Bellomo R, Myles P. Systematic review and meta-analysis of the perioperative use of vasoactive drugs on postoperative outcomes after ma­ jor abdominal surgery. Br J Anaesth. 2020;124:513–524. 8.	 Gregory A, Stapelfeldt WH, Khanna AK, et al. Intraoperative hypotension is

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sponses to laryngoscopy with and without tracheal intubation. Br J Anaesth. 1987;59:295–299. 32 Drummond JC, Blake JL, Patel PM, et al. An observational study of the

influence of “white-coat hypertension” on day-of-surgery blood pressure determinations. J Neurosurg Anesthesiol. 2013;25:154–161. 33.	 Ahuja S, Mascha EJ, Yang D, et al. Associations of intraoperative radial arte­ rial systolic, diastolic, mean, and pulse pressures with myocardial and acute kidney injury after noncardiac surgery: a retrospective cohort analysis. An­ esthesiology. 2020;132:291–306. 34.	 Wanner PM, Wulff DU, Djurdjevic M, et al. Targeting higher intraoperative blood pressures does not reduce adverse cardiovascular events following noncardiac surgery. J Am Coll Cardiol. 2021;78:1753–1764. 35.	 Briesenick L, Flick M, Saugel B. Postoperative blood pressure management in patients treated in the ICU after noncardiac surgery. Curr Opin Crit Care. 2021;27:694–700. 36.	 Marik PE, Varon J. Perioperative hypertension: a review of current and emerging therapeutic agents. J Clin Anesth. 2009;21:220–229. 37.	 Lee SM, Takemoto S, Wallace AW. Association between withholding an­ giotensin receptor blockers in the early postoperative period and 30-day mortality: a cohort study of the Veterans Affairs Healthcare System. Anes­ thesiology. 2015;123:288–306. 38.	 Mudumbai SC, Takemoto S, Cason BA, et al. Thirty-day mortality risk as­ sociated with the postoperative nonresumption of angiotensin-converting enzyme inhibitors: a retrospective study of the Veterans Affairs Healthcare System. J Hosp Med. 2014;9:289–296. 39.	 Anderson TS, Jing B, Auerbach A, et al. Clinical outcomes after intensify­

ing antihypertensive medication regimens among older adults at hospital discharge. JAMA Intern Med. 2019;179:1528–1536.

6.3 Heart Failure 1.	 Kietaibl AT, Fasching P, Glaser K, et al. New diabetic medication sodium-

glucose cotransporter-2 inhibitors can induce euglycemic ketoacidosis and mimic surgical diseases: a case report and review of literature. Front Surg. 2022;9:828649. 2.	 Milder DA, Milder TY, Kam PCA. Sodium-glucose co-transporter type-2 inhibitors: pharmacology and peri-operative considerations. Anaesthesia. 2018;73:1008–1018. 3.	 US FDA. FDA revises lables of SGLT2 inhibitors for diabetes to include warnings about too much acid in the blood and serious urinary tract in­ fections. Accessed October 16, 2022. https://www.fda.gov/drugs/ drug-safety-and-availability/fda-revises-labels-sglt2-inhibitors-diabetesinclude-warnings-about-too-much-acid-blood-and-serious 4.	 Gilstrap LG, Fonarow GC, Desai AS, et al. Initiation, continuation, or with­ drawal of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers and outcomes in patients hospitalized with heart failure with re­ duced ejection fraction. J Am Heart Assoc. 2017;6:e004675. 5.	 Maisel A, Xue Y, van Veldhuisen DJ, et al. Effect of spironolactone on 30day death and heart failure rehospitalization (from the COACH Study). Am J Cardiol. 2014;114:737–742. 6.	 Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure: a systematic review and meta-analysis. JACC Heart Fail. 2015;3:647–653. 7.	 Tran RH, Aldemerdash A, Chang P, et al. Guideline-directed medical therapy and survival following hospitalization in patients with heart failure. Pharma­ cotherapy. 2018;38:406–416. 8.	 Fonarow GC, Abraham WT, Albert NM, et al. Influence of beta-blocker continuation or withdrawal on outcomes in patients hospitalized with heart failure: findings from the OPTIMIZE-HF program. J Am Coll Cardiol. 2008;52:190–199. 9.	 Smilowitz NR, Banco D, Katz SD, et al. Association between heart failure and perioperative outcomes in patients undergoing non-cardiac surgery. Eur Heart J Qual Care Clin Outcomes. 2021;7:68–75. 10.	 Lerman BJ, Popat RA, Assimes TL, et al. Association of left ventricular ejec­ tion fraction and symptoms with mortality after elective noncardiac surgery among patients with heart failure. JAMA. 2019;321:572–579. 11.	 van Diepen S, Bakal JA, McAlister FA, et al. Mortality and readmission of patients with heart failure, atrial fibrillation, or coronary artery disease un­ dergoing noncardiac surgery: an analysis of 38047 patients. Circulation. 2011;124:289–296. 12.	 Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guide­ line for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Prac­ tice Guidelines. Circulation. 2022;145:e895–e1032. 13.	 Ackland GL, Patel A, Abbott TEF, et al. Discontinuation vs. continuation of

renin-angiotensin system inhibition before non-cardiac surgery: the SPACE trial. Eur Heart J. 2023;ehad716.

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VR, et al. Diabetes care in the hospital: standards of medical care in diabetes-2022. Diabetes Care. 2022;45:S244–S253. 6.3.1. Hypertrophic Cardiomyopathy 1.	 Dhillon A, Khanna A, Randhawa MS, et al. Perioperative outcomes of pa­ tients with hypertrophic cardiomyopathy undergoing non-cardiac surgery. Heart. 2016;102:1627–1632. 2.	 Hensley N, Dietrich J, Nyhan D, et al. Hypertrophic cardiomyopathy: a re­ view. Anesth Analg. 2015;120:554–569. 3.	 Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diag­ nosis and treatment of patients with hypertrophic cardiomyopathy: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2020;142:e558– e631. 4.	 Haering JM, Comunale ME, Parker RA, et al. Cardiac risk of noncardiac surgery in patients with asymmetric septal hypertrophy. Anesthesiology. 1996;85:254–259. 5.	 Xuan TM, Zeng Y, Zhu WL. Risk of patients with hypertrophic cardiomyopa­ thy undergoing noncardiac surgery. Chin Med Sci J. 2007;22:211–215. 6.	 Hreybe H, Zahid M, Sonel A, et al. Noncardiac surgery and the risk of death and other cardiovascular events in patients with hypertrophic cardiomyopa­ thy. Clin Cardiol. 2006;29:65–68. 7.	 Thompson RC, Liberthson RR, Lowenstein E. Perioperative anesthetic risk

of noncardiac surgery in hypertrophic obstructive cardiomyopathy. JAMA. 1985;254:2419–2421. 6.3.2. Pulmonary Hypertension 1.	 Meyer S, McLaughlin VV, Seyfarth HJ, et al. Outcomes of noncardiac, non­ obstetric surgery in patients with PAH: an international prospective survey. Eur Respir J. 2013;41:1302–1307. 2.	 Smilowitz NR, Armanious A, Bangalore S, et al. Cardiovascular outcomes of patients with pulmonary hypertension undergoing noncardiac surgery. Am J Cardiol. 2019;123:1532–1537. 3.	 Fayad A, Shillcutt S, Meineri M, et al. Comparative effectiveness and harms of intraoperative transesophageal echocardiography in noncardiac surgery: a systematic review. Semin Cardiothorac Vasc Anesth. 2018;22:122–136. 4.	 Rajaram SS, Desai NK, Kalra A, et al. Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Syst Rev. 2013;CD003408. 5.	 Ramakrishna G, Sprung J, Ravi BS, et al. Impact of pulmonary hypertension on the outcomes of noncardiac surgery: predictors of perioperative morbid­ ity and mortality. J Am Coll Cardiol. 2005;45:1691–1699. 6.	 Rajagopal S, Ruetzler K, Ghadimi K, et al. Evaluation and management of pulmonary hypertension in noncardiac surgery: a scientific statement from the American Heart Association. Circulation. 2023;147:1317–1343. 7.	 Price LC, Martinez G, Brame A, et al. Perioperative management of patients with pulmonary hypertension undergoing non-cardiothoracic, non-obstetric surgery: a systematic review and expert consensus statement. Br J Anaesth. 2021;126:774–790. 8.	 Ammash NM, Connolly HM, Abel MD, et al. Noncardiac surgery in Eisen­ menger syndrome. J Am Coll Cardiol. 1999;33:222–227. 9.	 Krowka MJ, Plevak DJ, Findlay JY, et al. Pulmonary hemodynamics and peri­ operative cardiopulmonary-related mortality in patients with portopulmonary hypertension undergoing liver transplantation. Liver Transpl. 2000;6:443– 450. 10.	 Lai HC, Lai HC, Wang KY, et al. Severe pulmonary hypertension complicates postoperative outcome of non-cardiac surgery. Br J Anaesth. 2007;99:184– 190. 11.	 Memtsoudis SG, Ma Y, Chiu YL, et al. Perioperative mortality in patients with pulmonary hypertension undergoing major joint replacement. Anesth Analg. 2010;111:1110–1116. 12.	 Price LC, Montani D, Jais X, et al. Noncardiothoracic nonobstetric surgery in mild-to-moderate pulmonary hypertension. Eur Respir J. 2010;35:1294– 1302. 13.	 Kaw R, Pasupuleti V, Deshpande A, et al. Pulmonary hypertension: an im­ portant predictor of outcomes in patients undergoing non-cardiac surgery. Respir Med. 2011;105:619–624. 14.	 Bennett C, Klingenberg SL, Langholz E, et al. Tranexamic acid for upper gastrointestinal bleeding. Cochrane Database Syst Rev. 2014;CD006640. 15.	 Kim D, Jules-Elysee K, Turteltaub L, et al. Clinical outcomes in patients with pulmonary hypertension undergoing total hip arthroplasty. Hss j. 2014;10:131–135. 16.	 Deljou A, Sabov M, Kane GC, et al. Outcomes after noncardiac surgery for

