European Heart Journal (2024) 00, 1–101 ESC GUIDELINES

https://doi.org/10.1093/eurheartj/ehae176

2024 ESC Guidelines for the management

of atrial fibrillation developed in collaboration

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with the European Association
for Cardio-Thoracic Surgery (EACTS)
Developed by the task force for the management of atrial fibrillation of the
European Society of Cardiology (ESC), with the special contribution of the
European Heart Rhythm Association (EHRA) of the ESC.
Endorsed by the European Stroke Organisation (ESO)

Authors/Task Force Members: Isabelle C. Van Gelder *†, (Chairperson)

(Netherlands), Michiel Rienstra ±, (Task Force Co-ordinator) (Netherlands),
Karina V. Bunting ±, (Task Force Co-ordinator) (United Kingdom),
Ruben Casado-Arroyo (Belgium), Valeria Caso 1 (Italy), Harry J.G.M. Crijns
(Netherlands), Tom J.R. De Potter (Belgium), Jeremy Dwight (United Kingdom),
Luigina Guasti (Italy), Thorsten Hanke 2 (Germany), Tiny Jaarsma (Sweden),
Maddalena Lettino (Italy), Maja-Lisa Løchen (Norway), R. Thomas Lumbers
(United Kingdom), Bart Maesen 2 (Netherlands), Inge Mølgaard (Denmark),
Giuseppe M.C. Rosano (United Kingdom), Prashanthan Sanders (Australia),
2
Renate B. Schnabel (Germany), Piotr Suwalski (Poland), Emma Svennberg
(Sweden), Juan Tamargo (Spain), Otilia Tica (Romania), Vassil Traykov
(Bulgaria), Stylianos Tzeis (Greece), Dipak Kotecha *†, (Chairperson)
(United Kingdom), and ESC Scientific Document Group

* Corresponding authors: Isabelle C. Van Gelder, Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. Tel: +31 50 361 1327.
Email: [email protected]; and Dipak Kotecha, Institute of Cardiovascular Sciences, University of Birmingham, United Kingdom & NIHR Birmingham Biomedical Research Centre,
University Hospitals Birmingham NHS Foundation Trust, Birmingham, United Kingdom. Tel: +44 121 371 8124. Email: [email protected]
†
The two Chairpersons contributed equally to the document and are joint corresponding authors.
±
The two Task Force Co-ordinators contributed equally to the document.
Author/Task Force Member affiliations are listed in author information.
1
Representing European Stroke Organisation (ESO).
2
Representing European Association for Cardio-Thoracic Surgery (EACTS).
ESC Clinical Practice Guidelines (CPG) Committee: listed in the Appendix.
ESC subspecialty communities having participated in the development of this document:
Associations: Association of Cardiovascular Nursing & Allied Professions (ACNAP), Association for Acute CardioVascular Care (ACVC), European Association of Cardiovascular Imaging
(EACVI), European Association of Preventive Cardiology (EAPC), European Association of Percutaneous Cardiovascular Interventions (EAPCI), European Heart Rhythm Association (EHRA),
Heart Failure Association (HFA).
Councils: Council for Cardiology Practice, Council of Cardio-Oncology, Council on Cardiovascular Genomics, Council on Stroke.
Working Groups: Cardiac Cellular Electrophysiology, Cardiovascular Pharmacotherapy, E-Cardiology, Thrombosis.
Patient Forum
© The European Society of Cardiology 2024. All rights reserved. For permissions, please email: [email protected].
2 ESC Guidelines

Document Reviewers: Nikolaos Dagres, (CPG Review Co-ordinator) (Germany), Bianca Rocca, (CPG Review
Co-ordinator) (Italy), Syed Ahsan (United Kingdom)2, Pietro Ameri (Italy), Elena Arbelo (Spain), Axel Bauer
(Austria), Michael A. Borger (Germany), Sergio Buccheri (Sweden), Barbara Casadei (United Kingdom),
Ovidiu Chioncel (Romania), Dobromir Dobrev (Germany), Laurent Fauchier (France), Bruna Gigante (Sweden),
Michael Glikson (Israel), Ziad Hijazi (Sweden), Gerhard Hindricks (Germany), Daniela Husser (Germany),
Borja Ibanez (Spain), Stefan James (Sweden), Stefan Kaab (Germany), Paulus Kirchhof (Germany), Lars Køber
(Denmark), Konstantinos C. Koskinas (Switzerland), Thomas Kumler (Denmark), Gregory Y.H. Lip
(United Kingdom), John Mandrola (United States of America), Nikolaus Marx (Germany), John William Mcevoy

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(Ireland), Borislava Mihaylova (United Kingdom), Richard Mindham (United Kingdom), Denisa Muraru (Italy),
Lis Neubeck (United Kingdom), Jens Cosedis Nielsen (Denmark), Jonas Oldgren (Sweden), Maurizio Paciaroni
(Italy)1, Agnes A. Pasquet (Belgium), Eva Prescott (Denmark), Filip Rega2 (Belgium), Francisco Javier Rossello
(Spain), Marcin Rucinski (Poland), Sacha P. Salzberg2 (Switzerland), Sam Schulman (Canada), Philipp Sommer
(Germany), Jesper Hastrup Svendsen (Denmark), Jurrien M. ten Berg (Netherlands), Hugo Ten Cate
(Netherlands), Ilonca Vaartjes (Netherlands), Christiaan Jm. Vrints (Belgium), Adam Witkowski (Poland), and
Katja Zeppenfeld (Netherlands)

All experts involved in the development of these guidelines have submitted declarations of interest
which are reported in a supplementary document to the guidelines. See the European Heart Journal online or
www.escardio.org/guidelines for supplementary documents as well as evidence tables.

Disclaimer. The ESC Guidelines represent the views of the ESC and were produced after careful consideration of the scientific and
medical knowledge and the evidence available at the time of their publication. The ESC is not responsible in the event of any contradiction,
discrepancy and/or ambiguity between the ESC Guidelines and any other official recommendations or guidelines issued by the relevant
public health authorities, in particular in relation to good use of healthcare or therapeutic strategies. Health professionals are encouraged
to take the ESC Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the
implementation of preventive, diagnostic or therapeutic medical strategies; however, the ESC Guidelines do not override, in any way
whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each
patient’s health condition and in consultation with that patient and, where appropriate and/or necessary, the patient’s caregiver. Nor do
the ESC Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated
recommendations or guidelines issued by the competent public health authorities, in order to manage each patient’s case in light of the
scientifically accepted data pursuant to their respective ethical and professional obligations. It is also the health professional’s
responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription. The ESC
warns readers that the technical language may be misinterpreted and declines any responsibility in this respect.

Permissions. The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational
use only. No commercial use is authorized. No part of the ESC Guidelines may be translated or reproduced in any form without written
permission from the ESC. Permissions can be obtained upon submission of a written request to Oxford University Press, the publisher of
the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC ([email protected]).

-Keywords
-----------------------------------------------------------------------------------------------------------------------------------------------------------
Guidelines • Atrial fibrillation • AF-CARE • Comorbidity • Risk factors • Anticoagulation • Rate control • Rhythm
control • Cardioversion • Antiarrhythmic drugs • Catheter ablation • AF surgery • Evaluation • Stroke •
Thromboembolism
ESC Guidelines 3

Table of contents 7.2.6. Anticoagulation in patients undergoing catheter ablation . 46

7.2.7. Endoscopic and hybrid AF ablation ............................................. 47
1. Preamble ...................................................................................................................... 6 7.2.8. AF ablation during cardiac surgery ............................................... 48
2. Introduction ............................................................................................................... 8 7.2.9. Atrial tachycardia after pulmonary vein isolation .................. 48
2.1. What is new ..................................................................................................... 9 8. [E] Evaluation and dynamic reassessment .................................................. 48
3. Definitions and clinical impact ......................................................................... 13 8.1. Implementation of dynamic care ........................................................... 49
3.1. Definition and classification of AF ......................................................... 13 8.2. Improving treatment adherence ............................................................ 49
3.2. Diagnostic criteria for AF ......................................................................... 14 8.3. Cardiac imaging ............................................................................................. 49

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3.3. Symptoms attributable to AF ................................................................. 15 8.4. Patient-reported outcome measures .................................................. 50
3.4. Diagnostic evaluation of new AF ........................................................... 15 9. The AF-CARE pathway in specific clinical settings ................................. 51
3.5. Adverse events associated with AF ...................................................... 16 9.1. AF-CARE in unstable patients ................................................................ 51
3.6. Atrial flutter .................................................................................................... 17 9.2. AF-CARE in acute and chronic coronary syndromes .................. 51
4. Patient pathways and management of AF .................................................. 17 9.3. AF-CARE in vascular disease ................................................................... 53
4.1. Patient-centred, multidisciplinary AF management ....................... 17 9.4. AF-CARE in acute stroke or intracranial haemorrhage .............. 53
4.1.1. The patient at the heart of care ................................................... 17 9.4.1. Management of acute ischaemic stroke ..................................... 53
4.1.2. Education and shared decision-making ...................................... 18 9.4.2. Introduction or re-introduction of anticoagulation after
4.1.3. Education of healthcare professionals ........................................ 19 ischaemic stroke ............................................................................................... 54
4.1.4. Inclusive management of AF ........................................................... 19 9.4.3. Introduction or re-introduction of anticoagulation after
4.2. Principles of AF-CARE ............................................................................... 19 haemorrhagic stroke ....................................................................................... 54
5. [C] Comorbidity and risk factor management ........................................ 25 9.5. AF-CARE for trigger-induced AF .......................................................... 54
5.1. Hypertension .................................................................................................. 26 9.6. AF-CARE in post-operative patients ................................................... 55
5.2. Heart failure .................................................................................................... 26 9.7. AF-CARE in embolic stroke of unknown source ........................... 55
5.3. Type 2 diabetes mellitus ............................................................................ 27 9.8. AF-CARE during pregnancy ..................................................................... 56
5.4. Obesity ............................................................................................................. 27 9.9. AF-CARE in congenital heart disease .................................................. 57
5.5. Obstructive sleep apnoea ......................................................................... 27 9.10. AF-CARE in endocrine disorders ....................................................... 57
5.6. Physical inactivity .......................................................................................... 27 9.11. AF-CARE in inherited cardiomyopathies and primary
5.7. Alcohol excess ............................................................................................... 28 arrhythmia syndromes ........................................................................................ 57
6. [A] Avoid stroke and thromboembolism ................................................... 28 9.12. AF-CARE in cancer ................................................................................... 58
6.1. Initiating oral anticoagulation ................................................................... 28 9.13. AF-CARE in older, multimorbid, or frail patients ........................ 58
6.1.1. Decision support for anticoagulation in AF ............................. 28 9.14. AF-CARE in atrial flutter ........................................................................ 58
6.2. Oral anticoagulants ...................................................................................... 30 10. Screening and prevention of AF .................................................................. 58
6.2.1. Direct oral anticoagulants ................................................................ 31 10.1. Epidemiology of AF ................................................................................... 58
6.2.2. Vitamin K antagonists ........................................................................ 32 10.2. Screening tools for AF ............................................................................. 59
6.2.3. Clinical vs. device-detected subclinical AF ................................ 32 10.3. Screening strategies for AF .................................................................... 60
6.3. Antiplatelet drugs and combinations with anticoagulants .......... 33 10.3.1. Single timepoint screening ‘snapshot’ ....................................... 61
6.4. Residual ischaemic stroke risk despite anticoagulation ................ 33 10.3.2. Prolonged screening ........................................................................ 61
6.5. Percutaneous left atrial appendage occlusion .................................. 33 10.4. Factors associated with incident AF .................................................. 62
6.6. Surgical left atrial appendage occlusion .............................................. 34 10.5. Primary prevention of AF ...................................................................... 62
6.7. Bleeding risk .................................................................................................... 35 10.5.1. Hypertension ...................................................................................... 63
6.7.1. Assessment of bleeding risk ............................................................ 35 10.5.2. Heart failure ........................................................................................ 63
6.7.2. Management of bleeding on anticoagulant therapy .............. 35 10.5.3. Type 2 diabetes mellitus ................................................................ 63
7. [R] Reduce symptoms by rate and rhythm control .............................. 38 10.5.4. Obesity .................................................................................................. 63
7.1. Management of heart rate in patients with AF ............................... 38 10.5.5. Sleep apnoea syndrome ................................................................. 63
7.1.1. Indications and target heart rate ................................................... 39 10.5.6. Physical activity ................................................................................... 63
7.1.2. Heart rate control in the acute setting ...................................... 39 10.5.7. Alcohol intake ..................................................................................... 64
7.1.3. Long-term heart rate control ......................................................... 39 11. Key messages ....................................................................................................... 64
7.1.4. Atrioventricular node ablation and pacemaker 12. Gaps in evidence ................................................................................................. 64
implantation ........................................................................................................ 40 13. ‘What to do’ and ‘What not to do’ messages from the guidelines 66
7.2. Rhythm control strategies in patients with AF ................................ 40 14. Evidence tables .................................................................................................... 69
7.2.1. General principles and anticoagulation ...................................... 40 15. Data availability statement .............................................................................. 69
7.2.2. Electrical cardioversion ..................................................................... 43 16. Author information ........................................................................................... 69
7.2.3. Pharmacological cardioversion ....................................................... 43 17. Appendix ................................................................................................................ 70
7.2.4. Antiarrhythmic drugs ......................................................................... 44 18. References ............................................................................................................. 71
7.2.5. Catheter ablation ................................................................................. 45
4 ESC Guidelines

Tables of Recommendations Recommendation Table 26 — Recommendations for management

of post-operative AF (see also Evidence Table 26) .................................... 55
Recommendation Table 1 — Recommendations for the diagnosis of Recommendation Table 27 — Recommendations for patients with
AF (see also Evidence Table 1) ............................................................................ 15 embolic stroke of unknown source (see also Evidence Table 27) ....... 56
Recommendation Table 2 — Recommendations for symptom Recommendation Table 28 — Recommendations for patients with
evaluation in patients with AF (see also Evidence Table 2) ..................... 15 AF during pregnancy (see also Evidence Table 28) ..................................... 56
Recommendation Table 3 — Recommendations for diagnostic Recommendation Table 29 — Recommendations for patients with
evaluation in patients with new AF (see also Evidence Table 3) .......... 15 AF and congenital heart disease (see also Evidence Table 29) .............. 57