patients with pulmonary hypertension: a historical cohort study. J Cardiotho­ rac Vasc Anesth. 2020;34:1506–1513. 17 Simonneau G, Montani D, Celermajer DS, et al. Haemodynamic definitions

and updated clinical classification of pulmonary hypertension. Eur Respir J. 2019;53:1801913. 18.	 Humbert M, Kovacs G, Hoeper MM, et al. 2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022;43:3618–3731. 19.	 Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and management of right-sided heart failure: a scientific statement from the American Heart Association. Circulation. 2018;137:e578–e622. 20.	 American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Practice guidelines for pulmonary artery catheteriza­ tion: an updated report by the American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Anesthesiology. 2003;99:988– 1014. 21.	 Ceccarelli P, Bigatello LM, Hess D, et al. Inhaled nitric oxide delivery by anesthesia machines. Anesth Analg. 2000;90:482–488. 22.	 Vizza CD, Rocca GD, Roma AD, et al. Acute hemodynamic effects of inhaled nitric oxide, dobutamine and a combination of the two in patients with mild to moderate secondary pulmonary hypertension. Crit Care. 2001;5:355– 361. 23.	 Ghadimi K, Cappiello J, Cooter-Wright M, et al. Inhaled pulmonary vasodila­

tor therapy in adult lung transplant: a randomized clinical trial. JAMA Surg. 2022;157:e215856. 6.3.3. Adult Congenital Heart Disease 1.	 Maxwell BG, Williams GD, Ramamoorthy C. Knowledge and attitudes of an­ esthesia providers about noncardiac surgery in adults with congenital heart disease. Congenit Heart Dis. 2014;9:45–53. 2.	 Ammash NM, Connolly HM, Abel MD, et al. Noncardiac surgery in Eisen­ menger syndrome. J Am Coll Cardiol. 1999;33:222–227. 3.	 Maxwell BG, Wong JK, Lobato RL. Perioperative morbidity and mortality after noncardiac surgery in young adults with congenital or early acquired heart disease: a retrospective cohort analysis of the National Surgical Qual­ ity Improvement Program database. Am Surg. 2014;80:321–326. 4.	 Eagle SS, Daves SM. The adult with Fontan physiology: systematic ap­ proach to perioperative management for noncardiac surgery. J Cardiothorac Vasc Anesth. 2011;25:320–334. 5.	 Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139:e698–e800. 6.	 Williamson CG, Ebrahimian S, Ascandar N, et al. Major elective non-cardiac operations in adults with congenital heart disease. Heart. 2023;109:202– 207. 7.	 Maxwell BG, Wong JK, Kin C, et al. Perioperative outcomes of major non­ cardiac surgery in adults with congenital heart disease. Anesthesiology. 2013;119:762–769. 8.	 Muller MJ, Norozi K, Caroline J, et al. Morbidity and mortality in adults with congenital heart defects in the third and fourth life decade. Clin Res Cardiol. 2022;111:900–911. 9.	 Maxwell BG, Posner KL, Wong JK, et al. Factors contributing to adverse perioperative events in adults with congenital heart disease: a structured analysis of cases from the closed claims project. Congenit Heart Dis. 2015;10:21–29. 10.	 Rabbitts JA, Groenewald CB, Mauermann WJ, et al. Outcomes of general

anesthesia for noncardiac surgery in a series of patients with Fontan pallia­ tion. Paediatr Anaesth. 2013;23:180–187. 6.3.4. Left Ventricular Assist Devices 1.	 Kirklin JK, Pagani FD, Kormos RL, et al. Eighth annual INTERMACS report: special focus on framing the impact of adverse events. J Heart Lung Trans­ plant. 2017;36:1080–1086. 2.	 Kormos RL, Antonides CFJ, Goldstein DJ, et al. Updated definitions of ad­ verse events for trials and registries of mechanical circulatory support: a consensus statement of the mechanical circulatory support academic re­ search consortium. J Heart Lung Transplant. 2020;39:735–750. 3.	 Bhat G, Kumar S, Aggarwal A, et al. Experience with noncardiac surgery in destination therapy left ventricular assist devices patients. ASAIO J. 2012;58:396–401. 4.	 Briasoulis A, Chehab O, Alvarez P. In-hospital outcomes of left ventricular assist devices (LVAD) patients undergoing noncardiac surgery. ASAIO J. 2021;67:144–148. 5.	 Mentias A, Briasoulis A, Vaughan Sarrazin MS, et al. Trends, perioperative

adverse events, and survival of patients with left ventricular assist devices undergoing noncardiac surgery. JAMA Netw Open. 2020;3:e2025118.

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noncardiac surgery in patients with implanted left ventricular assist devices. ASAIO J. 2015;61:648–651. 7.	 Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation guidelines for mechanical circu­ latory support: executive summary. J Heart Lung Transplant. 2013;32:157– 187. 8.	 Mehra MR, Uriel N, Naka Y, et al. A fully magnetically levitated left ventricu­

lar assist device: final report. N Engl J Med. 2019;380:1618–1627. 6.3.5. Heart Transplantation Recipients 1.	 Colvin MM, Smith JM, Ahn YS, et al. OPTN/SRTR 2022 annual data report: heart. Am J Transplant. 2024;24:S305–S393. 2.	 Jurgens PT, Aquilante CL, Page RL 2nd, et al. Perioperative management of cardiac transplant recipients undergoing noncardiac surgery: unique chal­ lenges created by advancements in care. Semin Cardiothorac Vasc Anesth. 2017;21:235–244. 3.	 Velleca A, Shullo MA, Dhital K, et al. The International Society for Heart and

Lung Transplantation (ISHLT) guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2023;42:e1–e141. 6.4. Valvular Heart Disease 1.	 Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the

management of patients with valvular heart disease: a report of the Ameri­ can College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143:e72–e227. 6.4.1. Aortic Stenosis 1.	 Luis SA, Dohaei A, Chandrashekar P, et al. Impact of aortic valve replace­ ment for severe aortic stenosis on perioperative outcomes following major noncardiac surgery. Mayo Clin Proc. 2020;95:727–737. 2.	 Taniguchi T, Morimoto T, Shiomi H, et al. Elective non-cardiac surgery in patients with severe aortic stenosis: observations from the CURRENT AS Registry. Circ J. 2020;84:1173–1182. 3.	 Calicchio F, Guarracino F, Giannini C, et al. Balloon aortic valvuloplasty be­ fore noncardiac surgery in severe aortic stenosis: a single-center experi­ ence. J Cardiovasc Med (Hagerstown). 2017;18:109–113. 4.	 Kwok CS, Bagur R, Rashid M, et al. Aortic stenosis and noncardiac surgery: a systematic review and meta-analysis. Int J Cardiol. 2017;240:145–153. 5.	 Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043–1049. 6.	 Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143:e72–e227. 7.	 Baumgartner H, Hung J, Bermejo J, et al. Recommendations on the echo­ cardiographic assessment of aortic valve stenosis: a focused update from the European Association of Cardiovascular Imaging and the American So­ ciety of Echocardiography. J Am Soc Echocardiogr. 2017;30:372–392. 8.	 Agarwal S, Rajamanickam A, Bajaj NS, et al. Impact of aortic stenosis on postoperative outcomes after noncardiac surgeries. Circ Cardiovasc Qual Outcomes. 2013;6:193–200. 9.	 Goldman L, Caldera DL, Nussbaum SR, et al. Multifactorial index of car­ diac risk in noncardiac surgical procedures. N Engl J Med. 1977;297:845– 850. 10.	 Tashiro T, Pislaru SV, Blustin JM, et al. Perioperative risk of major noncardiac surgery in patients with severe aortic stenosis: a reappraisal in con­ temporary practice. Eur Heart J. 2014;35:2372–2381. 11.	 Kogoj P, Devjak R, Bunc M. Balloon aortic valvuloplasty (BAV) as a bridge to aortic valve replacement in cancer patients who require urgent non-cardiac surgery. Radiol Oncol. 2014;48:62–66. 12.	 Yamamoto M, Kagase A, Shimura T, et al. Percutaneous aortic valve inter­ vention in patients scheduled for noncardiac surgery: a Japanese multi­ center study. Cardiovasc Revasc Med. 2020;21:621–628. 13.	 Debry N, Altes A, Vincent F, et al. Balloon aortic valvuloplasty for se­ vere aortic stenosis before urgent non-cardiac surgery. EuroIntervention. 2021;17:e680–e687. 14.	 Bansal A, Kumar A, Kalra A, et al. Temporal trends in the utilization and outcomes of balloon aortic valvuloplasty in the pre-transcatheter aortic valve implantation (TAVI) and TAVI eras. Am J Cardiol. 2022;180:91–98. 15.	 Sorrentino R, Santoro C, Bardi L, et al. Non-cardiac surgery in patients with

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incorporating commissural morphology and leaflet displacement to the prediction of outcome for patients undergoing percutaneous mitral valvulo­ plasty. Circulation. 2014;129:886–895. 2.	 Bouleti C, Iung B, Laouenan C, et al. Late results of percutaneous mitral commissurotomy up to 20 years: development and validation of a risk score predicting late functional results from a series of 912 patients. Circulation. 2012;125:2119–2127. 3.	 Meneguz-Moreno RA, Costa JR Jr, Gomes NL, et al. Very long term followup after percutaneous balloon mitral valvuloplasty. J Am Coll Cardiol Interv. 2018;11:1945–1952. 4.	 Rifaie O, Abdel-Dayem MK, Ramzy A, et al. Percutaneous mitral valvotomy versus closed surgical commissurotomy. Up to 15 years of follow-up of a prospective randomized study. J Cardiol. 2009;53:28–34. 5.	 Yang B, DeBenedictus C, Watt T, et al. The impact of concomitant pulmonary hypertension on early and late outcomes following surgery for mitral steno­ sis. J Thorac Cardiovasc Surg. 2016;152:394–400.e1. 6.	 Cardoso LF, Grinberg M, Pomerantzeff PM, et al. Comparison of open com­ missurotomy and balloon valvuloplasty in mitral stenosis. A five-year followup. Arq Bras Cardiol. 2004;83:248–252; 243–247. 7.	 Cotrufo M, Renzulli A, Ismeno G, et al. Percutaneous mitral commissurotomy versus open mitral commissurotomy: a comparative study. Eur J Cardiotho­ rac Surg. 1999;15:646–651; discussion 651–652. 8.	 Song JK, Kim MJ, Yun SC, et al. Long-term outcomes of percutaneous mitral balloon valvuloplasty versus open cardiac surgery. J Thorac Cardiovasc Surg. 2010;139:103–110. 9.	 Arora R, Nair M, Kalra GS, et al. Immediate and long-term results of balloon and surgical closed mitral valvotomy: a randomized comparative study. Am Heart J. 1993;125:1091–1094. 10.	 Ben Farhat M, Ayari M, Maatouk F, et al. Percutaneous balloon versus surgi­ cal closed and open mitral commissurotomy: seven-year follow-up results of a randomized trial. Circulation. 1998;97:245–250. 11.	 Patel JJ, Shama D, Mitha AS, et al. Balloon valvuloplasty versus closed com­ missurotomy for pliable mitral stenosis: a prospective hemodynamic study. J Am Coll Cardiol. 1991;18:1318–1322. 12.	 Reyes VP, Raju BS, Wynne J, et al. Percutaneous balloon valvuloplasty com­ pared with open surgical commissurotomy for mitral stenosis. N Engl J Med. 1994;331:961–967. 13.	 Turi ZG, Reyes VP, Raju BS, et al. Percutaneous balloon versus surgical closed commissurotomy for mitral stenosis. A prospective, randomized trial. Circulation. 1991;83:1179–1185. 14.	 Reichart DT, Sodian R, Zenker R, et al. Long-term (</= 50 years) results of patients after mitral valve commissurotomy-a single-center experience. J Thorac Cardiovasc Surg. 2012;143:S96–S98. 15.	 Bouleti C, Iung B, Himbert D, et al. Relationship between valve calcification and long-term results of percutaneous mitral commissurotomy for rheumat­ ic mitral stenosis. Circ Cardiovasc Interv. 2014;7:381–389. 16.	 Cannan CR, Nishimura RA, Reeder GS, et al. Echocardiographic as­ sessment of commissural calcium: a simple predictor of outcome after percutaneous mitral balloon valvotomy. J Am Coll Cardiol. 1997;29:175– 180. 17.	 El Sabbagh A, Reddy YNV, Barros-Gomes S, et al. Low-gradient severe mi­ tral stenosis: hemodynamic profiles, clinical characteristics, and outcomes. J Am Heart Assoc. 2019;8:e010736. 18.	 Saggu DK, Narain VS, Dwivedi SK, et al. Effect of ivabradine on heart rate and duration of exercise in patients with mild-to-moderate mitral steno­ sis: a randomized comparison with metoprolol. J Cardiovasc Pharmacol. 2015;65:552–554. 19.	 Parakh N, Chaturvedi V, Kurian S, et al. Effect of ivabradine vs atenolol on heart rate and effort tolerance in patients with mild to moderate mitral ste­ nosis and normal sinus rhythm. J Card Fail. 2012;18:282–288. 20.	 Agrawal V, Kumar N, Lohiya B, et al. Metoprolol vs ivabradine in patients with mitral stenosis in sinus rhythm. Int J Cardiol. 2016;221:562–566. 21.	 Rajesh GN, Sajeer K, Sajeev CG, et al. A comparative study of ivabradine and atenolol in patients with moderate mitral stenosis in sinus rhythm. Indian Heart J. 2016;68:311–315. 22.	 Esteves CA, Munoz JS, Braga S, et al. Immediate and long-term followup of percutaneous balloon mitral valvuloplasty in pregnant patients with rheumatic mitral stenosis. Am J Cardiol. 2006;98:812–816. 23.	 Nercolini DC, da Rocha Loures Bueno R, Eduardo Guerios E, et al. Percu­

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patient with valvular heart disease undergoing noncardiac surgery. Semin Cardiothorac Vasc Anesth. 2008;12:33–59. 6.4.4. Previous Transcatheter Aortic Valve Implantation or Mitral Valve Transcatheter Edge-to Edge Repair 1.	 Omoto T, Aoki A, Maruta K, et al. Influence of transcatheter aortic valve

replacement on patients with severe aortic stenosis undergoing non-cardiac surgery. J Cardiothorac Surg. 2020;15:198. 2.	 Okuno T, Yahagi K, Horiuchi Y, et al. The role of transcatheter aortic valve replacement in the patients with severe aortic stenosis requiring major noncardiac surgery. Cardiovasc Interv Ther. 2019;34:345–351. 3.	 Okuno T, Demirel C, Tomii D, et al. Risk and timing of noncardiac sur­ gery after transcatheter aortic valve implantation. JAMA Netw Open. 2022;5:e2220689. 4.	 Kalbacher D, Schafer U, RS VB, et al. Long-term outcome, survival and predictors of mortality after MitraClip therapy: results from the German Transcatheter Mitral Valve Interventions (TRAMI) registry. Int J Cardiol. 2019;277:35–41. 5.	 Hohmann C, Ludwig M, Walker J, et al. Real-world anticoagulatory treatment after percutaneous mitral valve repair using MitraClip: a retrospective, observational study on 1300 patients. Clin Res Cardiol. 2022;111:889–899. 6.	 Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS guidelines for the management of valvular heart disease. Eur Heart J. 2022;43:561–632. 7.	 Brouwer J, Nijenhuis VJ, Delewi R, et al. Aspirin with or without clopi­ dogrel after transcatheter aortic-valve implantation. N Engl J Med. 2020;383:1447–1457. 8.	 Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143:e72– e227. 9.	 Maisano F, Franzen O, Baldus S, et al. Percutaneous mitral valve inter­

ventions in the real world: early and 1-year results from the ACCESS- EU, a prospective, multicenter, nonrandomized post-approval study of the MitraClip therapy in Europe. J Am Coll Cardiol. 2013;62:1052–1061. 6.5. Atrial Fibrillation 1.	 Gundlund A, Kumler T, Bonde AN, et al. Comparative thromboembolic risk in atrial fibrillation with and without a secondary precipitant-Danish nationwide cohort study. BMJ Open. 2019;9:e028468. 2.	 Arrigo M, Jaeger N, Seifert B, et al. Disappointing success of electrical car­ dioversion for new-onset atrial fibrillation in cardiosurgical ICU patients. Crit Care Med. 2015;43:2354–2359. 3.	 Siontis KC, Gersh BJ, Weston SA, et al. Associations of atrial fibrillation after noncardiac surgery with stroke, subsequent arrhythmia, and death: a cohort study. Ann Intern Med. 2022;175:1065–1072. 4.	 Butt JH, Olesen JB, Havers-Borgersen E, et al. Risk of thromboembolism associated with atrial fibrillation following noncardiac surgery. J Am Coll Car­ diol. 2018;72:2027–2036. 5.	 Elharram M, Samuel M, AlTurki A, et al. Anticoagulant use and the risk of thromboembolism and bleeding in postoperative atrial fibrillation after non­ cardiac surgery. Can J Cardiol. 2021;37:391–399. 6.	 Lin MH, Kamel H, Singer DE, et al. Perioperative/postoperative atrial fibrilla­ tion and risk of subsequent stroke and/or mortality. Stroke. 2019;50:1364– 1371. 7.	 Abdelmoneim SS, Rosenberg E, Meykler M, et al. The incidence and natural progression of new-onset postoperative atrial fibrillation. JACC Clin Electro­ physiol. 2021;7:1134–1144. 8.	 Charitos EI, Herrmann FEM, Ziegler PD. Atrial fibrillation recurrence and spontaneous conversion to sinus rhythm after cardiac surgery: insights from 426 patients with continuous rhythm monitoring. J Cardiovasc Electrophysiol. 2021;32:2171–2178. 9.	 El-Chami MF, Merchant FM, Smith P, et al. Management of new-onset postoperative atrial fibrillation utilizing insertable cardiac monitor technol­ ogy to observe recurrence of AF (MONITOR-AF). Pacing Clin Electrophysiol. 2016;39:1083–1089. 10.	 Sanna T, Diener HC, Passman RS, et al. Cryptogenic stroke and atrial fibril­ lation. N Engl J Med. 2014;371:1261. 11.	 Ha ACT, Verma S, Mazer CD, et al. Effect of continuous electrocardiogram monitoring on detection of undiagnosed atrial fibrillation after hospital­ ization for cardiac surgery: a randomized clinical trial. JAMA Netw Open. 2021;4:e2121867. 12.	 Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS