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Recommendation Table 4 — Recommendations for patient-centred Recommendation Table 30 — Recommendations for prevention of
care and education (see also Evidence Table 4) ........................................... 19 thromboembolism in atrial flutter (see also Evidence Table 30) .......... 58
Recommendation Table 5 — Recommendations for comorbidity Recommendation Table 31 — Recommendations for screening for
and risk factor management in AF (see also Evidence Table 5) ............ 26 AF (see also Evidence Table 31) ......................................................................... 61
Recommendation Table 6 — Recommendations to assess and Recommendation Table 32 — Recommendations for primary
manage thromboembolic risk in AF (see also Evidence Table 6) ......... 29 prevention of AF (see also Evidence Table 32) ............................................ 63
Recommendation Table 7 — Recommendations for oral
anticoagulation in AF (see also Evidence Table 7) ....................................... 31
Recommendation Table 8 — Recommendations for combining
List of tables
antiplatelet drugs with anticoagulants for stroke prevention (see also Table 1 Classes of recommendations .................................................................. 7
Evidence Table 8) ....................................................................................................... 33 Table 2 Levels of evidence ........................................................................................ 7
Recommendation Table 9 — Recommendations for Table 3 New recommendations ............................................................................ 9
thromboembolism despite anticoagulation (see also Evidence Table 4 Revised recommendations .................................................................... 12
Table 9) .......................................................................................................................... 33 Table 5 Definitions and classifications for the temporal pattern of AF 14
Recommendation Table 10 — Recommendations for percutaneous Table 6 Other clinical concepts relevant to AF ............................................ 14
left atrial appendage occlusion (see also Evidence Table 10) ................. 34 Table 7 The modified European Heart Rhythm Association
Recommendation Table 11 — Recommendations for surgical left (mEHRA) symptom classification ........................................................................ 16
atrial appendage occlusion (see also Evidence Table 11) ......................... 35 Table 8 Diagnostic work-up for patients with AF ....................................... 17
Recommendation Table 12 — Recommendations for assessment of Table 9 Achieving patient-centred AF management .................................. 18
bleeding risk (see also Evidence Table 12) ...................................................... 35 Table 10 Updated definitions for the CHA2DS2-VA score .................... 29
Recommendation Table 13 — Recommendations for management Table 11 Recommended doses for direct oral anticoagulant therapy 32
of bleeding in anticoagulated patients (see also Evidence Table 13) ... 38 Table 12 Drugs for rate control in AF ............................................................. 39
Recommendation Table 14 — Recommendations for heart rate Table 13 Antiarrhythmic drugs for sinus rhythm restoration ................ 44
control in patients with AF (see also Evidence Table 14) ........................ 38 Table 14 Non-cardiac conditions associated with trigger-induced AF 54
Recommendation Table 15 — Recommendations for general Table 15 Tools for AF screening ......................................................................... 60
concepts in rhythm control (see also Evidence Table 15) ....................... 42 Table 16 Factors associated with incident AF ............................................... 62
Recommendation Table 16 — Recommendations for electrical Table 17 ‘What to do’ and ‘what not to do’ ................................................. 66
cardioversion of AF (see also Evidence Table 16) ....................................... 43
Recommendation Table 17 — Recommendations for
pharmacological cardioversion of AF (see also Evidence Table 17) .... 43
List of figures
Recommendation Table 18 — Recommendations for Figure 1 Impacts and outcomes associated with clinical AF. AF, atrial
antiarrhythmic drugs for long-term maintenance of sinus rhythm fibrillation ....................................................................................................................... 16
(see also Evidence Table 18) ................................................................................. 45 Figure 2 Multidisciplinary approach to AF management ........................... 18
Recommendation Table 19 — Recommendations for catheter Figure 3 Central illustration. Patient pathway for AF-CARE (see Figures
ablation of AF (see also Evidence Table 19) .................................................. 46 4, 5, 6, and 7 for the [R] pathways for first-diagnosed, paroxysmal,
Recommendation Table 20 — Recommendations for persistent and permanent AF) ...................................................................................... 20
anticoagulation in patients undergoing catheter ablation (see also Figure 4 [R] Pathway for patients with first-diagnosed AF ...................... 21
Evidence Table 20) .................................................................................................... 47 Figure 5 [R] Pathway for patients with paroxysmal AF ............................ 22
Recommendation Table 21 — Recommendations for endoscopic Figure 6 [R] Pathway for patients with persistent AF ............................... 23
and hybrid AF ablation (see also Evidence Table 21) ................................ 47 Figure 7 [R] Pathway for patients with permanent AF ............................. 24
Recommendation Table 22 — Recommendations for AF ablation Figure 8 Management of key comorbidities to reduce AF recurrence 25
during cardiac surgery (see also Evidence Table 22) .................................. 48 Figure 9 Common drug interactions with oral anticoagulants ............... 30
Recommendation Table 23 — Recommendations to improve Figure 10 Modifying the risk of bleeding associated with OAC ............ 36
patient experience (see also Evidence Table 23) ......................................... 51 Figure 11 Management of oral anticoagulant-related bleeding in
Recommendation Table 24 — Recommendations for patients with patients with AF ......................................................................................................... 37
acute coronary syndromes or undergoing percutaneous Figure 12 Approaches for cardioversion in patients with AF ................. 41
intervention (see also Evidence Table 24) ...................................................... 53 Figure 13 Relevance of echocardiography in the AF-CARE pathway . 50
Recommendation Table 25 — Recommendations for Figure 14 Antithrombotic therapy in patients with AF and acute or
trigger-induced AF (see also Evidence Table 25) ......................................... 55 chronic coronary syndromes ................................................................................ 52
ESC Guidelines 5

Figure 15 Non-invasive diagnostic methods for AF screening ............... 59 CABANA Catheter Ablation versus Anti-arrhythmic Drug
Figure 16 Approaches to screening for AF .................................................... 61 Therapy for Atrial Fibrillation (trial)
CAD Coronary artery disease
CASTLE-AF Catheter Ablation versus Standard Conventional
Abbreviations and acronyms Treatment in Patients With Left Ventricle (LV)
AAD Antiarrhythmic drugs
ACE Angiotensin-converting enzyme Dysfunction and AF (trial)
CASTLE-HTx Catheter Ablation for Atrial Fibrillation in Patients
ACEi Angiotensin-converting enzyme inhibitor
With End-Stage Heart Failure and Eligibility for
ACS Acute coronary syndromes

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Heart Transplantation (trial)
ACTIVE W Atrial fibrillation Clopidogrel Trial with Irbesartan
CCS Chronic coronary syndrome
for prevention of Vascular Events (trial)
CHADS2 Congestive heart failure, hypertension, age >75
AF Atrial fibrillation
years, diabetes; previous stroke (2 points)
AF-CARE Atrial fibrillation—[C] Comorbidity and risk factor CHA2DS2-VA Congestive heart failure, hypertension, age ≥75 years
management, [A] Avoid stroke and (2 points), diabetes mellitus, prior stroke/transient
thromboembolism, [R] Reduce symptoms by rate and ischaemic attack/arterial thromboembolism (2
rhythm control, [E] Evaluation and dynamic points), vascular disease, age 65–74 years (score)
reassessment CHA2DS2-VASc Congestive heart failure, hypertension, age ≥75
AFEQT Atrial Fibrillation Effect on QualiTy-of-Life years (2 points), diabetes mellitus, prior stroke or
(questionnaire) TIA or thromboembolism (2 points), vascular
AFFIRM Atrial Fibrillation Follow-up Investigation of disease, age 65–74 years, sex category
Rhythm Management (trial) CKD Chronic kidney disease
AFL Atrial flutter CMR Cardiac magnetic resonance
AFQLQ Atrial Fibrillation Quality of Life Questionnaire COMPASS Cardiovascular Outcomes for People Using
AF-QoL Atrial Fibrillation Quality of Life (questionnaire) Anticoagulation Strategies (trial)
AFSS Atrial Fibrillation Severity Scale CPAP Continuous positive airway pressure
AI Artificial intelligence CrCl Creatinine clearance
APACHE-AF Apixaban After Anticoagulation-associated CRT Cardiac resynchronization therapy
Intracerebral Haemorrhage in Patients With Atrial CT Computed tomography
Fibrillation (trial) CTA Computed tomography angiography
APAF-CRT Ablate and Pace for Atrial Fibrillation—cardiac CTI Cavo-tricuspid isthmus
resynchronization therapy DAPT Dual antiplatelet therapy
ARB Angiotensin receptor blocker DOAC Direct oral anticoagulant
ARTESiA Apixaban for the Reduction of Thromboembolism EAST-AFNET 4 Early treatment of Atrial fibrillation for Stroke
in Patients With Device-Detected Sub-Clinical prevention Trial
Atrial Fibrillation (trial) ECG Electrocardiogram
AT Atrial tachycardia ECV Electrical cardioversion
ATHENA A Placebo-Controlled, Double-Blind, Parallel Arm EHRA European Heart Rhythm Association
Trial to Assess the Efficacy of Dronedarone 400 mg ELAN Early versus Late initiation of direct oral
twice daily for the Prevention of Cardiovascular Anticoagulants in post-ischaemic stroke patients
Hospitalization or Death from Any Cause in with atrial fibrillatioN (trial)
Patients with Atrial Fibrillation/Atrial Flutter (trial) ESUS Embolic stroke of undetermined source
AUGUSTUS An open-label, 2 × 2 factorial, randomized controlled, FFP Fresh frozen plasma
clinical trial to evaluate the safety of apixaban vs. GI Gastrointestinal
vitamin k antagonist and aspirin vs. aspirin placebo in GWAS Genome-wide association studies
patients with atrial fibrillation and acute coronary HAS-BLED Hypertension, Abnormal renal/liver function,
syndrome or percutaneous coronary intervention Stroke, Bleeding history or predisposition, Labile
AVERROES Apixaban Versus Acetylsalicylic Acid to Prevent international normalized ratio, Elderly (>65 years),
Stroke in Atrial Fibrillation Patients Who Have Drugs/alcohol concomitantly (score)
Failed or Are Unsuitable for Vitamin K Antagonist HAVOC Hypertension, age, valvular heart disease,
Treatment (trial) peripheral vascular disease, obesity, congestive
AVN Atrioventricular node heart failure, and coronary artery disease
b.p.m. Beats per minute HbA1c Haemoglobin A1c (glycated or glycosylated
BMI Body mass index haemoglobin)
BNP B-type natriuretic peptide HCM Hypertrophic cardiomyopathy
BP Blood pressure HF Heart failure
C2HEST Coronary artery disease or chronic obstructive HFmrEF Heart failure with mildly reduced ejection fraction
pulmonary disease (1 point each); hypertension HFpEF Heart failure with preserved ejection fraction
(1 point); elderly (age ≥75 years, 2 points); systolic HFrEF Heart failure with reduced ejection fraction
heart failure (2 points); thyroid disease HR Hazard ratio
(hyperthyroidism, 1 point) i.v. Intravenous
6 ESC Guidelines

ICH Intracranial haemorrhage SAVE Sleep Apnea cardioVascular Endpoints (trial)

ICHOM International Consortium for Health Outcomes SBP Systolic blood pressure
Measurement SGLT2 Sodium-glucose cotransporter-2
IMT Intima-media thickness SIC-AF Successful Intravenous Cardioversion for Atrial
INR International normalized ratio (of prothrombin Fibrillation
time) SORT-AF Supervised Obesity Reduction Trial for AF
LA Left atrium Ablation Patients (trial)
LAA Left atrial appendage SoSTART Start or STop Anticoagulants Randomised Trial

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LAAO Left atrial appendage occlusion SR Sinus rhythm
LAAOS III Left Atrial Appendage Occlusion Study STEEER-AF Stroke prevention and rhythm control Therapy:
LEGACY Long-Term Effect of Goal directed weight Evaluation of an Educational programme of the
management on Atrial Fibrillation Cohort: a 5 Year European Society of Cardiology in a cluster-
follow-up study Randomised trial in patients with Atrial Fibrillation
LMWH Low molecular weight heparin (trial)
LOOP Atrial Fibrillation Detected by Continuous ECG STEMI ST-segment elevation myocardial infarction
Monitoring (trial) STROKESTOP Systematic ECG Screening for Atrial Fibrillation
LV Left ventricle Among 75 Year Old Subjects in the Region of
LVEF Left ventricular ejection fraction Stockholm and Halland, Sweden (trial)
LVH Left ventricular hypertrophy TE Thromboembolism
mEHRA Modified European Heart Rhythm Association TIA Transient ischaemic attack
score TIMING Timing of Oral Anticoagulant Therapy in Acute
MI Myocardial infarction Ischemic Stroke With Atrial Fibrillation (trial)
MRI Magnetic resonance imaging TOE Transoesophageal echocardiography
NOAH Non-vitamin K Antagonist Oral Anticoagulants TSH Thyroid-stimulating hormone
in Patients With Atrial High Rate Episodes (trial) TTE Transthoracic echocardiogram
NSAID Non-steroidal anti-inflammatory drug TTR Time in therapeutic range
NT-proBNP N-terminal pro-B-type natriuretic peptide UFH Unfractionated heparin
NYHA New York Heart Association VKA Vitamin K antagonist
OAC Oral anticoagulant(s)
OR Odds ratio
OSA Obstructive sleep apnoea 1. Preamble
PAD Peripheral arterial disease
Guidelines evaluate and summarize available evidence with the aim of
PCC Prothrombin complex concentrate
assisting health professionals in proposing the best diagnostic or thera­
PCI Percutaneous intervention
peutic approach for an individual patient with a given condition.
PFO Patent foramen ovale
Guidelines are intended for use by health professionals and the
POAF Post-operative atrial fibrillation
European Society of Cardiology (ESC) makes its Guidelines freely
PPG Photoplethysmography
available.
PROM Patient-reported outcome measure
ESC Guidelines do not override the individual responsibility of
PVD Peripheral vascular disease
health professionals to make appropriate and accurate decisions in
PVI Pulmonary vein isolation
consideration of each patient’s health condition and in consultation
QLAF Quality of Life in Atrial Fibrillation (questionnaire)
with that patient or the patient’s caregiver where appropriate and/
QRS Q wave, R wave, and S wave, the ‘QRS complex’
or necessary. It is also the health professional’s responsibility to verify
represents ventricular depolarization
the rules and regulations applicable in each country to drugs and de­
RACE 7 Rate Control versus Electrical Cardioversion
vices at the time of prescription and to respect the ethical rules of their
ACWAS Trial 7—Acute Cardioversion versus Wait and See
profession.
(trial)
RACE I RAte Control versus Electrical cardioversion study ESC Guidelines represent the official position of the ESC on a given
RACE II Rate Control Efficacy in Permanent Atrial topic and are regularly updated when warranted by new evidence. ESC
Fibrillation (trial) Policies and Procedures for formulating and issuing ESC Guidelines can
RACE 3 Routine versus Aggressive upstream rhythm be found on the ESC website (https://www.escardio.org/Guidelines/
Control for prevention of Early AF in heart failure Clinical-Practice-Guidelines/Guidelines-development/Writing-ESC-
(trial) Guidelines). This guideline updates and replaces the previous version
RACE 4 IntegRAted Chronic Care Program at Specialized from 2020.
AF Clinic Versus Usual CarE in Patients with Atrial The Members of this task force were selected by the ESC to include
Fibrillation (trial) professionals involved with the medical care of patients with this path­
RATE-AF RAte control Therapy Evaluation in permanent ology as well as patient representatives and methodologists. The selec­
Atrial Fibrillation (trial) tion procedure included an open call for authors and aimed to include
RCT Randomized controlled trial members from across the whole of the ESC region and from relevant
RR Relative risk ESC Subspecialty Communities. Consideration was given to diversity
ESC Guidelines 7

and inclusion, notably with respect to gender and country of origin. patient-reported experience measures were also evaluated as the ba­
The task force performed a critical review and evaluation of the sis for recommendations and/or discussion in these guidelines. The
published literature on diagnostic and therapeutic approaches includ­ task force followed ESC voting procedures and all approved recom­
ing assessment of the risk–benefit ratio. The strength of every recom­ mendations were subject to a vote and achieved at least 75% agree­
mendation and the level of evidence supporting them were weighed ment among voting members. Members of the task force with
and scored according to predefined scales as outlined in Tables 1 declared interests on specific topics were asked to abstain from voting
and 2 below. Patient-reported outcome measures (PROMs) and on related recommendations.