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able continuous ECG monitoring patch on detection of undiagnosed atrial fibrillation: the mSToPS randomized clinical trial. JAMA. 2018;320:146– 155. 6.6. Cardiovascular Implantable Electronic Devices 1.	 Schulman PM, Rozner MA. Case report: use caution when applying magnets to pacemakers or defibrillators for surgery. Anesth Analg. 2013;117:422– 427. 2.	 Costelloe CM, Murphy WA Jr, Gladish GW, et al. Radiography of pace­ makers and implantable cardioverter defibrillators. AJR Am J Roentgenol. 2012;199:1252–1258. 3.	 Navas-Blanco JR, Williams DV, Modak RK. Analyzing the impact of pre­ operative interrogation of cardiac implantable electronic devices. Ann Card Anaesth. 2021;24:447–451. 4.	 Mahlow WJ, Craft RM, Misulia NL, et al. A perioperative management al­ gorithm for cardiac rhythm management devices: the PACED-OP protocol. Pacing Clin Electrophysiol. 2013;36:238–248. 5.	 Rooke GA, Lombaard SA, Van Norman GA, et al. Initial experience of an anesthesiology-based service for perioperative management of pace­ makers and implantable cardioverter defibrillators. Anesthesiology. 2015;123:1024–1032. 6.	 Ellis MKM, Treggiari MM, Robertson JM, et al. Process improvement ini­ tiative for the perioperative management of patients with a cardiovascular implantable electronic device. Anesth Analg. 2017;125:58–65. 7.	 Wong DT, Middleton W. Electrocautery-induced tachycardia in a rateresponsive pacemaker. Anesthesiology. 2001;94:710–711. 8.	 Gifford J, Larimer K, Thomas C, et al. Randomized controlled trial of periop­ erative ICD management: magnet application versus reprogramming. Pac­ ing Clin Electrophysiol. 2014;37:1219–1224. 9.	 Schulman PM, Treggiari MM, Yanez ND, et al. Electromagnetic interference with protocolized electrosurgery dispersive electrode positioning in patients with implantable cardioverter defibrillators. Anesthesiology. 2019;130:530– 540. 10.	 Hauser RG, Kallinen L. Deaths associated with implantable cardioverter de­

fibrillator failure and deactivation reported in the United States Food and Drug Administration Manufacturer and User Facility Device Experience Da­ tabase. Heart Rhythm. 2004;1:399–405. 11.	 Reddy VY, Exner DV, Cantillon DJ, et al. Percutaneous implantation of an

entirely intracardiac leadless pacemaker. N Engl J Med. 2015;373:1125– 1135. 12.	 McFaul CM, Lombaard S, Arora V, et al. Unexpected shocks from a subcu­ taneous implantable cardioverter-defibrillator despite attempted reprogram­ ming and magnet use: a case report. A A Pract. 2020;14:e01178. 13.	 Neubauer H, Wellmann M, Herzog-Niescery J, et al. Comparison of periop­ erative strategies in ICD patients: the Perioperative ICD Management study (PIM study). Pacing Clin Electrophysiol. 2018;41:1536–1542. 14.	 Friedman H, Higgins JV, Ryan JD, et al. Predictors of intraoperative electrosurgery-induced implantable cardioverter defibrillator (ICD) detec­ tion. J Interv Card Electrophysiol. 2017;48:21–26. 15.	 Ip JE, Liu TJ, Chen CL, et al. Asystole during pacemaker magnet application. Pacing Clin Electrophysiol. 2017;40:1176–1179. 16.	 Crossley GH, Poole JE, Rozner MA, et al. The Heart Rhythm Society (HRS)/ American Society of Anesthesiologists (ASA) expert consensus statement on the perioperative management of patients with implantable defibrillators, pacemakers and arrhythmia monitors: facilities and patient management this document was developed as a joint project with the American Society of Anesthesiologists (ASA), and in collaboration with the American Heart As­ sociation (AHA), and the Society of Thoracic Surgeons (STS). Heart Rhythm. 2011;8:1114–1154. 17.	 Jaiyeola C, Chen AY, Kalarickal PL, et al. An unexpected magnet response of a Biotronik pacemaker in automatic mode: a case report. A A Pract. 2022;16:e01617. 18.	 Tully BW, Gerstein NS, Schulman PM. Electromagnetic interference with an underbody dispersive electrode in a patient with an implantable cardioverter-defibrillator undergoing noncardiac surgery: a case report. A A Pract. 2020;14:e01285. 19.	 Karuppiah S, Prielipp R, Banik RK. Anesthetic consideration for patients

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vention of stroke in patients with stroke and transient ischemic attack: a guideline from the American Heart Association/American Stroke Associa­ tion. Stroke. 2021;52:e364–e467. 6.8. Obstructive Sleep Apnea 1.	 Devaraj U, Rajagopala S, Kumar A, et al. Undiagnosed obstructive sleep apnea and postoperative outcomes: a prospective observational study. Res­ piration. 2017;94:18–25. 2.	 Wang S, Li S, Zhao Y, et al. Preoperative screening of patients at high risk of obstructive sleep apnea and postoperative complications: a systematic review and meta-analysis. J Clin Anesth. 2022;79:110692. 3.	 Chan MTV, Wang CY, Seet E, et al. Association of unrecognized obstructive sleep apnea with postoperative cardiovascular events in patients undergo­ ing major noncardiac surgery. JAMA. 2019;321:1788–1798. 4.	 Yeghiazarians Y, Jneid H, Tietjens JR, et al. Obstructive sleep apnea and cardiovascular disease: a scientific statement from the American Heart As­ sociation. Circulation. 2021;144:E56–E67. 5.	 Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea: types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol. 2017;69:841–858. 6.	 Ng KT, Lee ZX, Ang E, et al. Association of obstructive sleep apnea and postoperative cardiac complications: a systematic review and meta-analysis with trial sequential analysis. J Clin Anesth. 2020;62:109731. 7.	 Sun X, Yu J, Luo J, et al. Meta-analysis of the association between ob­

structive sleep apnea and postoperative complications. Sleep Med. 2022;91:1–11.

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7.1 Statins 1.	 Lindenauer PK, Pekow P, Wang K, et al. Lipid-lowering therapy and in-

hospital mortality following major noncardiac surgery. JAMA. 2004;291:2092–2099. 2.	 Berwanger O, Le Manach Y, Suzumura EA, et al. Association between pre-operative statin use and major cardiovascular complications among patients undergoing non-cardiac surgery: the VISION study. Eur Heart J. 2016;37:177–185. 3.	 London MJ, Schwartz GG, Hur K, et al. Association of perioperative statin use with mortality and morbidity after major noncardiac surgery. JAMA Intern Med. 2017;177:231–242. 4.	 Durazzo AE, Machado FS, Ikeoka DT, et al. Reduction in cardiovascular events after vascular surgery with atorvastatin: a randomized trial. J Vasc Surg. 2004;39:967–975. discussion 975–976. 5.	 Yu W, Wang B, Zhan B, et al. Statin therapy improved long-term prognosis in patients with major non-cardiac vascular surgeries: a systematic review and meta-analysis. J Vasc Surg. 2018;68:1608. 6.	 Kertai MD, Boersma E, Westerhout CM, et al. A combination of statins and beta-blockers is independently associated with a reduction in the incidence of perioperative mortality and nonfatal myocardial infarction in patients un­ dergoing abdominal aortic aneurysm surgery. Eur J Vasc Endovasc Surg. 2004;28:343–352. 7.	 Raju MG, Pachika A, Punnam SR, et al. Statin therapy in the reduction of cardiovascular events in patients undergoing intermediate-risk noncardiac, nonvascular surgery. Clin Cardiol. 2013;36:456–461. 8.	 Putzu A, de Carvalho e Silva CMPD, de Almeida JP, et al. Perioperative statin therapy in cardiac and non-cardiac surgery: a systematic review and metaanalysis of randomized controlled trials. Ann Intensive Care. 2018;8:95. 9.	 Dunkelgrun M, Boersma E, Schouten O, et al. Bisoprolol and fluvastatin for the reduction of perioperative cardiac mortality and myocardial infarction in intermediate-risk patients undergoing noncardiovascular surgery: a ran­ domized controlled trial (DECREASE-IV). Ann Surg. 2009;249:921–926. 10.	 Berwanger O, de Barros ESPG, Barbosa RR, et al. Atorvastatin for highrisk statin-naive patients undergoing noncardiac surgery: the Lowering the Risk of Operative Complications Using Atorvastatin Loading Dose (LOAD) randomized trial. Am Heart J. 2017;184:88–96. 11.	 Xia J, Qu Y, Shen H, et al. Patients with stable coronary artery disease re­ ceiving chronic statin treatment who are undergoing noncardiac emergency surgery benefit from acute atorvastatin reload. Cardiology. 2014;128:285– 292. 12.	 Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/

ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the man­ agement of blood cholesterol: a report of the American College of Cardiol­ ogy/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139:e1046–e1081. 7.2. Renin-Angiotensin-Aldosterone System Inhibitors 1.	 Shiffermiller JF, Monson BJ, Vokoun CW, et al. Prospective randomized eval­ uation of preoperative angiotensin-converting enzyme inhibition (PREOP- ACEI). J Hosp Med. 2018;13:661–667. 2.	 Hollmann C, Fernandes NL, Biccard BM. A systematic review of outcomes associated with withholding or continuing angiotensin-converting enzyme inhibitors and angiotensin receptor blockers before noncardiac surgery. Anesth Analg. 2018;127:678–687. 3.	 Coriat P, Richer C, Douraki T, et al. Influence of chronic angiotensinconverting enzyme inhibition on anesthetic induction. Anesthesiology. 1994;81:299–307. 4.	 Bertrand M, Godet G, Meersschaert K, et al. Should the angiotensin II an­

tagonists be discontinued before surgery? Anesth Analg. 2001;92:26–30. 5 Schirmer U, Schurmann W. [Preoperative administration of angiotensin-

converting enzyme inhibitors]. Anaesthesist. 2007;56:557–561. 6.	 Ackland GL, Patel A, Abbott TEF, et al. Discontinuation vs. continuation of renin-angiotensin system inhibition before non-cardiac surgery: the SPACE trial. Eur Heart J. 2023;ehad716. 7.	 Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guide­ line for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Prac­ tice Guidelines. Circulation. 2022;145:e895–e1032. 8.	 Wesselink EM, Wagemakers SH, van Waes JAR, et al. Associations be­ tween intraoperative hypotension, duration of surgery and postoperative myocardial injury after noncardiac surgery: a retrospective single-centre cohort study. Br J Anaesth. 2022;129:487–496. 9.	 Ling Q, Gu Y, Chen J, et al. Consequences of continuing renin angiotensin aldosterone system antagonists in the preoperative period: a systematic re­ view and meta-analysis. BMC Anesthesiol. 2018;18:26. 10.	 Misra S, Parida S, Sahajanandan R, et al. The effect of continuing versus withholding angiotensin-converting enzyme inhibitors/angiotensin II recep­ tor blockers on mortality and major adverse cardiovascular events in hyper­ tensive patients undergoing elective non-cardiac surgery: study protocol for a multi-centric open-label randomised controlled trial. Trials. 2022;23:670. 11.	 Legrand M, Futier E, Leone M, et al. Impact of renin-angiotensin system in­ hibitors continuation versus discontinuation on outcome after major surgery: protocol of a multicenter randomized, controlled trial (STOP-or-NOT trial). Trials. 2019;20:160. 12.	 Marcucci M, Painter TW, Conen D, et al. Hypotension-avoidance versus

hypertension-avoidance strategies in noncardiac surgery: an international randomized controlled trial (POISE-3). Ann Intern Med. 2023;176:605–614.

7.3. Calcium Channel Blockers 1.	 Wijeysundera DN, Beattie WS. Calcium channel blockers for reducing cardiac morbidity after noncardiac surgery: a meta-analysis. Anesth Analg. 2003;97:634–641. 2.	 Lin Y, Ma L. Blood pressure lowering effect of calcium channel blockers on perioperative hypertension: a systematic review and meta-analysis. Medicine (Baltimore). 2018;97:e13152. 3.	 Duncan D, Sankar A, Beattie WS, et al. Alpha-2 adrenergic agonists for

the prevention of cardiac complications among adults undergoing surgery. Cochrane Database Syst Rev. 2018;3:CD004126.

7.4. Alpha-2 Receptor Agonists 1.	 Devereaux PJ, Sessler DI, Leslie K, et al. Clonidine in patients undergoing noncardiac surgery. N Engl J Med. 2014;370:1504–1513. 2.	 Martin PR, Ebert MH, Gordon EK, et al. Catecholamine metabolism during clonidine withdrawal. Psychopharmacology (Berl). 1984;84:58–63. 3.	 Duncan D, Sankar A, Beattie WS, et al. Alpha-2 adrenergic agonists for

the prevention of cardiac complications among adults undergoing surgery. Cochrane Database Syst Rev. 2018;3:CD004126. 7.5. Antiplatelet Therapy and Timing of Noncardiac Surgery in Patients With Coronary Artery Disease 1.	 Cao D, Chandiramani R, Capodanno D, et al. Non-cardiac surgery in patients with coronary artery disease: risk evaluation and periprocedural manage­ ment. Nat Rev Cardiol. 2021;18:37–57. 2.	 Childers CP, Maggard-Gibbons M, Ulloa JG, et al. Perioperative man­ agement of antiplatelet therapy in patients undergoing non-cardiac sur­ gery following coronary stent placement: a systematic review. Syst Rev. 2018;7:4. 3.	 Graham LA, Hollis RH, Richman JS, et al. Frequency of surgery cancella­ tions associated with myocardial infarction or death 6 months after coronary stent placement. JAMA Surg. 2015;150:1199–1201. 4.	 Rossini R, Tarantini G, Musumeci G, et al. A multidisciplinary approach on the perioperative antithrombotic management of patients with coronary stents undergoing surgery: surgery after stenting 2. J Am Coll Cardiol Intv. 2018;11:417–434. 5.	 Smilowitz NR, Lorin J, Berger JS. Risks of noncardiac surgery early after percutaneous coronary intervention. Am Heart J. 2019;217:64–71. 6.	 Wijeysundera DN, Wijeysundera HC, Yun L, et al. Risk of elective major noncardiac surgery after coronary stent insertion: a population-based study. Circulation. 2012;126:1355–1362. 7.	 Kim C, Kim JS, Kim H, et al. Consensus decision-making for the manage­

ment of antiplatelet therapy before non-cardiac surgery in patients who underwent percutaneous coronary intervention with second-generation drug-eluting stents: a cohort study. J Am Heart Assoc. 2021;10:e020079.

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and mortality after major noncardiac surgery. N Engl J Med. 2005;353:349– 361. 7.8. Perioperative Management of Blood Glucose 1.	 Han HS, Kang SB. Relations between long-term glycemic control and post­ operative wound and infectious complications after total knee arthroplasty in type 2 diabetics. Clin Orthop Surg. 2013;5:118–123. 2.	 Underwood P, Askari R, Hurwitz S, et al. Preoperative A1C and clinical out­ comes in patients with diabetes undergoing major noncardiac surgical pro­ cedures. Diabetes Care. 2014;37:611–616. 3.	 Godshaw BM, Ojard CA, Adams TM, et al. Preoperative glycemic control predicts perioperative serum glucose levels in patients undergoing total joint arthroplasty. J Arthroplasty. 2018;33:S76–S80. 4.	 van den Boom W, Schroeder RA, Manning MW, et al. Effect of A1C and glucose on postoperative mortality in noncardiac and cardiac surgeries. Dia­ betes Care. 2018;41:782–788. 5.	 ElSayed NA, Aleppo G, Aroda VR, et al. Diabetes care in the hospital: stan­ dards of care in diabetes, 2023. Diabetes Care. 2023;46:S267–S278. 6.	 Kuzulugil D, Papeix G, Luu J, et al. Recent advances in diabetes treatments and their perioperative implications. Curr Opin Anaesthesiol. 2019;32:398– 404. 7.	 Thiruvenkatarajan V, Meyer EJ, Nanjappa N, et al. Perioperative diabetic ketoacidosis associated with sodium-glucose co-transporter-2 inhibitors: a systematic review. Br J Anaesth. 2019;123:27–36. 8.	 Charytan DM, Solomon SD, Ivanovich P, et al. Metformin use and cardiovas­ cular events in patients with type 2 diabetes and chronic kidney disease. Diabetes Obes Metab. 2019;21:1199–1208. 9.	 Aharaz A, Pottegard A, Henriksen DP, et al. Risk of lactic acidosis in type 2 diabetes patients using metformin: a case control study. PLoS One. 2018;13:e0196122. 10.	 Rena G, Lang CC. Repurposing metformin for cardiovascular disease. Circu­ lation. 2018;137:422–424. 11.	 Loi H, Boal F, Tronchere H, et al. Metformin protects the heart against hy­ pertrophic and apoptotic remodeling after myocardial infarction. Front Phar­ macol. 2019;10:154. 12.	 Younis A, Eskenazi D, Goldkorn R, et al. The addition of vildagliptin to met­ formin prevents the elevation of interleukin 1ss in patients with type 2 dia­ betes and coronary artery disease: a prospective, randomized, open-label study. Cardiovasc Diabetol. 2017;16:69. 13.	 US Food and Drug Administration. FDA revises lables of SGLT2 in­ hibitors for diabetes to include warnings about too much acid in the blood and serious urinary tract infections. Accessed October 16, 2022. https://www.fda.gov/drugs/drug-safety-and-availability/fda-reviseslabels-sglt2-inhibitors-diabetes-include-warnings-about-too-muchacid-blood-and-serious 14.	 DHHS. Centers for Disease Control and Prevention: national diabetes sta­ tistics report, 2020. 2022. Accessed January 7, 2023. https://www.cdc. gov/diabetes/data/statistics-report/index.html. 15.	 Duggan EW, Carlson K, Umpierrez GE. Perioperative hyperglycemia man­ agement: an update. Anesthesiology. 2017;126:547–560. 16.	 Todd LA, Vigersky RA. Evaluating perioperative glycemic control of non-cardiac surgical patients with diabetes. Mil Med. 2021;186:e867– e872. 17.	 Halperin I, Malcolm J, Moore S, et al. Suggested Canadian standards for perioperative/periprocedure glycemic management in patients with type 1 and type 2 diabetes. Can J Diabetes. 2022;46:99–107.e105. 18.	 American Society of Anesthesiologists Task Force on Preoperative Fast­ ing. Consensus based guidance on preoperative management of patients (adults and children) on glucagon-like peptide-1 (GLP-1) receptor agonists. Accessed January 15, 2024. https://www.asahq.org/about-asa/news­ room/news-releases/2023/06/american-society-of-anesthesiologistsconsensus-based-guidance-on-preoperative 19.	 Alexanian SM, McDonnell ME, Akhtar S. Creating a perioperative glycemic control program. Anesthesiol Res Pract. 2011;2011:465974. 20.	 Noordzij PG, Boersma E, Schreiner F, et al. Increased preoperative glucose levels are associated with perioperative mortality in patients undergoing noncardiac, nonvascular surgery. Eur J Endocrinol. 2007;156:137–142. 21.	 Abdelmalak BB, Knittel J, Abdelmalak JB, et al. Preoperative blood glucose

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22 Patoulias D, Manafis A, Mitas C, et al. Sodium-glucose cotransporter 2 in­