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Table 1 Classes of recommendations

Definition Wording to use

Classes of recommendations

Class I Evidence and/or general agreement Is recommended or is indicated

that a given treatment or procedure is
beneficial, useful, effective.

Class II Conflicting evidence and/or a divergence of opinion about the usefulness/

efficacy of the given treatment or procedure.

Class IIa Weight of evidence/opinion is in Should be considered

favour of usefulness/efficacy.

Class IIb Usefulness/efficacy is less well May be considered

established by evidence/opinion.

Class III Evidence or general agreement that the Is not recommended

given treatment or procedure is not

©ESC 2024
useful/effective, and in some cases
may be harmful.

Table 2 Levels of evidence

Level of Data derived from multiple randomized clinical trials

evidence A or meta-analyses.

Level of Data derived from a single randomized clinical trial

evidence B or large non-randomized studies.

Level of Consensus of opinion of the experts and/or small studies,

evidence C retrospective studies, registries.
©ESC 2024
8 ESC Guidelines

The experts of the writing and reviewing panels provided declaration of The typical drivers of AF onset and progression are a range of co­
interest forms for all relationships that might be perceived as real or po­ morbidities and associated risk factors. To achieve optimal care for pa­
tential sources of conflicts of interest. Their declarations of interest were tients with AF, it is now widely accepted that these comorbidities and
reviewed according to the ESC declaration of interest rules which can be risk factors must be managed early and in a dynamic way. Failure to do
found on the ESC website (http://www.escardio.org/guidelines) and have so contributes to recurrent cycles of AF, treatment failure, poor patient
been compiled in a report published in a supplementary document with outcomes, and a waste of healthcare resources. In this iteration of the
the guidelines. Funding for the development of ESC Guidelines is derived European Society of Cardiology (ESC) practice guidelines on AF, the
entirely from the ESC with no involvement of the healthcare industry. task force has consolidated and evolved past approaches to develop

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The ESC Clinical Practice Guidelines (CPG) Committee supervises and the AF-CARE framework (Atrial Fibrillation—[C] Comorbidity and
co-ordinates the preparation of new guidelines and is responsible for the risk factor management, [A] Avoid stroke and thromboembolism, [R]
approval process. In addition to review by the CPG Committee, ESC Reduce symptoms by rate and rhythm control, [E] Evaluation and dy­
Guidelines undergo multiple rounds of double-blind peer review by exter­ namic reassessment). Comorbidities and risk factors is placed as the ini­
nal experts, including members from across the whole of the ESC region, all tial and central component of patient management. This should be
National Cardiac Societies of the ESC and from relevant ESC Subspecialty considered first as it applies to all patients with AF, regardless of their
Communities. After appropriate revisions, the guidelines are signed off by thromboembolic risk factors or any symptoms that might warrant
all the experts in the task force. The finalized document is signed off by the intervention. This is followed by considering how best to [A] avoid
CPG Committee for publication in the European Heart Journal. stroke and thromboembolism, and then the options available to reduce
ESC Guidelines are based on analyses of published evidence, chiefly on symptoms, and in some cases improve prognosis, through [R] rate and
clinical trials and meta-analyses of trials, but potentially including other rhythm control. [E] Evaluation and reassessment should be individua­
types of studies. Evidence tables summarizing key information from rele­ lized for every patient, with a dynamic approach that accounts for
vant studies are generated early in the guideline development process to how AF and its associated conditions change over time.
facilitate the formulation of recommendations, to enhance comprehension Patient empowerment is critical in any long-term medical problem
of recommendations after publication, and reinforce transparency in the to achieve better outcomes, encourage adherence, and to seek timely
guidelines development process. The tables are published in their guidance on changes in clinical status. A patient-centred, shared
own section of ESC Guidelines and reference specific recommenda­ decision-making approach will facilitate the choice of management
tion tables. that suits each individual patient, particularly in AF where some ther­
Off-label use of medication may be presented in this guideline if a suf­ apies and interventions improve clinical outcomes, and others are
ficient level of evidence shows that it can be considered medically focused on addressing symptoms and quality of life. Education and
appropriate for a given condition. However, the final decisions con­ awareness are essential, not only for patients but also healthcare pro­
cerning an individual patient must be made by the responsible health fessionals in order to constrain the impact of AF on patients and
professional giving special consideration to: healthcare services.
With this in mind, the task force have created a range of patient
• The specific situation of the patient. Unless otherwise provided for
pathways that cover the major aspects of AF-CARE. At present, these re­
by national regulations, off-label use of medication should be limited
main based on the time-orientated classification of AF (first-diagnosed,
to situations where it is in the patient’s interest with regard to the
paroxysmal, persistent, and permanent), but ongoing research may allow
quality, safety, and efficacy of care, and only after the patient has
for pathology-based classifications and a future of personalized medicine.
been informed and has provided consent.
Clinical practice guidelines can only cover common scenarios with an evi­
• Country-specific health regulations, indications by governmental
dence base, and so there remains a need for healthcare professionals to
drug regulatory agencies, and the ethical rules to which health profes­
care for patients within a local multidisciplinary team. While guideline-
sionals are subject, where applicable.
adherent care has repeatedly been shown to improve patient outcomes,
the actual implementation of guidelines is often poor in many healthcare
settings. This has been demonstrated in the ESC’s first randomized con­
2. Introduction trolled trial (RCT), STEEER-AF (Stroke prevention and rhythm control
Atrial fibrillation (AF) is one of the most commonly encountered heart Therapy: Evaluation of an Educational programme of the European
conditions, with a broad impact on all health services across primary Society of Cardiology in a cluster-Randomised trial in patients with Atrial
and secondary care. The prevalence of AF is expected to double in Fibrillation), which has sought to improve guideline adherence in parallel
the next few decades as a consequence of the ageing population, an in­ to guideline production. The task force developing the 2024 AF
creasing burden of comorbidities, improved awareness, and new tech­ Guidelines have made implementation a key goal by focusing on the under­
nologies for detection. pinning evidence and using a consistent writing style for each recommen­
The effects of AF are variable across individual patients; however, mor­ dation (the intervention proposed, the population it should be applied to,
bidity from AF remains highly concerning. Patients with AF can suffer and the potential value to the patient, followed by any exceptions). Tables 3
from a variety of symptoms and poor quality of life. Stroke and heart and 4 below outline new recommendations and those with important re­
failure as consequences of AF are now well appreciated by healthcare visions. These initiatives have been designed to make the 2024 ESC
professionals, but AF is also linked to a range of other thromboembolic Guidelines for the management of AF easier to read, follow, and implement,
outcomes. These include subclinical cerebral damage (potentially leading with the aim of improving the lives of patients with AF. A patient version of
to vascular dementia), and thromboembolism to every other organ, all of these guidelines is also available at http://www.escardio.org/Guidelines/
which contribute to the higher risk of mortality associated with AF. guidelines-for-patients.
ESC Guidelines 9

2.1. What is new

Table 3 New recommendations

Classa Levelb

Diagnostic evaluation of new AF—Section 3.4

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A transthoracic echocardiogram is recommended in patients with an AF diagnosis where this will guide treatment decisions. I C
Principles of AF-CARE—Section 4.2
Education directed to patients, family members, caregivers, and healthcare professionals is recommended to optimize shared
I C
decision-making, facilitating open discussion of both the benefit and risk associated with each treatment option.
Access to patient-centred management according to the AF-CARE principles is recommended in all patients with AF, regardless of gender,
I C
ethnicity, and socioeconomic status, to ensure equality in healthcare provision and improve outcomes.
Patient-centred AF management with a multidisciplinary approach should be considered in all patients with AF to optimize management and
IIa B
improve outcomes.
[C] Comorbidity and risk factor management—Section 5
Diuretics are recommended in patients with AF, HF, and congestion to alleviate symptoms and facilitate better AF management. I C
Appropriate medical therapy for HF is recommended in AF patients with HF and impaired LVEF to reduce symptoms and/or HF
I B
hospitalization and prevent AF recurrence.
Sodium-glucose cotransporter-2 inhibitors are recommended for patients with HF and AF regardless of left ventricular ejection fraction to
I A
reduce the risk of HF hospitalization and cardiovascular death.
Effective glycaemic control is recommended as part of comprehensive risk factor management in individuals with diabetes mellitus and AF,
I C
to reduce burden, recurrence, and progression of AF.
Bariatric surgery may be considered in conjunction with lifestyle changes and medical management in individuals with AF and body mass
IIb C
index ≥40 kg/m2 c where a rhythm control strategy is planned, to reduce recurrence and progression of AF.
Management of obstructive sleep apnoea may be considered as part of a comprehensive management of risk factors in individuals with AF to
IIb B
reduce recurrence and progression.
When screening for obstructive sleep apnoea in individuals with AF, using only symptom-based questionnaires is not recommended. III B
Initiating oral anticoagulation—Section 6.1
Oral anticoagulation is recommended in patients with clinical AF at elevated thromboembolic risk to prevent ischaemic stroke and
I A
thromboembolism.
A CHA2DS2-VA score of 2 or more is recommended as an indicator of elevated thromboembolic risk for decisions on initiating oral
I C
anticoagulation.
A CHA2DS2-VA score of 1 should be considered an indicator of elevated thromboembolic risk for decisions on initiating oral
IIa C
anticoagulation.
Oral anticoagulation is recommended in all patients with AF and hypertrophic cardiomyopathy or cardiac amyloidosis, regardless of
I B
CHA2DS2-VA score, to prevent ischaemic stroke and thromboembolism.
Individualized reassessment of thromboembolic risk is recommended at periodic intervals in patients with AF to ensure anticoagulation is
I B
started in appropriate patients.
Direct oral anticoagulant therapy may be considered in patients with asymptomatic device-detected subclinical AF and elevated
IIb B
thromboembolic risk to prevent ischaemic stroke and thromboembolism, excluding patients at high risk of bleeding.
Oral anticoagulants—Section 6.2
A reduced dose of DOAC therapy is not recommended, unless patients meet DOAC-specific criteria, to prevent underdosing and
III B
avoidable thromboembolic events.
Maintaining VKA treatment rather than switching to a DOAC may be considered in patients aged ≥75 years on clinically stable therapeutic
IIb B
VKA with polypharmacy to prevent excess bleeding risk.
Antiplatelet drugs and combinations with anticoagulants—Section 6.3
Adding antiplatelet treatment to oral anticoagulation is not recommended in AF patients for the goal of preventing ischaemic stroke or
III B
thromboembolism.
Continued
10 ESC Guidelines

Residual ischaemic stroke risk despite anticoagulation—Section 6.4

A thorough diagnostic work-up should be considered in patients taking an oral anticoagulant and presenting with ischaemic stroke or
thromboembolism to prevent recurrent events, including assessment of non-cardioembolic causes, vascular risk factors, dosage, and IIa B
adherence.
Adding antiplatelet treatment to anticoagulation is not recommended in patients with AF to prevent recurrent embolic stroke. III B
Switching from one DOAC to another, or from a DOAC to a VKA, without a clear indication is not recommended in patients with AF to
III B
prevent recurrent embolic stroke.

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Surgical left atrial appendage occlusion—Section 6.6
Surgical closure of the left atrial appendage should be considered as an adjunct to oral anticoagulation in patients with AF undergoing
IIa C
endoscopic or hybrid AF ablation to prevent ischaemic stroke and thromboembolism.
Stand-alone endoscopic surgical closure of the left atrial appendage may be considered in patients with AF and contraindications for
IIb C
long-term anticoagulant treatment to prevent ischaemic stroke and thromboembolism.
Management of bleeding on anticoagulant therapy—Section 6.7.2
Specific antidotes should be considered in AF patients on a DOAC who develop a life-threatening bleed, or bleed into a critical site, to
IIa B
reverse the antithrombotic effect.
Management of heart rate in patients with AF—Section 7.1
Rate control therapy is recommended in patients with AF, as initial therapy in the acute setting, an adjunct to rhythm control therapies, or as
I B
a sole treatment strategy to control heart rate and reduce symptoms.
Beta-blockers, diltiazem, verapamil, or digoxin are recommended as first-choice drugs in patients with AF and LVEF >40% to control heart
I B
rate and reduce symptoms.
Atrioventricular node ablation combined with cardiac resynchronization therapy should be considered in severely symptomatic patients
with permanent AF and at least one hospitalization for HF to reduce symptoms, physical limitations, recurrent HF hospitalization, and IIa B
mortality.
General principles and anticoagulation—Section 7.2.1
Direct oral anticoagulants are recommended in preference to VKAs in eligible patients with AF undergoing cardioversion for
I A
thromboembolic risk reduction.
Cardioversion of AF (either electrical or pharmacological) should be considered in symptomatic patients with persistent AF as part of a
IIa B
rhythm control approach.
A wait-and-see approach for spontaneous conversion to sinus rhythm within 48 h of AF onset should be considered in patients without
IIa B
haemodynamic compromise as an alternative to immediate cardioversion.
Implementation of a rhythm control strategy should be considered within 12 months of diagnosis in selected patients with AF at risk of
IIa B
thromboembolic events to reduce the risk of cardiovascular death or hospitalization.
Early cardioversion is not recommended without appropriate anticoagulation or transoesophageal echocardiography if AF duration is
III C
longer than 24 h, or there is scope to wait for spontaneous cardioversion.
Electrical cardioversion—Section 7.2.2
Electrical cardioversion as a diagnostic tool should be considered in patients with persistent AF where there is uncertainty about the value of
IIa C
sinus rhythm restoration on symptoms, or to assess improvement in left ventricular function.
Antiarrhythmic drugs—Section 7.2.4
Antiarrhythmic drug therapy is not recommended in patients with advanced conduction disturbances unless antibradycardia pacing is
III C
provided.
Catheter ablation—Section 7.2.5
Sinus node disease/tachycardia–bradycardia syndrome
Atrial fibrillation catheter ablation should be considered in patients with AF-related bradycardia or sinus pauses on AF termination to
IIa C
improve symptoms and avoid pacemaker implantation.
Recurrence after catheter ablation
Repeat AF catheter ablation should be considered in patients with AF recurrence after initial catheter ablation, provided the patient’s
IIa B
symptoms were improved after the initial PVI or after failed initial PVI, to reduce symptoms, recurrence, and progression of AF.
Anticoagulation in patients undergoing catheter ablation—Section 7.2.6
Uninterrupted oral anticoagulation is recommended in patients undergoing AF catheter ablation to prevent peri-procedural ischaemic
I A
stroke and thromboembolism.
Continued
ESC Guidelines 11

Endoscopic and hybrid AF ablation—Section 7.2.7

Continuation of oral anticoagulation is recommended in patients with AF at elevated thromboembolic risk after concomitant, endoscopic,
I C
or hybrid AF ablation, independent of rhythm outcome or LAA exclusion, to prevent ischaemic stroke and thromboembolism.
Endoscopic and hybrid ablation procedures should be considered in patients with symptomatic persistent AF refractory to AAD therapy to
prevent symptoms, recurrence, and progression of AF, within a shared decision-making rhythm control team of electrophysiologists and IIa A
surgeons.
AF ablation during cardiac surgery—Section 7.2.8

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Intraprocedural imaging for detection of left atrial thrombus in patients undergoing surgical ablation is recommended to guide surgical
I C
strategy, independent of oral anticoagulant use, to prevent peri-procedural ischaemic stroke and thromboembolism.
Concomitant surgical ablation should be considered in patients undergoing non-mitral valve cardiac surgery and AF suitable for a rhythm
control strategy to prevent symptoms and recurrence of AF, with shared decision-making supported by an experienced team of IIa B
electrophysiologists and arrhythmia surgeons.
Patient-reported outcome measures—Section 8.4
Evaluating quality of care and identifying opportunities for improved treatment of AF should be considered by practitioners and institutions
IIa B
to improve patient experiences.
Acute and chronic coronary syndromes in patients with AF—Section 9.2
Recommendations for AF patients with chronic coronary or vascular disease
Antiplatelet therapy beyond 12 months is not recommended in stable patients with chronic coronary or vascular disease treated with oral
III B
anticoagulation, due to lack of efficacy and to avoid major bleeding.
Trigger-induced AF—Section 9.5
Long-term oral anticoagulation should be considered in suitable patients with trigger-induced AF at elevated thromboembolic risk to
IIa C
prevent ischaemic stroke and systemic thromboembolism.
Post-operative AF—Section 9.6
Peri-operative amiodarone therapy is recommended where drug therapy is desired to prevent post-operative AF after cardiac surgery. I A
Concomitant posterior peri-cardiotomy should be considered in patients undergoing cardiac surgery to prevent post-operative AF. IIa B
Patients with embolic stroke of unknown source (ESUS)—Section 9.7
Initiation of oral anticoagulation in ESUS patients without documented AF is not recommended due to lack of efficacy in preventing
III A
ischaemic stroke and thromboembolism.
Atrial flutter—Section 9.14
Oral anticoagulation is recommended in patients with atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and
I B
thromboembolism.
Screening strategies for AF—Section 10.3
Review of an ECG (12-lead, single, or multiple leads) by a physician is recommended to provide a definite diagnosis of AF and commence
I B
appropriate management.
Population-based screening for AF using a prolonged non-invasive ECG-based approach should be considered in individuals aged ≥75 years,
IIa B
or ≥65 years with additional CHA2DS2-VA risk factors to ensure earlier detection of AF.
Primary prevention of AF—Section 10.5
Maintaining optimal blood pressure is recommended in the general population to prevent AF, with ACE inhibitors or ARBs as first-line
I B
therapy.
Appropriate medical HF therapy is recommended in individuals with HFrEF to prevent AF. I B
Maintaining normal weight (BMI 20–25 kg/m2) is recommended for the general population to prevent AF. I B
Maintaining an active lifestyle is recommended to prevent AF, with the equivalent of 150–300 min per week of moderate intensity or 75–
I B
150 min per week of vigorous intensity aerobic physical activity.
Avoidance of binge drinking and alcohol excess is recommended in the general population to prevent AF. I B
© ESC 2024

Metformin or SGLT2 inhibitors should be considered for individuals needing pharmacological management of diabetes mellitus to prevent
IIa B
AF.
Weight reduction should be considered in obese individuals to prevent AF. IIa B

AAD, antiarrhythmic drugs; ACEi, angiotensin-converting enzyme inhibitor; AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor management, [A] Avoid stroke
and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; ARB, angiotensin receptor blocker; BMI, body mass index; CHA2DS2-VA,
congestive heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial thromboembolism (2 points), vascular disease, age 65–74
years; DOAC, direct oral anticoagulant; ECG, electrocardiogram; ESUS, embolic stroke of undetermined source; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; LAA, left
atrial appendage; LVEF, left ventricular ejection fraction; PVI, pulmonary vein isolation; SGLT2, sodium-glucose cotransporter-2; VKA, vitamin K antagonist.
a
Class of recommendation.
b
Level of evidence.
c
Or body mass index ≥35 kg/m2 with obesity-related complications.
12 ESC Guidelines

Table 4 Revised recommendations

Recommendations in 2020 version Classa Levelb Recommendations in 2024 version Classa Levelb

Section 3.2—Diagnostic criteria for AF

ECG documentation is required to establish the Confirmation by an electrocardiogram (12-lead,
diagnosis of AF. A standard 12-lead ECG recording or a multiple, or single leads) is recommended to establish
single-lead ECG tracing of ≥30 s showing heart rhythm the diagnosis of clinical AF and commence risk
I B I A

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with no discernible repeating P waves and irregular RR stratification and treatment.
intervals (when atrioventricular conduction is not
impaired) is diagnostic of clinical AF.
In patients with AF, it is recommended to: Evaluating the impact of AF-related symptoms is
• Evaluate AF-related symptoms (including fatigue, recommended before and after major changes in
tiredness, exertional shortness of breath, palpitations, treatment to inform shared decision-making and guide
and chest pain) and quantify the patient symptom treatment choices.
status using the modified EHRA symptom scale I C I B
before and after initiation of treatment.
• Evaluate AF-related symptoms before and after
cardioversion of persistent AF to aid rhythm control
treatment decisions.
Section 5—[C] Comorbidity and risk factor management
Attention to good BP control is recommended in AF Blood pressure lowering treatment is recommended in
patients with hypertension to reduce AF recurrences patients with AF and hypertension to reduce
I B I B
and risk of stroke and bleeding. recurrence and progression of AF and prevent adverse
cardiovascular events.
In obese patients with AF, weight loss together with Weight loss is recommended as part of comprehensive
management of other risk factors should be considered risk factor management in overweight and obese
IIa B I B
to reduce AF incidence, AF progression, AF individuals with AF to reduce symptoms and AF burden,
recurrences, and symptoms. with a target of 10% or more reduction in body weight.
Physical activity should be considered to help prevent A tailored exercise programme is recommended in
AF incidence or recurrence, with the exception of IIa C individuals with paroxysmal or persistent AF to improve I B
excessive endurance exercise, which may promote AF. cardiorespiratory fitness and reduce AF recurrence.
Advice and management to avoid alcohol excess should Reducing alcohol consumption to ≤3 standard drinks
be considered for AF prevention and in AF patients (≤30 grams of alcohol) per week is recommended as
IIa B I B
considered for OAC therapy. part of comprehensive risk factor management to
reduce AF recurrence.
Section 6.6—Surgical left atrial appendage occlusion
Surgical occlusion or exclusion of the LAA may be Surgical closure of the left atrial appendage is
considered for stroke prevention in patients with AF recommended as an adjunct to oral anticoagulation in
IIb C I B
undergoing cardiac surgery. patients with AF undergoing cardiac surgery to prevent
ischaemic stroke and thromboembolism.
Section 6.7—Bleeding risk
For a formal risk-score-based assessment of bleeding Assessment and management of modifiable bleeding
risk, the HAS-BLED score should be considered to help risk factors is recommended in all patients eligible for
address modifiable bleeding risk factors, and to identify oral anticoagulation, as part of shared decision-making
IIa B I B
patients at high risk of bleeding (HAS-BLED score ≥3) to ensure safety and prevent bleeding.
for early and more frequent clinical review and
follow-up.
Continued
ESC Guidelines 13

Section 7.2—Rhythm control strategies in patients with AF

AF catheter ablation for PVI should/may be considered Catheter ablation is recommended as a first-line option
as first-line rhythm control therapy to improve within a shared decision-making rhythm control
IIa B I A
symptoms in selected patients with symptomatic: strategy in patients with paroxysmal AF, to reduce
• Paroxysmal AF episodes. symptoms, recurrence, and progression of AF.
Thoracoscopic procedures—including hybrid surgical Endoscopic and hybrid ablation procedures may be
ablation—should be considered in patients who have considered in patients with symptomatic paroxysmal

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symptomatic paroxysmal or persistent AF refractory to AF refractory to AAD therapy and failed percutaneous
AAD therapy and have failed percutaneous AF ablation, catheter ablation strategy to prevent symptoms,
IIa B IIb B
or with evident risk factors for catheter ablation failure, recurrence, and progression of AF, within a shared
to maintain long-term sinus rhythm. The decision must decision-making rhythm control team of
be supported by an experienced team of electrophysiologists and surgeons.
electrophysiologists and surgeons.
Thoracoscopic procedures—including hybrid surgical Endoscopic and hybrid ablation procedures should be
ablation—may be considered in patients with persistent considered in patients with symptomatic persistent AF
AF with risk factors for recurrence, who remain refractory to AAD therapy to prevent symptoms,
IIb C IIa A
symptomatic during AF despite at least one failed AAD recurrence, and progression of AF, within a shared
and who prefer further rhythm control therapy. decision-making rhythm control team of
electrophysiologists and surgeons.
Concomitant AF ablation should be considered in Concomitant surgical ablation is recommended in
patients undergoing cardiac surgery, balancing the patients undergoing mitral valve surgery and AF suitable
benefits of freedom from atrial arrhythmias and the risk for a rhythm control strategy to prevent symptoms and
IIa A I A
factors for recurrence (left atrial dilatation, years in AF, recurrence of AF, with shared decision-making
age, renal dysfunction, and other cardiovascular risk supported by an experienced team of
factors). electrophysiologists and arrhythmia surgeons.
Section 9.6—Post-operative AF
Long-term OAC therapy to prevent thromboembolic Long-term oral anticoagulation should be considered in
events may be considered in patients at risk for stroke patients with post-operative AF after cardiac and

© ESC 2024
with post-operative AF after cardiac surgery, IIb B non-cardiac surgery at elevated thromboembolic risk, IIa B
considering the anticipated net clinical benefit of OAC to prevent ischaemic stroke and thromboembolism.
therapy and informed patient preferences.

AAD, antiarrhythmic drugs; AF, atrial fibrillation; BP, blood pressure; ECG, electrocardiogram; EHRA, European Heart Rhythm Association; HAS-BLED, Hypertension, Abnormal renal/liver
function, Stroke, Bleeding history or predisposition, Labile international normalized ratio, Elderly (>65 years), Drugs/alcohol concomitantly; LAA, left atrial appendage; OAC, oral
anticoagulant; PVI, pulmonary vein isolation; RR, relative risk.
a
Class of recommendation.
b
Level of evidence.

with AF develop atrial and ventricular damage, which can make at­
3. Definitions and clinical impact tempts at rhythm control futile. For this reason, or when patients
and physicians make a joint decision for rate control, AF is classified
3.1. Definition and classification of AF as permanent (the most common ‘type’ of AF in historical registries).1
Atrial fibrillation is one of the most common heart rhythm disorders. Despite many limitations, this task force have retained this temporal
A supraventricular arrhythmia with uncoordinated atrial activation, approach because most trials in patients with AF have used these de­
AF results in a loss of effective atrial contraction (see finitions. Classifying AF by underlying drivers could inform manage­
Supplementary data online for pathophysiology). AF is reflected on ment, but the evidence in support of the clinical use of such
the surface electrocardiogram (ECG) by the absence of discernible classification is currently lacking.
and regular P waves, and irregular activation of the ventricles. This re­ Several other classifications have been applied to patients with AF,
sults in no specific pattern to RR intervals, in the absence of an atrio­ many of which have limited evidence to support them. The definition
ventricular block. The definition of AF by temporal pattern is of AF is a developing field and ongoing research may allow for
presented in Table 5. It should be noted that these categories reflect pathology-based strategies that could facilitate personalized manage­
observed episodes of AF and do not suggest the underlying patho­ ment in the future. Table 6 presents some commonly used concepts
physiological process. Some patients may progress consecutively in current clinical practice. Due to the lack of supporting evidence (par­
through these categories, while others may need periodic reclassifica­ ticularly for the time periods stated), this task force have edited and up­
tion due to their individual clinical status. Over time, some patients dated these definitions by consensus.
14 ESC Guidelines

Table 5 Definitions and classifications for the temporal AF burden The overall time spent in AF during a
pattern of AF clearly specified and reported period of
monitoring, expressed as a percentage of
Temporal Definition
time.
classification
Recent-onset AF There is accumulating data on the value
First-diagnosed AF AF that has not been diagnosed before, of the term recent-onset AF in
regardless of symptom status, temporal pattern, decision-making for acute
or duration. pharmacological or electrical