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cose control in type 2 diabetes. N Engl J Med. 2008;359:1577–1589. 8.1. Choice of Anesthetic Technique and Agent 1.	 Lindholm EE, Aune E, Noren CB, et al. The anesthesia in abdominal aortic surgery (ABSENT) study: a prospective, randomized, controlled trial compar­ ing troponin T release with fentanyl-sevoflurane and propofol-remifentanil anesthesia in major vascular surgery. Anesthesiology. 2013;119:802–812. 2.	 Lurati Buse GA, Schumacher P, Seeberger E, et al. Randomized comparison of sevoflurane versus propofol to reduce perioperative myocardial ischemia in patients undergoing noncardiac surgery. Circulation. 2012;126:2696– 2704. 3.	 Zhang Y, Lin W, Shen S, et al. Randomized comparison of sevoflurane versus propofol-remifentanil on the cardioprotective effects in elderly patients with coronary heart disease. BMC Anesthesiol. 2017;17:104. 4.	 Bisgaard J, Torp-Pedersen C, Rasmussen BS, et al. Regional versus gen­ eral anaesthesia in peripheral vascular surgery: a propensity score matched nationwide cohort study of 17359 procedures in Denmark. Eur J Vasc En­ dovasc Surg. 2021;61:430–438. 5.	 Neuman MD, Feng R, Carson JL, et al. Spinal anesthesia or general anes­ thesia for hip surgery in older adults. N Engl J Med. 2021;385:2025–2035. 6.	 Pisansky AJB, Brovman EY, Kuo C, et al. Perioperative outcomes after re­ gional versus general anesthesia for above the knee amputations. Ann Vasc Surg. 2018;48:53–66. 7.	 Holse C, Aasvang EK, Vester-Andersen M, et al. Hyperoxia and antioxidants for myocardial injury in noncardiac surgery: a 2 × 2 factorial, blinded, ran­ domized clinical trial. Anesthesiology. 2022;136:408–419. 8.	 Reiterer C, Kabon B, Taschner A, et al. Perioperative supplemental oxygen and NT-proBNP concentrations after major abdominal surgery: a prospec­ tive randomized clinical trial. J Clin Anesth. 2021;73:110379. 9.	 Ruetzler K, Cohen B, Leung S, et al. Supplemental intraoperative oxygen does not promote acute kidney injury or cardiovascular complications after noncardiac surgery: subanalysis of an alternating intervention trial. Anesth Analg. 2020;130:933–940. 10.	 Landoni G, Fochi O, Bignami E, et al. Cardiac protection by volatile anes­ thetics in non-cardiac surgery? A meta-analysis of randomized controlled studies on clinically relevant endpoints. HSR Proc Intensive Care Cardiovasc Anesth. 2009;1:34–43. 11.	 Zangrillo A, Testa V, Aldrovandi V, et al. Volatile agents for cardiac protection in noncardiac surgery: a randomized controlled study. J Cardiothorac Vasc Anesth. 2011;25:902–907. 12.	 Van Waesberghe J, Stevanovic A, Rossaint R, et al. General vs. neuraxial

anaesthesia in hip fracture patients: a systematic review and meta-analysis. BMC Anesthesiol. 2017;17:87. 8.2. Pain Management 1.	 Guay J, Kopp S. Epidural pain relief versus systemic opioid-based pain relief for abdominal aortic surgery. Cochrane Database Syst Rev. 2016;CD005059. 2.	 Mohamad MF, Mohammad MA, Hetta DF, et al. Thoracic epidural analgesia reduces myocardial injury in ischemic patients undergoing major abdominal cancer surgery. J Pain Res. 2017;10:887–895. 3.	 Choi JV, Cheung RM, Mozel MR, et al. Perioperative outcomes after preop­ erative epidural analgesia in patients with hip fracture undergoing surgical repair: a systematic review. Pain Med. 2022;23:234–245. 4.	 Sandoval Y, Jaffe AS. Type 2 myocardial infarction: JACC review topic of the week. J Am Coll Cardiol. 2019;73:1846–1860. 5.	 Ljungqvist O, de Boer HD, Balfour A, et al. Opportunities and challenges for the next phase of enhanced recovery after surgery: a review. JAMA Surg. 2021;156:775–784. 6.	 Verret M, Lauzier F, Zarychanski R, et al. Perioperative use of gabapenti­ noids for the management of postoperative acute pain: a systematic review and meta-analysis. Anesthesiology. 2020;133:265–279. 7.	 Hah J, Mackey SC, Schmidt P, et al. Effect of perioperative gabapentin on postoperative pain resolution and opioid cessation in a mixed surgical co­ hort: a randomized clinical trial. JAMA Surg. 2018;153:303–311. 8.	 Park CM, Inouye SK, Marcantonio ER, et al. Perioperative gabapentin use

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esophageal echocardiography during intraoperative cardiac arrest in non­ cardiac surgery. Anesth Analg. 2006;102:1653–1657. 2.	 Shillcutt SK, Markin NW, Montzingo CR, et al. Use of rapid “rescue” peri­ operative echocardiography to improve outcomes after hemodynamic instability in noncardiac surgical patients. J Cardiothorac Vasc Anesth. 2012;26:362–370. 3.	 Navas-Blanco JR, Louro J, Reynolds J, et al. Intraoperative focused car­ diac ultrasound for assessment of hypotension: a systematic review. Anesth Analg. 2021;133:852–859. 4.	 Markin NW, Coker BJ, Tuck BC, et al. Focused cardiac ultrasound in the operating room: another important tool for the assessment of the unstable patient. Anesth Analg. 2021;133:848–851. 5.	 Eisenberg MJ, London MJ, Leung JM, et al. Monitoring for myocardial isch­ emia during noncardiac surgery. A technology assessment of transesopha­ geal echocardiography and 12-lead electrocardiography. The Study of Perioperative Ischemia Research Group. JAMA. 1992;268:210–216. 6.	 London MJ, Tubau JF, Wong MG, et al. The “natural history” of segmental wall motion abnormalities in patients undergoing noncardiac surgery. S.P.I. Research Group. Anesthesiology. 1990;73:644–655. 7.	 De Marchi L, Wang CJ, Skubas NJ, et al. Safety and benefit of transesopha­ geal echocardiography in liver transplant surgery: a position paper from the Society for the Advancement of Transplant Anesthesia (SATA). Liver Transpl. 2020;26:1019–1029. 8.	 Task Force on Transesophageal Echocardiography. Practice guidelines for perioperative transesophageal echocardiography. An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists. Anesthesiology. 2010;112:1084–1096. 9.	 Michelena HI, Abel MD, Suri RM, et al. Intraoperative echocardiography in valvular heart disease: an evidence-based appraisal. Mayo Clin Proc. 2010;85:646–655. 10.	 Hahn RT, Abraham T, Adams MS, et al. Guidelines for performing a com­ prehensive transesophageal echocardiographic examination: recommenda­ tions from the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26:921– 964. 11.	 Reeves ST, Finley AC, Skubas NJ, et al. Basic perioperative transesophageal echocardiography examination: a consensus statement of the American So­ ciety of Echocardiography and the Society of Cardiovascular Anesthesiolo­ gists. J Am Soc Echocardiogr. 2013;26:443–456. 12.	 Spencer KT, Kimura BJ, Korcarz CE, et al. Focused cardiac ultrasound: rec­ ommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2013;26:567–581. 13.	 Via G, Hussain A, Wells M, et al. International evidence-based recommenda­ tions for focused cardiac ultrasound. J Am Soc Echocardiogr. 2014;27:683. e681–683.e633. 14.	 Bilotta F, Tempe DK, Giovannini F, et al. Perioperative transoesophageal echocardiography in noncardiac surgery. Ann Card Anaesth. 2006;9:108– 113. 15.	 Fayad A, Shillcutt S, Meineri M, et al. Comparative effectiveness and harms of intraoperative transesophageal echocardiography in noncardiac surgery: a systematic review. Semin Cardiothorac Vasc Anesth. 2018;22:122–136. 16.	 Mahmood F, Shernan SK. Perioperative transoesophageal echocardiogra­ phy: current status and future directions. Heart. 2016;102:1159–1167. 17.	 Fayad A, Shillcutt SK. Perioperative transesophageal echocardiography for non-cardiac surgery. Can J Anaesth. 2018;65:381–398. 18.	 Cote G, Denault A. Transesophageal echocardiography-related complica­ tions. Can J Anaesth. 2008;55:622–647. 19.	 Kallmeyer IJ, Collard CD, Fox JA, et al. The safety of intraoperative trans­ esophageal echocardiography: a case series of 7200 cardiac surgical pa­ tients. Anesth Analg. 2001;92:1126–1130. 20.	 ACGME. ACGME program requirements for gradudate medical education in anesthesiology. Accessed March 15, 2024. https://www.acgme.org/glo­ balassets/pfassets/programrequirements/040_anesthesiology_2022.pdf. 21.	 ABA. Applied exam objective structured clinical examination content outline. American Board of Anesthesiology. https://www.theaba.org/pdfs/OSCE_ Content_Outline.pdf 22.	 American Society of Anesthesiologists and Society of Cardiovascular An­