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Paroxysmal AF AF which terminates spontaneously within 7 cardioversion of AF. The cut-off time
days or with the assistance of an intervention. interval to define this entity has not yet
Evidence suggests that most self-terminating been established.8–10
paroxysms last <48 h.2 Trigger-induced AF New AF episode in close proximity to a
Persistent AF AF episodes which are not self-terminating. precipitating and potentially reversible
Many intervention trials have used 7 days as a factor.11–14
cut-off for defining persistent AF.3,4 Early AF The time since diagnosis that qualifies for
Long-standing persistent AF is arbitrarily defined early AF is dissociated from any
as continuous AF of at least 12 months’ duration underlying atrial cardiomyopathy and is
but where rhythm control is still a treatment not well defined, broadly ranging from 3
option in selected patients, distinguishing it from to 24 months.15–17 The definition of early
permanent AF. AF also does not necessarily determine
© ESC 2024

Permanent AF AF for which no further attempts at restoration early timing of intervention.

of sinus rhythm are planned, after a shared Self-terminating AF Paroxysmal AF which terminates
decision between the patient and physician. spontaneously.2 This definition may be of
value for decisions on acute rhythm
AF, atrial fibrillation.
control taken jointly by the patient and
healthcare provider.
Non-self-terminating AF Atrial fibrillation which does not
terminate spontaneously and, if needed,
Table 6 Other clinical concepts relevant to AF
termination can be achieved only with an
Clinical concept Definition intervention.
Atrial cardiomyopathy A combination of structural, electrical, or
Clinical AF Symptomatic or asymptomatic AF that is functional changes in the atria that leads
clearly documented by an ECG (12-lead to clinical impact (e.g. progression/
ECG or other ECG devices). The recurrence of AF, limited effectiveness of
minimum duration to establish the AF therapy, and/or development of heart
diagnosis of clinical AF for ambulatory failure).18,19 Atrial cardiomyopathy
ECG is not clear and depends on the includes inflammatory and
clinical context. Periods of 30 s or more prothrombotic remodelling of the atria,

© ESC 2024
may indicate clinical concern, and trigger neurohormonal activation (thereby
further monitoring or risk stratification affecting the ventricles), and fibrosis of
for thromboembolism. myocardial tissue.20
Device-detected Device-detected subclinical AF refers to
AF, atrial fibrillation; b.p.m., beats per minute; ECG, electrocardiogram.
subclinical AF asymptomatic episodes of AF detected a
Atrial high-rate episodes are defined as episodes generally lasting more than 5 min with an
on continuous monitoring devices. These atrial lead rate ≥170 b.p.m.,7,21–24 detected by implanted cardiac devices that allow for
devices include implanted cardiac automated continuous monitoring and storage of atrial rhythm. Atrial high-rate episodes
need to be visually inspected because some may be electrical artefacts or false positives.
electronic devices, for which most atrial
high-rate episodesa may be AF, as well as
consumer-based wearable monitors.
Confirmation is needed by a competent 3.2. Diagnostic criteria for AF
professional reviewing intracardiac
In many patients, the diagnosis of AF is straightforward, e.g. typical
electrograms or an ECG-recorded symptoms associated with characteristic features on a standard
rhythm.5,6 Device-detected subclinical 12-lead ECG that indicate the need for AF management. Diagnosis be­
AF is a predictor of future clinical AF.7 comes more challenging in the context of asymptomatic episodes or AF
Continued detected on longer-term monitoring devices, particularly those that do
ESC Guidelines 15

not provide an ECG (see Section 10). To guard against inappropriate patient-related effects of symptoms from AF over time can alterna­
diagnosis of AF, this task force continues to recommend that ECG tively be evaluated using patient-reported outcome measures (see
documentation is required to initiate risk stratification and AF manage­ Section 8.4).
ment. In current practice, ECG confirmation can include multiple op­
tions: not only where AF persists across a standard 12-lead ECG, but
also single- and multiple-lead devices that provide an ECG (see Recommendation Table 2 — Recommendations for
Supplementary data online, Additional Evidence Table S1). This does symptom evaluation in patients with AF (see also
not include non-ECG wearables and other devices that typically use Evidence Table 2)

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photoplethysmography. Note that many pivotal AF trials required
Recommendations Classa Levelb
two or more ECGs documenting AF, or an established AF diagnosis be­
fore randomization.25–29 The time period of AF required for diagnosis Evaluating the impact of AF-related symptoms is

© ESC 2024
on monitoring devices is not clear cut. A standard 12-lead ECG mea­ recommended before and after major changes in
I B
sures 10 s, while 30 s or more on single-lead or multiple-lead ECG de­ treatment to inform shared decision-making and
vices has generally been the consensus opinion, albeit with limited guide treatment choices.17,36,46–55
evidence.
AF, atrial fibrillation.
a
Class of recommendation.
b
Level of evidence.

Recommendation Table 1 — Recommendations for the

diagnosis of AF (see also Evidence Table 1)

Recommendations Classa Levelb 3.4. Diagnostic evaluation of new AF

All patients with AF should be offered a comprehensive diagnostic as­
Confirmation by an electrocardiogram (12-lead, sessment and review of medical history to identify risk factors and/or
© ESC 2024

multiple, or single leads) is recommended to establish comorbidities needing active treatment. Table 8 displays the essential
I A
the diagnosis of clinical AF and commence risk diagnostic work-up for a patient with AF.
25–29
stratification and treatment. A 12-lead ECG is warranted in all AF patients to confirm rhythm, de­
AF, atrial fibrillation. termine ventricular rate, and look for signs of structural heart disease,
a
Class of recommendation. conduction defects, or ischaemia.56 Blood tests should be carried out
b
Level of evidence. (kidney function, serum electrolytes, liver function, full blood count, glu­
cose/glycated haemoglobin [HbA1c], and thyroid tests) to detect any
concomitant conditions that may exacerbate AF or increase the risk
of bleeding and/or thromboembolism.57,58
3.3. Symptoms attributable to AF Other investigations will depend on individualized assessment and
Symptoms related to episodes of AF are variable and broad, and not the planned treatment strategy.59–65 A transthoracic echocardiogram
just typical palpitations (Figure 1). Asymptomatic episodes of AF can (TTE) should be carried out in the initial work-up, where this will guide
occur,30 although 90% of patients with AF describe symptoms with management decisions, or in patients where there is a change in cardio­
variable severity.31 Even in symptomatic patients, some episodes of vascular signs or symptoms. The task force recognizes that accessibility
AF may remain asymptomatic.32,33 The presence or absence of symp­ to TTE might be limited or delayed in the primary care setting, but this
toms is not related to incident stroke, systemic embolism, or mortal­ should not delay initiation of oral anticoagulation (OAC) or other com­
ity.34 However, symptoms do impact on patient quality of life.35,36 ponents of AF-CARE where indicated.66 Further details on TTE and re­
Cardiac-specific AF symptoms such as palpitations are less common assessment (e.g. if elevated heart rate limits diagnostic imaging, or
than non-specific symptoms such as fatigue, but they significantly where there is a change in clinical status) are presented in Section 8.3.
impair quality of life.36,37 Although women are often underrepresented Additional imaging using different modalities may be required to assist
in clinical trials of AF,38–40 the available literature suggests that with comorbidity and AF-related management (see Supplementary
women with AF appear to be more symptomatic and have poorer data online, Figure S1).
quality of life.41,42 Patients with AF report a higher burden of anxiety
and severity of depression (odds ratio [OR], 1.08; 95% confidence
interval [CI], 1.02–1.15; P = .009) as compared with the general
population,43,44 with higher prevalence of these symptoms in women
with AF.45 Recommendation Table 3 — Recommendations for
Assessment of AF-related symptoms should be recorded initially, diagnostic evaluation in patients with new AF (see also
Evidence Table 3)
after a change in treatment, or before and after intervention. The
modified European Heart Rhythm Association score (mEHRA) Recommendations Classa Levelb
symptom classification (Table 7) is similar to the New York
© ESC 2024

Heart Association (NYHA) functional class for heart failure. It cor­ A transthoracic echocardiogram is recommended in
relates with quality of life scores in clinical trials, is associated with patients with an AF diagnosis where this will guide I C
clinical progress and events, and may be a valuable starting point treatment decisions.59,65,67
in routine practice to assess the burden and impact of symptoms to­
AF, atrial fibrillation.
gether with the patient.46–48 Note that symptoms may also relate to a
Class of recommendation.
associated comorbidities and not just the AF component. The b
Level of evidence.
16 ESC Guidelines

Patient symptoms
Palpitations Poor exercise capacity
Shortness of breath Fainting (syncope)
Fatigue Anxiety

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Chest pain Depressed mood
Dizziness Disordered sleep

ial fibrillation
Atr
Adverse outcomes
Recurrent Cognitive decline and
hospitalization vascular dementia
Heart failure Depression
Ischaemic stroke Impaired quality of life
Thromboembolism Death
Im es
pac
t a n d o utc o m

Healthcare and society Doubling of AF

2010 2060
Increasing prevalence
High economic cost Lifetime risk
1 in 5 1 in 3
Impact on individuals,
families and communities 1–2% of healthcare
expenditure

Figure 1 Impacts and outcomes associated with clinical AF. AF, atrial fibrillation.

Table 7 The modified European Heart Rhythm 3.5. Adverse events associated with AF
Association (mEHRA) symptom classification
Atrial fibrillation is associated with a range of serious adverse events
Score Symptoms Description (Figure 1) (see Supplementary data online, Additional Evidence
Table S2). Patients with AF also have high rates of hospitalization
1 None AF does not cause any symptoms and complications from coexisting medical conditions. The most com­
2a Mild Normal daily activity not affected by symptoms mon non-fatal outcome in those with AF is heart failure, occurring in
related to AF around half of patients over time. Patients with AF have a four- to five-
2b Moderate Normal daily activity not affected by symptoms fold increase in the relative risk (RR) of heart failure compared with
related to AF, but patient troubled by those without AF, as demonstrated in two meta-analyses (RR, 4.62;
symptoms 95% CI, 3.13–6.83 and RR, 4.99; 95% CI, 3.0–8.22).68,69 The next
most common adverse impacts from AF are ischaemic stroke (RR,
© ESC 2024

3 Severe Normal daily activity affected by symptoms

2.3; 95% CI, 1.84–2.94), ischaemic heart disease (RR, 1.61; 95% CI,
related to AF
1.38–1.87), and other thromboembolic events.69–71 The latter typic­
4 Disabling Normal daily activity discontinued
ally include arterial thromboembolic events (preferred to the term
AF, atrial fibrillation. systemic), although venous thromboembolism is also associated
ESC Guidelines 17

Table 8 Diagnostic work-up for patients with AF Atrial fibrillation is also associated with increased mortality. In
2017, AF contributed to over 250 000 deaths globally, with an
All patients Selected patients age-standardized mortality rate of 4.0 per 100 000 people (95% un­
certainty interval 3.9–4.2).81 The most frequent cause of death in pa­
• Medical history to determine AF • Ambulatory ECG monitoring for
tients with AF is heart failure related,70 with complex relationships to
pattern, relevant family history, assessing AF burden and
cardiovascular and non-cardiovascular disease.82 There is up to a
and comorbidities, and to assess ventricular rate control
two-fold increased risk of all-cause mortality (RR, 1.95; 95% CI,
risk factors for thromboembolism • Exercise ECG to evaluate rate
1.50–2.54),68 and cardiovascular mortality (RR, 2.03; 95% CI, 1.79–
and bleeding control or effects of class IC
2.30)69 in AF compared with sinus rhythm. Even in the absence of

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antiarrhythmic drugs
major thromboembolic risk factors, the incidence of death is 15.5
• 12-lead ECG • Further blood tests for per 1000 person-years in those with AF exposure, compared
investigation of cardiovascular with 9.4 per 1000 person-years without (adjusted HR, 1.44; 95% CI,
disease and refinement of stroke/ 1.38–1.50; P < .001).78 Patients with OAC-related bleeding have
bleeding risk (e.g. NT-proBNP, higher mortality, including both minor and major bleeding (as
troponin) defined by the International Society on Thrombosis and
• Assess symptoms and functional • Transoesophageal Haemostasis scale).83 Despite OAC, patients with AF remain at high
impairment echocardiography for left atrial residual risk of death, highlighting the importance of attention to con­
thrombus and valvular disease comitant disease.84
assessment
• Collect generic or AF-specific • Coronary CT, angiography, or 3.6. Atrial flutter
patient-reported outcome ischaemia imaging for suspected Atrial flutter (AFL) is the among the most common atrial tachyarrhyth­
measures CAD mias, with an overall incidence rate of 88 per 100 000 person-years, ris­
• Blood tests (full blood count, • CMR for evaluation of atrial and ing to 317 per 100 000 person-years in people over 50 years of age.85
kidney function, serum ventricular cardiomyopathies, Risk factors for AFL and AF are similar, and more than half of all patients
electrolytes, liver function, and to plan interventional
with AFL will develop AF.85 Observational studies suggest that
thromboembolic risk is elevated in AFL.86 In direct comparison of
glucose/HbA1c, and thyroid procedures
AFL with AF, some studies suggest a similar risk of stroke and others
function)
a lower risk in AFL,87–90 possibly due to different comorbidity burdens
• Transthoracic echocardiography • Brain imaging and cognitive
and the impact of confounders such as AFL/AF ablation and anticoagu­
© ESC 2024

where this will guide AF-CARE function assessment for

lation (more frequently stopped in AFL).91
management decisions cerebrovascular disease and
dementia risk

AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor
4. Patient pathways and
management, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate
and rhythm control, [E] Evaluation and dynamic reassessment; CAD, coronary artery
management of AF
disease; CMR, cardiac magnetic resonance; CT, computed tomography; CTA, computed
tomography angiography; ECG, electrocardiogram; HbA1c, glycated haemoglobin; 4.1. Patient-centred, multidisciplinary AF
NT-proBNP, N-terminal pro-B-type natriuretic peptide. management
4.1.1. The patient at the heart of care
with AF.72,73 Patients with AF also have an increased risk of cognitive A patient-centred and integrated approach to AF management means
impairment (adjusted hazard ratio [HR], 1.39; 95% CI, 1.25–1.53)74 working with a model of care that respects the patient’s experience,
and dementia (OR, 1.6; 95% CI, 1.3–2.0).75–77 It should be noted values, needs, and preferences for planning, co-ordination, and delivery
that most of the observational studies on adverse events have a mix of care. A central component of this model is the therapeutic relationship
of patients taking and not taking OAC. When carefully controlling between the patient and the multidisciplinary team of healthcare profes­
for the confounding effects of stroke, comorbidities, and OAC, AF ex­ sionals (Figure 2). In patient-centred AF management, patients are seen
posure was still significantly associated with vascular dementia (HR, not as passive recipients of health services, but as active participants
1.68; 95% CI, 1.33–2.12; P < .001), but not Alzheimer’s disease (HR, who work as partners alongside healthcare professionals. Patient-
0.85; 95% CI, 0.70–1.03; P = .09).78 centred AF management requires integration of all aspects of AF man­
Hospital admission rates due to AF vary widely depending on the agement. This includes symptom control, lifestyle recommendations,
population studied, and may be skewed by selection bias. In a Dutch psychosocial support, and management of comorbidities, alongside op­
RCT including first-diagnosed AF patients (mean age 64 years), car­ timal medical treatment consisting of pharmacotherapy, cardioversion,
diovascular hospitalization rates were 7.0% to 9.4% per year.79 An and interventional or surgical ablation (Table 9). Services should be de­
Australian study identified 473 501 hospitalizations for AF during signed to ensure that all patients have access to an organized model of
15 years of follow-up (300 million person-years), with a relative in­ AF management, including tertiary care specialist services when indi­
crease in AF hospitalizations of 203% over the study period, in con­ cated (see Supplementary data online, Table S1, Evidence Table 4 and
trast to an increase for all hospitalizations of 71%. The age-specific Additional Evidence Table S3). It is equally important to maintain path­
incidence of hospital admission increased particularly in the older ways for patients to promptly re-engage with specialist services when
age groups.80 their condition alters.
18 ESC Guidelines

Atrial fibrillation
ient-centred
Pat

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in t
egr RE
ate d A F- C A

C E
Comorbidity
and risk factor
management
A R Evaluation and
dynamic
reassessment

Lifestyle help Reduce symptoms Primary care

Avoid stroke and
Primary care by rate and Cardiology
thromboembolism
Cardiology rhythm control Pharmacy
Internal medicine Nursing
Nursing care Primary care Primary care Family/carers
Other Cardiology Cardiology e-Health
Neurology Electrophysiology
Nursing care Cardiac surgeons
Anticoagulation e-Health
services
e-Health

Figure 2 Multidisciplinary approach to AF management. Principal caregivers are involved in the community and hospital settings to provide optimal,
patient-centred care for patients living with AF. AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor management, [A] Avoid stroke and
thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment.

Table 9 Achieving patient-centred AF management

Components of patient-centred AF management: 4.1.2. Education and shared decision-making

Clear advice about the rationale for treatments, the possibility of
• Optimal treatment according to the AF-CARE pathway, which includes: treatment modification, and shared decision-making can help patients
∘ [C] Comorbidity and risk factor management live with AF (see Supplementary data online, Table S2).92 An open and
∘ [A] Avoid stroke and thromboembolism effective relationship between the patient and the healthcare profes­
∘ [R] Reduce symptoms by rate and rhythm control sional is critical, with shared decision-making found to improve
∘ [E] Evaluation and dynamic reassessment outcomes for OAC and arrhythmia management.93,94 In using a
shared approach, both the clinician and patient are involved in the
• Lifestyle recommendations
decision-making process (to the extent that the patient prefers).
• Psychosocial support
Information is shared in both directions. Furthermore, both the
• Education and awareness for patients, family members, and caregivers clinician and the patient express their preferences and discuss the
• Seamless co-ordination between primary care and specialized AF care options. Of the potential treatment decisions, no treatment is
How to implement patient-centred AF management: also a possibility.95 There are several toolkits available to facilitate
• Shared decision-making this, although most are focused on anticoagulation decisions. For ex­
• Multidisciplinary team approach ample, the Shared Decision-Making Toolkit (http://afibguide.com,
http://afibguide.com/clinician) and the Successful Intravenous
© ESC 2024

• Patient education and empowerment, with emphasis on self-care

Cardioversion for Atrial Fibrillation (SIC-AF) score have been shown
• Structured educational programmes for healthcare professionals
to reduce decisional conflict compared with usual care in patients
• Technology support (e-Health, m-Health, telemedicine)a
with AF.93,94 Patient-support organizations can also make an import­
AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor ant contribution to providing understandable and actionable knowl­
management, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate edge about AF and its treatments (e.g. local support groups and
and rhythm control, [E] Evaluation and dynamic reassessment.
a international charities, such as http://afa-international.org). As AF is a
e-Health refers to healthcare services provided using electronic methods; m-Health,
refers to healthcare services supported by mobile devices; and telemedicine refers to chronic or recurrent disease in most patients, education is central
remote diagnosis or treatment supported by telecommunications technology. to empower patients, their families, and caregivers.
ESC Guidelines 19

4.1.3. Education of healthcare professionals factors is considered next, focused on appropriate use of anticoagu­
Gaps in knowledge and skills across all domains of AF care are consist­ lant therapy. Reducing AF-related symptoms and morbidity by effect­
ently described among cardiologists, neurologists, internal medicine ive use of heart rate and rhythm control [R] is then applied, which in
specialists, emergency physicians, general practitioners, nurses, and al­ selected patients may also reduce hospitalization or improve progno­
lied health practitioners.96–98 Healthcare professionals involved in sis. The potential benefit of rhythm control, accompanied by consid­
multidisciplinary AF management should have a knowledge of all avail­ eration of all risks involved, should be considered in all patients at each
able options for diagnosis and treatment.99–101 In the STEEER-AF contact point with healthcare professionals. As AF, and its related co­
trial,99 real-world adherence to clinical practice guidelines for AF morbidities, changes over time, different levels of evaluation [E] and

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across six ESC countries was poor. These findings highlight the critical re-evaluation are required in each patient, and these approaches
need for appropriate training and education of healthcare should be dynamic. Due to the wide variability in response to therapy,
professionals.102 and the changing pathophysiology of AF as age and comorbidities ad­
Specifically targeted education for healthcare professionals can in­ vance, reassessment should be built into the standard care pathway to
crease knowledge and lead to more appropriate use of OAC for prevent adverse outcomes for patients and improve population
prevention of thromboembolism.103 However, educational interventions health.
for healthcare providers are often not enough to sustainably impact be­ AF-CARE builds upon prior ESC Guidelines, e.g. the five-step
haviour.104 Other tools may be needed, such as active feedback,103 outcome-focused integrated approach in the 2016 ESC Guidelines for
clinical decision support tools,105 expert consultation,106 or e-Health the management of AF,119 and the AF Better Care (ABC) pathway in
learning.107 the 2020 ESC Guidelines for the diagnosis and management of AF.120
The reorganization into AF-CARE was based on the parallel develop­
ments in new approaches and technologies (in particular for rhythm
4.1.4. Inclusive management of AF control), with new evidence consistently suggesting that all aspects of
Evidence is growing on differences in AF incidence, prevalence, risk fac­ AF management are more effective when comorbidities and risk factors
tors, comorbidities, and outcomes according to gender.108 Women di­ have been considered. This includes management relating to symptom
agnosed with AF are generally older, have more hypertension and heart benefit, improving prognosis, prevention of thromboembolism, and the
failure with preserved ejection fraction (HFpEF), and have less diag­ response to rate and rhythm control strategies. AF-CARE makes expli­
nosed coronary artery disease (CAD).109 Registry studies have re­ cit the need for individualized evaluation and follow-up in every patient,
ported differences in outcomes, with higher morbidity and mortality with an active approach that accounts for how patients, their AF, and
in women, although these may be confounded by age and comorbidity associated comorbidities change over time. The AF-CARE principles
burden.110–112 Women with AF may be more symptomatic, and report have been applied to different patient pathways for ease of implemen­
a lower quality of life.41,113 It is unclear whether this is related to de­ tation into routine clinical care. This includes the management of first-
layed medical assessment in women, or whether there are genuine diagnosed AF (Figure 4), paroxysmal AF (Figure 5), persistent AF
sex differences. Despite a higher symptom load, women are less likely (Figure 6), and permanent AF (Figure 7).
to undergo AF ablation than men, even though antiarrhythmic drug
therapy seems to be associated with more proarrhythmic events in
women.109 These observations call for more research on gender Recommendation Table 4 — Recommendations for
differences in order to prevent disparities and inequality in care. patient-centred care and education (see also Evidence
Other diversity aspects such as age, race, ethnicity, and transgender Table 4)
issues, as well as social determinants (including socioeconomic status,
disability, education level, health literacy, and rural/urban location) are Recommendation Classa Levelb
important contributors to inequality that should be actively considered Education directed to patients, family members,
to improve patient outcomes.114 caregivers, and healthcare professionals is
recommended to optimize shared decision-making, I C
4.2. Principles of AF-CARE facilitating open discussion of both the benefit and
The 2024 ESC Guidelines for the management of AF have compiled and risk associated with each treatment option.94,103
evolved past approaches to create principles of management to aid im­ Access to patient-centred management according to
plementation of these guidelines, and hence improve patient care and the AF-CARE principles is recommended in all
outcomes. There is growing evidence that clinical support tools115–118 patients with AF, regardless of gender, ethnicity, and I C
can aid best-practice management, with the caveat that any tool is a socioeconomic status, to ensure equality in
guide only, and that all patients require personalized attention. The healthcare provision and improve outcomes.
AF-CARE approach covers many established principles in the manage­ Patient-centred AF management with a
ment of AF, but does so in a systematic, time-orientated format with
© ESC 2024

multidisciplinary approach should be considered in all

four essential treatment pillars (Figure 3; central illustration). Joint man­ IIa B
patients with AF to optimize management and
agement with each patient forms the starting point of the AF-CARE ap­ improve outcomes.79,121–124
proach. Notably, it takes account of the growing evidence base that
therapies for AF are most effective when associated health conditions AF, atrial fibrillation; AF-CARE, Atrial fibrillation—[C] Comorbidity and risk factor
management, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate
are addressed. A careful search for these comorbidities and risk factors
and rhythm control, [E] Evaluation and dynamic reassessment.
[C] is critical and should be applied in all patients with a diagnosis of AF. a
Class of recommendation.
Avoidance of stroke and thromboembolism [A] in patients with risk b
Level of evidence.
20 ESC Guidelines

AF
Equality in healthcare provision (gender, ethnicity, socioeconomic) (Class I)

Education for patients, families and healthcare professionals (Class I)

C A R E Patient-centred AF management with a multidisciplinary approach (Class IIa)

Comorbidity and risk factor management

C Overweight Obstructive sleep

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Hypertension Heart failure Alcohol
or obese apnoea
Blood pressure Diuretics for Weight loss Management Reduce to �3
lowering treatment congestion (target 10%)a of OSAa drinks per week
(Class I) (Class I) (Class I) (Class IIb) (Class I)
Appropriate HFrEF Bariatric surgery
Diabetes medical therapy if rhythm controla Exercise Other risk factors/
mellitus (Class I) (Class IIb) capacity comorbidities
Effective Tailored Identify and manage
SGLT2 inhibitors
glycaemic controla exercise programme aggressivelya
(Class 1)
(Class I) (Class I) (Class I)

Avoid stroke and thromboembolism

A Risk of
thrombo-
embolism
Use locally-validated
risk score
or CHA2DS2-VA
Choice of
anticoagulant
Assess
bleeding risk
Prevent
bleeding

Use DOAC, except Assess and manage Do not combine

Start oral OAC if CHA2DS2-VA
mechanical valve or all modifiable risk antiplatelets and OAC
anticoagulation score = 2 or more
mitral stenosis factors for bleeding for stroke prevention
(Class I) (Class I)
(Class I) (Class I) (Class III)

Temporal pattern OAC if CHA2DS2-VA If VKA: Do not use risk Avoid antiplatelets
of AF not relevant score = 1 Target INR 2.0–3.0; scores to withhold beyond 12 months
(Class III) (Class IIa) (Class I) anticoagulation in OAC treated
>70% INR range; (Class III) CCS/PVD
Antiplatelet therapy
(Class IIa) (Class III)
not an alternative
(Class III) or switch to DOAC
(Class I)

Reduce symptoms by rate and rhythm control

R First-diagnosed AF
See patient pathways for:

Paroxysmal AF Persistent AF Permanent AF

Consider:
Rate control drugs Cardioversion Antiarrhythmic drugs Catheter ablation Endoscopic/hybrid ablation Surgical ablation Ablate and pace

Evaluation and dynamic reassessment

E Re-evaluate when AF episodes or non-AF admissions

Regular re-evaluation: 6 months after presentation, and then at least annually or based on clinical need

ECG, blood tests, Continue OAC

Assess new and Stratify risk Check impact of AF Assess and manage
cardiac imaging, despite rhythm
existing risk factors for stroke and symptoms before modifiable bleeding
ambulatory ECG, control if risk
and comorbidities thromboembolism and after treatment risk factors
other imaging of thromboembolism
(Class I) (Class I) (Class I) (Class I)
as needed (Class I)

Figure 3 Central illustration. Patient pathway for AF-CARE (see Figures 4, 5, 6, and 7 for the [R] pathways for first-diagnosed, paroxysmal, persistent and
permanent AF). AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor management, [A] Avoid stroke and thromboembolism,
[R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; CCS, chronic coronary syndrome; CHA2DS2-VA, congest­
ive heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial thromboembolism (2 points),
vascular disease, age 65–74 years; DOAC, direct oral anticoagulant; ECG, electrocardiogram; HFrEF, heart failure with reduced ejection fraction; INR,
international normalized ratio of prothrombin time; OAC, oral anticoagulant; OSA, obstructive sleep apnoea; PVD, peripheral vascular disease; SGLT2,
sodium-glucose cotransporter-2; VKA, vitamin K antagonist. aAs part of a comprehensive management of cardiometabolic risk factors.
ESC Guidelines 21

Patient with first-diagnosed AF

Y Haemodynamically stable N

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Electrical cardioversion
(Class I)

Follow AF-CARE for [C] comorbidity and risk factor management & [A] avoid stroke and thromboembolism

Initial rate control

(Class I)

Y LVEF ≤40% N

Beta-blocker Beta-blocker, digoxin,

or digoxin diltiazem or verapamil
(Class I) (Class I)

Combination Combination
rate control therapy rate control therapy
(Class IIa) (Class IIa)