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membrane oxygenation rescue in a patient with pulmonary hypertension presenting for revision total hip arthroplasty: a case report and narrative review. Cureus. 2022;14:e28234. 5.	 den Uil CA, Van Mieghem NM, M BB, et al. Primary intra-aortic balloon sup­

port versus inotropes for decompensated heart failure and low output: a randomised trial. EuroIntervention. 2019;15:586–593. 6.	 Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guide­ line for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Prac­ tice Guidelines. Circulation. 2022;145:e895–e1032. 7.	 Faerber G, Doenst T. Ventricular assist device-promoted recovery and tech­ nical aspects of explant. JTCVS Tech. 2021;7:182–188. 8.	 Umei N, Ichiba S, Ujike Y, et al. Successful application of venoarterialvenous extracorporeal membrane oxygenation in the reversal of severe car­ diorespiratory failure. BMJ Case Rep. 2015;2015:bcr2015209901. 9.	 Ge C, Liu J, Fu Y, et al. A case report of early application of veno-arterial extracorporeal membrane oxygenation in amniotic fluid embolism. Medicine (Baltimore). 2021;100:e27896. 10.	 Georgeson S, Coombs AT, Eckman MH. Prophylactic use of the intra-aortic balloon pump in high-risk cardiac patients undergoing noncardiac surgery: a decision analytic view. Am J Med. 1992;92:665–678. 11.	 Montisci A, Micheletto G, Sibilio S, et al. Impella 5.0 supported oncological surgery as bridge to LVAD. ESC Heart Fail. 2021;8:167–170. 12.	 Schmidt R, Kasper M, Gerula C, et al. Intra-aortic balloon pump prior to non­ cardiac surgery: a forgotten remedy? J Invasive Cardiol. 2011;23:E26–E30. 13.	 Samad K, Khan FA. The role of prophylactic intra-aortic balloon pump coun­ terpulsation (IABP) in emergency non-cardiac surgery. J Pak Med Assoc. 2006;56:42–43. 14.	 Millat MH, Cameron EW. Intra-aortic balloon pump in patients with isch­ aemic heart disease undergoing oesophagogastrectomy. Ir J Med Sci. 2003;172:177–179. 15.	 Samalavicius RS, Puodziukaite L, Radaviciute I, et al. Prophylactic use of an intra-aortic balloon pump in a high-risk patient with peripartum cardiomy­ opathy requiring cesarean delivery. Int J Obstet Anesth. 2018;33:67–71. 16.	 Ouyang D, Gulati G, Ha R, et al. Incidence of temporary mechanical circu­ latory support before heart transplantation and impact on post-transplant outcomes. J Heart Lung Transplant. 2018;37:1060–1066. 17.	 Kelly B, Carton E. Extended indications for extracorporeal membrane oxy­ genation in the operating room. J Intensive Care Med. 2020;35:24–33. 18.	 Foong TW, Ramanathan K, Chan KKM, et al. Extracorporeal membrane oxy­ genation during adult noncardiac surgery and perioperative emergencies: a narrative review. J Cardiothorac Vasc Anesth. 2021;35:281–297. 19.	 Koster AA, Pappalardo F, Silvetti S, et al. Cesarean section in a patient with non-compaction cardiomyopathy managed with ECMO. Heart Lung Vessel. 2013;5:183–186. 20.	 Chestovich PJ, Kwon MH, Cryer HG, et al. Surgical procedures for patients receiving mechanical cardiac support. Am Surg. 2011;77:1314–1317. 21.	 Eckhauser AE, Melvin WV, Sharp KW. Management of general surgical prob­ lems in patients with left ventricular assist devices. Am Surg. 2006;72:158– 161. 22.	 Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation guidelines for mechanical circu­ latory support: executive summary. J Heart Lung Transplant. 2013;32:157– 187. 23.	 Schmid C, Wilhelm M, Dietl KH, et al. Noncardiac surgery in patients with left ventricular assist devices. Surgery. 2001;129:440–444. 24.	 Stehlik J, Nelson DM, Kfoury AG, et al. Outcome of noncardiac surgery in patients with ventricular assist devices. Am J Cardiol. 2009;103:709–712. 25.	 Goldstein DJ, Mullis SL, Delphin ES, et al. Noncardiac surgery in longterm implantable left ventricular assist-device recipients. Ann Surg. 1995;222:203–207. 26.	 Kirklin JK, Pagani FD, Goldstein DJ, et al. American Association for Thoracic

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37 Glance LG, Dick AW, Mukamel DB, et al. Association between intraopera­

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coronary heart disease screening in kidney and liver transplantation

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Appendix 1. Author Relationships With Industry and Other Entities―2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery

Committee Member Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness Annemarie Thompson, Chair Duke University Hospital—Professor of Anesthesiology, Medicine, and Population Health Sciences; Director, Anesthesiology Residency Program, ASA Perioperative Medicine Education Track Chair, Division of Cardiothoracic Anesthesiology and Critical Care None None None None None None Kirsten E. Fleischmann, Vice Chair UCSF School of Medicine—Profes­ sor of Clinical Medicine; Assistant Chair of Medicine for Faculty Experi­ ence; Associate Chief of Cardiology for Faculty Experi­ ence; Medical Director, Adult Car­ diac Stress & ECG Laboratories, UCSF Health None None None NOT RELEVANT •	 ADA grant, PI* NOT RELEVANT •	 Massachusetts Medical Society •	 NIH, Co-I† •	 PCORI •	 UCSF Health, Medical Director ECG/Stress Lab† None Nathaniel R. Smilowitz, Vice Chair NYU Langone Health, NYU School of Medicine—As­ sistant Professor of Medicine, Inter­ ventional Cardiol­ ogy, The Leon H. Charney Division of Cardiology RELEVANT •	 Abbott† None None None NOT RELEVANT •	 Abiomed‡ •	 AHA/Sarah Ross Soter Center for Women’s Cardiovascular Research at NYU Grossman School of Medicine‡ •	 BioCardia‡ •	 DOD/University of Florida‡ •	 NHLBI/NIH‡ None Niti R. Aggarwal Mayo Clinic— Assistant Profes­ sor of Medicine, Consultant, Depart­ ment of Cardiovascular Disease None None None None None None Faraz S. Ahmad Northwestern University Feinberg School of Medi­ cine—Assistant Pro­ fessor of Medicine (Cardiology) NOT RELEVANT •	 Teladoc Livongo†

RELEVANT •	 Pfizer None NOT RELEVANT •	 Healthority* NOT RELEVANT •	 AHA† •	 Atman Health† •	 CDC† •	 Duke University School of Medicine† •	 NIH† •	 PCORI†

RELEVANT •	 Pfizer None None

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Committee Member Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness Robert B. Allen Juris Doctor heart surgery patient (septal myectomy); AHA volunteer-SW Region Board; Prior Chair, Corporate Operations Coordi­ nating Committee None None None None None None S. Elissa Altin Yale School of Medicine—Assistant Professor None None None RELEVANT •	 Boston Scientific NOT RELEVANT •	 Bard‡ •	 Cardiovascular Systems, Inc.‡ •	 MicroPort‡ None Andrew Auerbach UCSF, Division of Hospital Medi­ cine—Professor of Medicine None None NOT RELEVANT •	 ADviCE* •	 Kuretic* None NOT RELEVANT •	 AHRQ† •	 FDA† •	 NHLBI† •	 UpToDate† None Jeffrey S. Berger NYU School of Medicine—As­ sociate Professor of Medicine and Surgery; Director, Center for the Pre­ vention of Cardio­ vascular Disease RELEVANT •	 Amgen •	 Janssen Pharmaceuti­ cals† None None RELEVANT •	 Amgen None None Benjamin Chow University of Ottawa Heart Institute—Professor of Medicine (Cardi­ ology and Nuclear Medicine) and Radiology None None None NOT RELEVANT •	 TD Bank†

RELEVANT •	 Artrya† •	 Siemens* None None

Habib A. Dakik American University of Beirut Medical Center—Professor of Medicine, Chief of Cardiology None NOT RELEVANT •	 GE Healthcare None None None None Lisa de las Fuentes Washington Uni­ versity School of Medicine in St. Louis—Professor of Medicine and Bio­ statistics NOT RELEVANT •	 Acceleron •	 Aerovate •	 Altavant •	 Bayer •	 CVR Consulting† •	 Express Scripts •	 Gossamer •	 Impact PH† •	 Johnson & Johnson† •	 Liquidia •	 Merck •	 Sommetrics* •	 Vaderis •	 V-Wave •	 WebMD, LLC† NOT RELEVANT •	 Ferrer •	 Simply Speaking† None NOT RELEVANT •	 Acceleron† •	 Altavant† •	 Bayer† •	 Gossamer† •	 Johnson & Johnson† •	 Medtronic† •	 PhaseBio† •	 Respira† •	 Trio Analytics† •	 United Therapeutics† •	 University of Kentucky (DSMB)* •	 University of Toronto (DSMB)* •	 Vaderis† NOT RELEVANT •	 ACC* •	 AHA† •	 NIH† •	 PHA† NOT RELEVANT •	 Plaintiff, patent infringement (Johnson & Johnson), 2022†

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Committee Member Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness Eric L. Eisenstein Duke University— Associate Professor Emeritus in Medi­ cine; University of Victoria, Canada— Adjunct Associate Professor, School of Health Informa­ tion Science None None None NOT RELEVANT •	 Burroughs Wellcome Fund— Innovation in Regu­ latory Science† •	 Eunice Kennedy Shriver National Institute of Child Health and Human Development* •	 NCATS* •	 NHLBI* •	 NIH* NOT RELEVANT •	 EHR2EDC (Sanofi)† None Marie Gerhard- Hermann Harvard Medical School—Associate Professor None None None NOT RELEVANT •	 Progeria Research Foundation† NOT RELEVANT •	 ABIM, Cardiovascular Exam Committee •	 NIH, NCATS None Kamrouz Ghadimi Duke University School of Medi­ cine—Associate Professor, Anesthe­ siology & Critical Care; Director, Clinical Research Unit, Department of Anesthesiology None None None NOT RELEVANT •	 IARS† •	 Octapharma* •	 PCORI None None Bessie Kachulis Columbia University Medical Center— Professor of Anes­ thesiology; Director of Evidence Based Medicine, Cardiothoracic Anesthesiology None None None None None None Jacinthe Leclerc Université Laval— Scientist; Quebec Heart & Lung Insti­ tute—Adjunct Pro­ fessor of Pharmacy None None None None NOT RELEVANT •	 JSS Medical Research (DSMB) None Christopher S. Lee Boston College, William F. Connell School of Nurs­ ing—Barry Family/ Goldman Sachs Endowed Professor None None None NOT RELEVANT •	 NIH† None None Tracy E. Macaulay University of Ken­ tucky College of Pharmacy—Clinical Professor of Phar­ macy & Medicine None None None None None None Gail Mates AHA National Spokesperson, Go Red for Women; You’re the Cure Committee Mem­ ber; Health for Good Chair; Mis­ sion Board Member None None None None None None