Cardioversion of symptomatic
persistent AF
(Class I)

Wait-and-see if sinus rhythm

restores spontaneously <48 h
(Class IIa)

Figure 4 [R] Pathway for patients with first-diagnosed AF. AF, atrial fibrillation; AF-CARE, Atrial fibrillation—[C] Comorbidity and risk factor man­
agement, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; LVEF,
left ventricular ejection fraction. After following the pathway for first-diagnosed AF, patients with recurrent AF should enter the AF-CARE [R] pathway
for paroxysmal, persistent, or permanent AF, depending on the type of their AF.
22 ESC Guidelines

Patient with paroxysmal AF

Follow AF-CARE for [C] comorbidity and risk factor management & [A] avoid stroke and thromboembolism

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Rate control target = resting heart rate <110 b.p.m. (lenient control),
with stricter control with continuing symptoms
(Class IIa)

Y LVEF ≤40% N

Beta-blocker Combination Beta-blocker, digoxin, Combination

or digoxin rate control therapy diltiazem or verapamil rate control therapy
(Class I) (Class IIa) (Class I) (Class IIa)

Shared decision-making on rhythm control

(Class I)

Antiarrhythmic drug therapy

Stable HFmrEF
Absence
HFrEF (LVEF 41–49%),
or minimal heart
(LVEF ≤40%) coronary heart disease,
disease
valvular heart disease

Amiodarone or Dronedarone, flecainide

Amiodarone Catheter ablationa
dronedarone or propafenone
(Class I) (Class I)
(Class I) (Class I)

Sotalol Sotalol
(Class IIb) (Class IIb)

Recurrence of AF symptoms

Shared decision-making
(Class I)

If failed antiarrhythmic If failed catheter

drug therapy ablation

Catheter ablation Re-do catheter ablation Surgical/hybrid ablation Antiarrhythmic drug

(Class I) (Class IIa) (Class IIb) therapy (see above)

Figure 5 [R] Pathway for patients with paroxysmal AF. AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor manage­
ment, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; b.p.m.,
beats per minute; HFmrEF, heart failure with mildly reduced ejection fraction; HFrEF, Heart failure with reduced ejection fraction; LVEF, left ventricular
ejection fraction. aIn patients with HFrEF: Class I if high probability of tachycardia-induced cardiomyopathy; and Class IIa in selected patients to improve
prognosis.
ESC Guidelines 23

Patient with persistent AF

Follow AF-CARE for [C] comorbidity and risk factor management & [A] avoid stroke and thromboembolism

Rate control target = resting heart rate <110 b.p.m. (lenient control),

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with stricter control with continuing symptoms
(Class IIa)

Y LVEF ≤40% N

Beta-blocker Combination Beta-blocker, digoxin, Combination

or digoxin rate control therapy diltiazem or verapamil rate control therapy
(Class I) (Class IIa) (Class I) (Class IIa)

Shared decision-making on rhythm control

(Class I)

Haemodynamic instability (Class I)

Electrical
Part of rhythm control strategy (Class IIa)
cardioversion
Clarify benefit from sinus rhythm (Class IIa)

Antiarrhythmic drug therapy

Stable HFmrEF
Absence
HFrEF (LVEF 41–49%),
or minimal heart
(LVEF ≤40%) coronary heart disease,
disease
valvular heart disease

Amiodarone or Dronedarone, flecainide

Amiodarone Catheter ablationa
dronedarone or propafenone
(Class I) (Class IIb)
(Class I) (Class I)

Sotalol Sotalol
(Class IIb) (Class IIb)

Recurrence of AF symptoms

Shared decision-making, considering all rhythm control options

(Class I)

If failed antiarrhythmic If failed catheter

drug therapy ablation

Catheter Endoscopic/ Re-do Endoscopic Antiarrhythmic Consider

ablation hybrid ablation catheter hybrid or drug therapy rate control
(Class I) (Class IIa) ablation surgical ablation (see above) strategy

Figure 6 [R] Pathway for patients with persistent AF. AF, atrial fibrillation; AF-CARE, Atrial fibrillation—[C] Comorbidity and risk factor management,
[A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; b.p.m., beats per
minute; HFmrEF, heart failure with mildly reduced ejection fraction; HFrEF, heart failure with reduced ejection fraction; LVEF, left ventricular ejection
fraction. aIn patients with HFrEF: Class I if high probability of tachycardia-induced cardiomyopathy; and Class IIa in selected patients to improve prognosis.
24 ESC Guidelines

Patient with permanent AF

Follow AF-CARE for [C] comorbidity and risk factor management & [A] avoid stroke and thromboembolism

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Severely symptomatic and
LVEF ≤40% LVEF >40%
HF hospitalization

Initiate beta-blocker,
Initiate beta-blocker Atrioventricular node
digoxin, diltiazem
or digoxin ablation and CRT
or verapamil
(Class I) (Class IIa)
(Class I)

Evaluation and dynamic Evaluation and dynamic

reassessment reassessment

Rate control target = resting Rate control target = resting

heart rate <110 b.p.m. heart rate <110 b.p.m.
(lenient control), Y (lenient control), Y
with stricter control with stricter control
with continuing symptoms with continuing symptoms
(Class IIa) (Class IIa)

N N

Combination beta-blocker
Combination Continue beta-blocker,
Continue beta-blocker with digoxin, or diltiazem/
beta-blocker with digoxin, digoxin, diltiazem
or digoxin verapamil with digoxin;
avoiding bradycardia or verapamil
(Class I) avoiding bradycardia
(Class IIa) (Class I)
(Class IIa)a

Rate control target = resting heart rate <110 b.p.m. (lenient control), with stricter control with continuing symptoms
(Class IIa)

N Y

Continue review and follow-up as per Intensify rate control therapy under
AF-CARE approach observation

Evaluation for atrioventricular node

ablation in combination with pacemaker
(Class IIa)

Figure 7 [R] Pathway for patients with permanent AF. AF, atrial fibrillation; AF-CARE, Atrial fibrillation—[C] Comorbidity and risk factor manage­
ment, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; b.p.m.,
beats per minute; CRT, cardiac resynchronization therapy; HF, heart failure; LVEF, left ventricular ejection fraction. Permanent AF is a shared decision
made between the patient and physician that no further attempts at restoration of sinus rhythm are planned. aNote that the combination of beta-
blockers with diltiazem or verapamil should only be used under specialist advice, and monitored with an ambulatory ECG to check for bradycardia.
ESC Guidelines 25

5. [C] Comorbidity and risk factor activity and reduce alcohol intake (see Supplementary data online,
Additional Evidence Table S4). Identification and treatment of these
management comorbidities and clusters of risk factors form an important part
A broad array of comorbidities are associated with the recurrence of effective AF-CARE (Figure 8), with the evidence outlined in the
and progression of AF. Managing comorbidities is also central to the rest of this section highlighting where management can improve
success of other aspects of care for patients with AF, with evidence patient outcomes or prevent AF recurrence. Many of these
available for hypertension, heart failure, diabetes mellitus, obesity, factors (and more) are also associated with incident AF (see
and sleep apnoea, along with lifestyle changes that improve physical Section 10).

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Shared Focus on key
decision-making risk factors

Setting individual Behavioural

targets for change
comorbidities
and risk factors
Achievable Provide information
targets without overloading

Suggested approach and targets

Integrated Identify and actively manage all risk factors and comorbidities
management (Class I)

Blood pressure treatment with target 120–129 mmHg /

Hypertension 70–79 mmHg in most adults (or as low as reasonably achievable)
(Class I)
Key targets
Optimize with diuretics to alleviate congestion appropriate,
Heart medical therapy for reduced LVEF, and SGLT2 inhibitors for all LVEF
failure (Class I)

Effective glycaemic control with diet/medication(s)

Diabetes (Class I)

Weight loss programme if overweight /obese,

Obesity with 10% or more weight loss
(Class I)

Management of obstructive sleep apnoea to minimize

Sleep apnoeic episodes
apnoea (Class IIb)

Tailored exercise programme aiming for regular

Physical moderate/vigorous activity
activity (Class I)

Alcohol Reduce alcohol consumption to 3 or less standard

intake drinks per week
(Class I)

Figure 8 Management of key comorbidities to reduce AF recurrence. LVEF, left ventricular ejection fraction; SGLT2, sodium-glucose
cotransporter-2.
26 ESC Guidelines

Recommendation Table 5 — Recommendations for 5.1. Hypertension

comorbidity and risk factor management in AF (see
Hypertension in patients with AF is associated with an increased risk of
also Evidence Table 5)
stroke, heart failure, major bleeding, and cardiovascular mortality.158–161
Recommendation Classa Levelb The target for treated systolic blood pressure (BP) in most adults is
120–129 mmHg. Where BP-lowering treatment is poorly tolerated,
Identification and management of risk factors and clinically significant frailty exists or the patient’s age is 85 years or
comorbidities is recommended as an integral part of I B older, a more lenient target of <140 mmHg is acceptable or ‘as low
AF care.39,125–127 as reasonably achievable’. On-treatment diastolic BP should ideally

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Blood pressure lowering treatment is recommended be 70–79 mmHg.162 In an individual participant data meta-analysis of
in patients with AF and hypertension to reduce 22 randomized trials reporting baseline AF, a 5 mmHg reduction in
I B
recurrence and progression of AF and prevent systolic BP reduced the risk of major cardiovascular events by 9%
adverse cardiovascular events. 126–130 (HR, 0.91; 95% CI, 0.83–1.00), with identical effect in patients with
Diuretics are recommended in patients with AF, HF, AF or sinus rhythm.129
and congestion to alleviate symptoms and facilitate I C In individuals with AF, hypertension often coexists with other
modifiable and non-modifiable risk factors that all contribute to re­
better AF management.
currence of AF, readmission to hospital, and ongoing symptoms after
Appropriate medical therapy for HF is
rhythm control.163–171 Optimal control of blood pressure should be
recommended in AF patients with HF and impaired
I B considered an essential component of treating AF and undertaken
LVEF to reduce symptoms and/or HF hospitalization
within a strategy of comprehensive risk factor management.126–128
and prevent AF recurrence.131–137 Although the majority of research has focused on clinical outcomes,
Sodium-glucose cotransporter-2 inhibitors are limited comparative data on hypertension medication suggests that
recommended for patients with HF and AF use of angiotensin-converting enzyme (ACE) inhibitors or angioten­
regardless of left ventricular ejection fraction to I A sin receptor blockers (ARB) may be superior for prevention of recur­
reduce the risk of HF hospitalization and rent AF.172–175
cardiovascular death.136,138–140
Effective glycaemic control is recommended as part
5.2. Heart failure
of comprehensive risk factor management in
I C Heart failure is a key determinant of prognosis in patients with AF, as
individuals with diabetes mellitus and AF, to reduce
well as an important factor associated with recurrence and progression
burden, recurrence, and progression of AF.
of AF.176,177 During 30 years of follow-up in the Framingham cohort,
Weight loss is recommended as part of 57% of those with new heart failure had concomitant AF, and 37% of
comprehensive risk factor management in those with new AF had heart failure.178 Numerous cardiovascular
overweight and obese individuals with AF to reduce I B and non-cardiovascular conditions impact the development of both
symptoms and AF burden, with a target of 10% or AF and heart failure, leading to the common pathway of atrial cardio­
more reduction in body weight.125–128 myopathy.18 In patients with acute heart failure attending the emer­
A tailored exercise programme is recommended in gency department, AF is one of the most prevalent triggering factors
individuals with paroxysmal or persistent AF to of the episode.179 The development of heart failure in patients with
I B
improve cardiorespiratory fitness and reduce AF AF is associated with a two-fold increase in stroke and thrombo­
recurrence.141–146 embolism,180 even after anticoagulation,181 and 25% higher all-cause
Reducing alcohol consumption to ≤3 standard drinks mortality.178 Prognosis may be affected by left ventricular ejection
(≤30 grams of alcohol) per week is recommended as fraction (LVEF), with the rate of death highest with the combination
I B of AF and heart failure with reduced ejection fraction (HFrEF)
part of comprehensive risk factor management to
reduce AF recurrence.126,127,147
(LVEF ≤ 40%), as compared with AF and HFpEF (LVEF ≥ 50%).
However, rates of stroke and incident heart failure hospitalization
Bariatric surgery may be considered in conjunction
are similar regardless of LVEF.182 Due to how common concomitant
with lifestyle changes and medical management in
AF and heart failure are in clinical practice, strategies to improve out­
individuals with AF and body mass index ≥40 kg/m2 c IIb C
comes in these patients are detailed within each component of the
where a rhythm control strategy is planned, to
AF-CARE pathway. However, it is also critical that heart failure itself
reduce recurrence and progression of AF. is managed appropriately in patients with AF to prevent avoidable ad­
Management of obstructive sleep apnoea may be verse events.
considered as part of a comprehensive management Optimization of heart failure management should follow current
IIb B
of risk factors in individuals with AF to reduce ESC Guidelines: 2023 Focused Update183 of the 2021 ESC Guidelines
recurrence and progression.126–128,148–154 for the diagnosis and treatment of acute and chronic heart failure.137
© ESC 2024

When screening for obstructive sleep apnoea in Achieving euvolaemia with diuretics is an important first step that not
individuals with AF, using only symptom-based III B only manages the heart failure component, but can also facilitate better
questionnaires is not recommended.155–157 control of heart rate in AF. For HFrEF, it should be highlighted that
many older guideline-recommended therapies lack specific evidence
AF, atrial fibrillation; HF, heart failure; LVEF, left ventricular ejection fraction.
a for benefit in patients with coexisting AF. No trial data are available
Class of recommendation.
b
Level of evidence. in this context for ACE inhibitors, there are conflicting data on
c
Or body mass index ≥35 kg/m2 with obesity-related complications. ARBs,132,184 and an individual patient-level analysis of RCTs found no
ESC Guidelines 27

difference between beta-blockers and placebo for all-cause mortality in provided in the 2023 ESC Guidelines for the management of cardiovas­
HFrEF with AF.133 However, these drugs have clear proof of safety and cular disease in patients with diabetes.207
there may be other indications for these therapies beyond prognosis,
including comorbidity management and symptom improvement. 5.4. Obesity
These and other therapies may also have dual functions, for example,
Obesity frequently coexists with other risk factors that have been inde­
beta-blockers or digoxin for rate control of AF, in addition to improving
pendently associated with the development of AF.208,209 Obesity (body
heart failure metrics and reducing hospitalization.48,185,186 More recent
mass index [BMI] ≥30 kg/m2) and being overweight (BMI >25 kg/m2)
additions to HFrEF management, such as eplerenone, sacubitril-
are associated with a greater risk of recurrent atrial arrhythmias after