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November 5, 2024 Circulation. 2024;150:e351–e442. DOI: 10.1161/CIR.0000000000001285 e438

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Committee Member Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness Geno J. Merli Thomas Jefferson University Sidney Kimmel Medical College—Profes­ sor, Co-Director, Jefferson Vascular Center; Thomas Jefferson University Hospital—Senior VP, Associate CMO NOT RELEVANT •	 LoweRisk, LLC* None None RELEVANT •	 Bristol Myers Squibb/Pfizer* None None Debabrata Mukherjee Texas Tech Univer­ sity Health Science Center El Paso— Chief, Cardiovascu­ lar Medicine; Chair­ man, Department of Internal Medicine NOT RELEVANT •	 ACC† None None None None None Purvi Par­ wani Loma Linda Uni­ versity Health—As­ sociate Professor of Medicine; Director, Echocardiography Laboratory RELEVANT •	 Medtronic RELEVANT •	 AstraZeneca None None NOT RELEVANT •	 SCMR None Jeanne E. Poole University of Wash­ ington—Professor of Medicine, Division of Cardiology None None None NOT RELEVANT •	 Boston Scientific (institutional research grant)

RELEVANT •	 AtriCure •	 Biotronik† •	 Kestra, Inc.† •	 Medtronic NOT RELEVANT •	 HRS† None

Michael W. Rich Washington Univer­ sity School of Medi­ cine—Professor of Medicine None None None None None None Kurt Ruetzler Cleveland Clinic— Assistant Professor of Anesthesiology, Department of Anesthesiology None None None None None None Steven C. Stain Lahey Hospital and Medical Center— Chair, Department of Surgery None None None None None None

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Committee Member Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness BobbieJean Sweitzer University of VA INOVA Health— Professor, Medical Education NOT RELEVANT •	 UpToDate None None None NOT RELEVANT •	 IARS† NOT RELEVANT •	 Defendant, elderly man died of aspergillosis, 2022† •	 Defendant, elderly man developed bradycardia during GA, 2022 •	 Plaintiff, hypoxic encephalopathy after NPPE after airway obstruction, 2022 •	 Plaintiff, patient with extreme obesity and OSA had to be intu­ bated urgently in ED, 2021 •	 Plaintiff, patient died after mas­ sive intraoperative hemorrhage during back surgery, 2021 •	 Plaintiff, elderly woman having elective spine surgery bled to death, 2021 •	 Plaintiff, ischemic optic neuritis with visual loss, 2021 •	 Plaintiff, patient had arm injury during transport from procedure room to the recovery room, 2021 •	 Plaintiff, cardiac arrest after gen­ eral anesthesia for shoulder sur­ gery, 2021 Amy W. Talbot§ AHA/ACC Science and Health Advisor, Guidelines None None None None None None Saraschan­ dra Vallab­ hajosyula Warren Alpert Medical School of Brown Univer­ sity and Lifespan Cardiovascular Institute—Assistant Professor of Medi­ cine, Division of Cardiology, Depart­ ment of Medicine; Medical Director, Cardiac Intensive Care Unit and Inpa­ tient Services None None None None NOT RELEVANT •	 Abiomed‡ •	 Tufts University‡ None

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Committee Member Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness John Whittle University College London Hospi­ tals—Clinical Lead, Perioperative Medi­ cine (Critical Care) and Prehabilitation; Honorary Associate Professor & Lead for Perioperative Translational Medicine NOT RELEVANT •	 EBPOM •	 Predicate HPG •	 SplendoHealth None None None NOT RELEVANT •	 Baxter •	 InBody •	 PhysioFlow •	 UCLH Charity •	 UK NIH None Kim Allan Williams, Sr. University of Lou­ isville School of Medicine—Chair, Department of Inter­ nal Medicine None None None None None None This table represents all relationships of committee members with industry and other entities that were reported by authors, including those not deemed to be relevant to this document, at the time this document was under development. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of ≥5% of the voting stock or share of the business entity, or ownership of ≥$5000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the previ­ ous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. Please refer to https://www.acc.org/guidelines/about-guidelines-and-clinical-documents/relationships-with-industry-policy for definitions of disclosure categories or additional information about the ACC/AHA Disclosure Policy for Writing Committees. *No financial benefit. †Significant relationship. ‡This disclosure was entered under the Clinical Trial Enroller category in the ACC’s disclosure system. To appear in this category, the author acknowledges that there is no direct or institutional relationship with the trial sponsor as defined in the (ACCF or AHA/ACC) Disclosure Policy for Writing Committees. §Amy Talbot is an ACC/AHA joint staff member and acts as the Science and Health Advisor. No relevant relationships to report. Nonvoting author on measures and not included/counted in the RWI balance for this committee. ABIM indicates American Board of Internal Medicine; ACC, American College of Cardiology; ADA, Americans with Disabilities; AHA, American Heart Association; AHRQ, Agency for Healthcare Research and Quality; ASA, American Society of Anesthesiologists; CDC, Centers for Disease Control and Prevention; CMO, chief medical officer; Co-I, co-investigator; DOD, US Department of Defense; DSMB, data and safety monitoring board; ECG, electrocardiogram; ED, emergency department; EBPOM, Evidence Based Perioperative Medicine; EHR2EDC, Electronic Health Records to Electronic Data Capture systems; FDA, US Food and Drug Administration; GA, general anesthesia; HRS, Heart Rhythm Society; IARS, International Anesthesia Research Society; NCATS, National Center for Advancing Translational Sciences; NHLBI, National Heart, Lung, and Blood Institute; NIH, National Institutes of Health; NPPE, negative pressure pulmonary edema; NYU, New York University; OSA, ob­ structive sleep apnea; PCORI, Patient-Centered Outcomes Research Institute; PHA, Pulmonary Hypertension Association; PI, Principal Investigator; SCMR, Society for Cardiovascular Magnetic Resonance; SW, Southwest; UCLH, University College London Hospitals; UCSF, University of California, San Francisco; UK, United Kingdom; VA, Virginia; and VP, vice president.

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Appendix 2. Peer Review Committee Relationships With Industry and Other Entities―2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/ SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery

Reviewer Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness Jacqueline E. Tamis-Holland, Chair Cleveland Clinic None •	 EBIX None •	 Concepts Medical* •	 CORSIRA II trial, Investigator •	 AHA* •	 NYS* None Marietta Ambrose University of Pennsylvania None None None None None None Danielle Blais Ohio State University Wexner Medical Center None None None None None None Jeanna Blitz Noridian Healthcare Solutions •	 Guidepoint •	 Providence Anesthesia Associates •	 Society for Advancement of Patient Blood Management None None None •	 Caption Health* •	 Society for Perioperative Assessment and Quality Improvement* None Renee Bullock-Palmer Deborah Heart and Lung Center None None None None •	 Abbott •	 AHA* •	 Amgen •	 ASNC* •	 IAC, Board of Directors* None Shea E. Hogan Denver Health None None None None •	 ACC •	 CPC Clinical Research† •	 Plaintiff (State of Colorado), review of stan­ dard of care, 2023 •	 Plaintiff (Rieback Legal, Inc.), 2023 •	 Plaintiff (Round Table), case review 2023 Michelle M. Kittleson Cedars-Sinai Smidt Heart Institute None •	 Encore Medical Education* None None •	 Actelion‡ •	 Eidos Therapeutics‡ •	 Gilead/One Legacy/Baylor‡ •	 Journal of Heart and Lung Transplantation* •	 NIH‡ •	 Sanofi (Genzyme Corporation)‡ •	 United Therapeutics‡ None Clauden Louis BayCare Medical System; Winter Haven Hospital; Bostick Heart Center None None None None None None

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Reviewer Employment Consultant Speakers Bureau Ownership/ Partnership/ Principal Personal Research Institutional, Organizational, or Other Financial Benefit Expert Witness Elizabeth Magnuson Saint Luke’s Mid America Heart Institute None None None None •	 Abbott† •	 ACC •	 AHA* •	 Ancora Heart† •	 Corvia† •	 Edwards Lifesciences† •	 NHLBI† •	 V-Wave† None Kanae Mukai (representing SCMR) Salinas Valley Health •	 Canon Medical Systems •	 Circle Cardiovascular Imaging None None None None None Grant Reed Cleveland Clinic Foundation •	 Boston Scientific† •	 Philips Healthcare None None None None None Jennifer Rymer (representing SVM) Duke University •	 Chiesi† •	 Medscape None None •	 AHA† •	 Idorsia† •	 Novo Nordisk, Inc.† •	 Vascular Cures† •	 Idorsia‡ None This table represents all reviewers’ relationships with industry and other entities that were reported at the time of peer review, including those not deemed to be relevant to this document, at the time this document was under review. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of ≥5% of the voting stock or share of the business entity, or ownership of ≥$5000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person’s gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. Please refer to http://www.acc.org/guidelines/about-guidelines-and-clinical-documents/relationships-with-industry-policy for definitions of disclosure categories or additional information about the ACC/AHA Disclosure Policy for Writing Committees. *No financial benefit. †Significant relationship. ‡This disclosure was entered under the Clinical Trial Enroller category in the ACC’s disclosure system. To appear in this category, the author acknowledges that there is no direct or institutional relationship with the trial sponsor as defined in the (ACCF or AHA/ACC) Disclosure Policy for Writing Committees. ACC indicates American College of Cardiology; AHA, American Heart Association; ASNC, American Society of Nuclear Cardiology; CORSIRA II, Efficacy of the Coro­ nary Sinus Reducer in Patients With Refractory Angina II; IAC, Intersocietal Accreditation Commission; NHLBI, National Heart, Lung, and Blood Institute; NIH, National Institutes of Health; NYS, New York state; SCMR, Society for Cardiovascular Magnetic Resonance; and SVM, Society for Vascular Medicine.

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