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valsartan, and sodium-glucose cotransporter-2 (SGLT2) inhibitors,
AF ablation (13% increase for every 5 kg/m2 higher BMI).210–212 In
had substantial numbers of patients with AF enrolled in RCTs, with
the setting of comprehensive risk factor management, weight loss of
no evidence that AF status affected their ability to reduce cardiovascu­
≥10% in overweight and obese individuals with AF has been associated
lar mortality/heart failure hospitalization.134–136 Cardiac resynchroniza­
with reduced AF symptoms and AF burden in an RCT (aiming for BMI
tion therapy (CRT) in the context of HFrEF and AF is discussed in detail
<27 kg/m2).125 Cohort studies have also shown a graded response to
in the 2021 ESC Guidelines on cardiac pacing and cardiac resynchroni­
maintenance of sinus rhythm,126 improved ablation outcomes,128 and
zation therapy, with an important focus on ensuring effective biventri­
reversal of the type of AF127 commensurate with the degree of weight
cular pacing (with a low threshold for considering atrioventricular node
loss and risk factor management. However, in the Supervised Obesity
ablation).187 Patients who have heart failure with mildly reduced ejec­
Reduction Trial for AF Ablation Patients (SORT-AF) randomized trial
tion fraction (HFmrEF) (LVEF 41%–49%) and AF should generally be
in AF ablation patients, a sole weight loss intervention that achieved
treated according to guidance for HFrEF,137 albeit with limited evidence
4% loss in weight over 12 months did not impact ablation outcomes.213
to date in AF.188–190 For treatment of HFpEF and AF,191 pre-specified
This is consistent with the findings in LEGACY (Long-Term Effect of
subgroup data on AF from multiple large trials show that the SGLT2
Goal directed weight management on Atrial Fibrillation Cohort: a 5
inhibitors dapagliflozin, empaglifozin, and sotagliflozin are effective in
Year follow-up study) that showed that weight loss of ≤3% had no im­
improving prognosis.138–140
pact on AF recurrence.126 Observational studies have raised the possi­
Appropriate management of heart failure has the potential to reduce
bility of a point of no return in terms of the benefit of weight loss,214 but
recurrence of AF, e.g. by reducing adverse atrial and ventricular myo­
also the possibility that bariatric surgery can improve symptoms and re­
cardial remodelling, but there are limited data for specific therapies.
duce AF recurrence.215–217
In the Routine versus Aggressive upstream rhythm Control for preven­
tion of Early AF in heart failure (RACE 3) trial, combined management
of mild-to-moderate heart failure with ACE inhibitors/ARBs, mineralo­ 5.5. Obstructive sleep apnoea
corticoid receptor antagonists, statins, and cardiac rehabilitation in­ Obstructive sleep apnoea (OSA) is a highly prevalent condition, particu­
creased the maintenance of sinus rhythm on ambulatory monitoring larly in patients with AF.157,218 Optimal screening tools in the AF popu­
at 12 months.39 This benefit was not preserved at the 5 year follow-up, lation are still under evaluation, although it may be reasonable to screen
although this may have been confounded by the lack of ongoing inter­ for OSA in patients where a rhythm control strategy is being pursued.
vention beyond the initial 12 months.192 Polysomnography or home sleep apnoea testing are suggested in pref­
erence to screening questionnaires.155–157,219 Questionnaires assessing
daytime sleepiness are poor predictors of moderate-to-severe OSA.155
5.3. Type 2 diabetes mellitus Which parameter should be used to focus on risk of AF in patients with
OSA, and to guide OSA treatment in patients with AF, is still
Diabetes mellitus is present in around 25% of patients with AF.193–195
unclear.220,221
Patients with both diabetes and AF have a worse prognosis,196 with in­
Observational studies have suggested that individuals with OSA not
creased healthcare utilization and excess mortality and cardiovascular
treated with continuous positive airway pressure (CPAP) respond
events. The prevalence and incidence of AF and type 2 diabetes are
poorly to treatments for AF, with an increased risk of recurrence
widely increasing, thus making the association of these two conditions
after cardioversion or ablation.222 Conversely, OSA patients treated
a public health challenge.195,197 Moreover, diabetes is a major factor in­
with CPAP seem to mitigate their propensity toward developing
fluencing thromboembolic risk.198,199 Following catheter ablation of AF,
AF.148–153,222–224 A small randomized trial of CPAP vs. no therapy de­
diabetes and higher HbA1c are associated with increased length of stay
monstrated reversal of atrial remodelling in individuals with moderate
and a greater recurrence of AF.200–203
OSA.154 However, other small RCTs have failed to show a benefit of
In cohort studies, the management of diabetes mellitus as part of
CPAP therapy on ablation outcomes225 or post-cardioversion.226
comprehensive risk factor management has been associated with re­
Data on the cardiovascular mortality benefit of CPAP therapy in
duced AF symptoms, burden, reversal of the type of AF (from persist­
OSA are inconclusive.227–230
ent to paroxysmal or no AF), and improved maintenance of sinus
rhythm.126–128 However, robust evidence is limited, and individual
glucose-lowering medications have had variable effects on AF.204–206 5.6. Physical inactivity
There are emerging data of the use of SGLT2 and glucagon-like Reduced cardiorespiratory fitness frequently coexists with other modi­
peptide-1 antagonists in patients with diabetes and AF that may impact fiable risk factors and has been associated with a greater recurrence of
on treatment choice in the near future. Importantly, diabetes frequently AF after catheter ablation.141 Better cardiorespiratory fitness has a de­
coexists with multiple risk factors in patients with AF, and a compre­ monstrated inverse relationship to AF burden in both middle-aged and
hensive approach to management is required. Further details are elderly people.141 Small RCTs, meta-analyses, and observational
28 ESC Guidelines

cohorts have shown that regular aerobic exercise may also improve Class IA recommendation for the use of OAC in patients at risk of
AF-related symptoms, quality of life, and exercise capacity.142,143 thromboembolism. However, in the absence of strong evidence for
Better cardiorespiratory fitness and a gain in cardiorespiratory fitness how to apply risk scores in real-world patients, this has been sepa­
over time are associated with a greater reduction in AF burden and im­ rated from the use of any particular risk score. This is also in line
proved maintenance of sinus rhythm.141–145 with regulatory approvals for direct oral anticoagulants (DOACs),
which do not stipulate risk scores or numerical thresholds.25–28,245
5.7. Alcohol excess Substantive changes have occurred in the decades since these risk
scores were developed in regards to population-level risk factor pro­
Alcohol consumption can increase the risk of adverse events in patients
files, therapies, and targets.198 Historical scores do not take into ac­

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with AF, such as thromboembolism, death, or AF-related hospitaliza­
count parameters that have been associated with thromboembolism
tion.231,232 Alcohol is associated with an increased risk of ischaemic
in contemporary cohorts, such as cancer, chronic kidney disease
stroke in patients with newly diagnosed AF, and alcohol abstinence after
(CKD), ethnicity, and a range of circulating biomarkers (including tropo­
AF diagnosis can reduce the risk of ischaemic stroke.233 In patients re­
nin and B-type natriuretic peptide [BNP]). As an example, for CKD
ceiving OAC, alcohol excess is associated with a greater risk of bleed­
there is a correlation between decreasing glomerular filtration rate
ing,234 mediated by poor adherence, alcohol–drug interactions, liver
and proteinuria with stroke risk,247–250 and cohort data suggest a two-
disease, and variceal bleeding.
fold increased risk of ischaemic stroke and mortality in AF patients with
Alcohol consumption is associated with a dose-dependent increase
CKD vs. without.251 Other factors, such as atrial enlargement, hyperlip­
in the recurrence of AF after catheter ablation.147,235 In an RCT among
idaemia, smoking, and obesity, have been identified in specific cohort
regular non-binge drinkers with AF, the goal of abstinence led to a sig­
studies as additional risk factors for ischaemic stroke in AF.70,252,253
nificant reduction in AF recurrence and burden; alcohol intake was re­
Biomarkers, such as troponin, natriuretic peptides, growth differenti­
duced from 16.8 to 2.1 standard drinks per week (≤30 grams or 3
ation factor-15, cystatin C, and interleukin-6, can also indicate residual
standard drinks of alcohol) in the intervention arm, with 61% attaining
stroke risk among anticoagulated AF patients.254,255 Biomarker-guided
abstinence.147 In observational data of patients undergoing catheter ab­
stroke prevention is currently being evaluated in an ongoing RCT
lation, reduction of consumption to ≤7 standard drinks (≤70 grams of
(NCT03753490). Until further validation within RCTs is available, this
alcohol) per week was associated with improved maintenance of sinus
task force continues to support using simple clinical classification for im­
rhythm.128,235
plementation of OAC. Clinicians should use tools that have been vali­
dated in their local population and take an individualized approach to
6. [A] Avoid stroke and thromboembolic risk stratification that considers the full range of
each patient’s specific risk factors. The absolute risk level at which to
thromboembolism start OAC in individual patients cannot be estimated from population-
level studies. It will vary depending on how those factors interact with
6.1. Initiating oral anticoagulation other medical issues, and the degree of risk acceptable or tolerated by
Atrial fibrillation is a major risk factor for thromboembolism, irre­ that person. In general, most of the available risk scores have a thresh­
spective of whether it is paroxysmal, persistent, or permanent.236,237 old of 0.6%–1.0% per annum of thromboembolic events for clinical AF
Left untreated, and dependent on other patient-specific factors, the to warrant OAC prescription.
risk of ischaemic stroke in AF is increased five-fold, and one in every Across Europe, the most popular risk score is CHA2DS2–VASc, giv­
five strokes is associated with AF.238 The default approach should ing points for congestive heart failure, hypertension, age ≥75 years
therefore be to provide OAC to all eligible patients, except those (2 points), diabetes mellitus, prior stroke/TIA/thromboembolism
at low risk of incident stroke or thromboembolism. The effectiveness (2 points), vascular disease, age 65–74 years and female sex.
of OAC to prevent ischaemic stroke in patients with AF is well estab­ However, implementation has varied in terms of gender. Female sex
lished.239,240 Antiplatelet drugs alone (aspirin, or aspirin in combin­ is an age-dependent stroke risk modifier rather than a risk factor per
ation with clopidogrel) are not recommended for stroke prevention se.112,256,257 The inclusion of gender complicates clinical practice both
in AF.241,242 for healthcare professionals and patients.258 It also omits individuals
who identify as non-binary, transgender, or are undergoing sex hor­
6.1.1. Decision support for anticoagulation in AF mone therapy. Previous guidelines from the ESC (and globally) have
Tools have been developed to enable easier implementation of OAC not actually used CHA2DS2-VASc; instead providing different score le­
in patients with clinical AF. The majority of OAC clinical trials have vels for women and men with AF to qualify for OAC. Hence,
used variations of the CHADS2 score to indicate those at risk (with CHA2DS2-VA (excluding gender) has effectively been in place
points for chronic heart failure, hypertension, age, diabetes, and 2 (Table 10).78 This task force proposes, in the absence of other locally
points for prior stroke/transient ischaemic attack [TIA]). Although validated alternatives, that clinicians and patients should use the
most available stroke risk scores are simple and practical, the predict­ CHA2DS2-VA score to assist in decisions on OAC therapy (i.e. without
ive value of scores is generally modest (see Supplementary data a criterion for birth sex or gender). Pending further trials in lower risk
online, Table S3).243–245 Classification and discrimination of adverse patients (NCT04700826,259 NCT02387229260), OAC are recom­
events is relatively poor for all scores and hence the benefit of using mended in those with a CHA2DS2-VA score of 2 or more and should
them to select patients for OAC is unclear. There is also considerable be considered in those with a CHA2DS2-VA score of 1, following a
variation in the definition of risk factors across countries,246 and a lack patient-centred and shared care approach. Healthcare professionals
of evidence from clinical trials on the ability of stroke risk scoring to should take care to assess for other thromboembolic risk factors
enhance clinical practice.243 This guideline continues to provide a that may also indicate the need for OAC prescription.
ESC Guidelines 29

Recommendation Table 6 — Recommendations to A CHA2DS2-VA score of 1 should be considered an

assess and manage thromboembolic risk in AF (see also indicator of elevated thromboembolic risk for IIa C
Evidence Table 6)
decisions on initiating oral anticoagulation.
Recommendations Class a
Level b Direct oral anticoagulant therapy may be considered
in patients with asymptomatic device-detected
Oral anticoagulation is recommended in patients subclinical AF and elevated thromboembolic risk to IIb B
with clinical AF at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism,
I A
prevent ischaemic stroke and excluding patients at high risk of bleeding.281,282

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thromboembolism.239,240 Antiplatelet therapy is not recommended as an
A CHA2DS2-VA score of 2 or more is recommended alternative to anticoagulation in patients with AF to
as an indicator of elevated thromboembolic risk for I C III A
prevent ischaemic stroke and
decisions on initiating oral anticoagulation. thromboembolism.242,283
Oral anticoagulation is recommended in all patients Using the temporal pattern of clinical AF

© ESC 2024
with AF and hypertrophic cardiomyopathy or (paroxysmal, persistent, or permanent) is not
cardiac amyloidosis, regardless of CHA2DS2-VA I B III B
recommended to determine the need for oral
score, to prevent ischaemic stroke and anticoagulation.284,285
thromboembolism.270–276
AF, atrial fibrillation; CHA2DS2-VA, congestive heart failure, hypertension, age ≥75 years (2
Individualized reassessment of thromboembolic risk
points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial
is recommended at periodic intervals in patients with thromboembolism (2 points), vascular disease, age 65–74 years; DOAC, direct oral
I B
AF to ensure anticoagulation is started in appropriate anticoagulant.
a
Class of recommendation.
patients.277–280 b
Level of evidence.
Continued

Table 10 Updated definitions for the CHA2DS2-VA score

CHA2DS2-VA component Definition and comments Points

awardeda

C Chronic heart failure Symptoms and signs of heart failure (irrespective of LVEF, thus including HFpEF, HFmrEF, and 1
HFrEF), or the presence of asymptomatic LVEF ≤40%.261–263
H Hypertension Resting blood pressure >140/90 mmHg on at least two occasions, or current antihypertensive 1
treatment. The optimal BP target associated with lowest risk of major cardiovascular events is
120–129/70–79 mmHg (or keep as low as reasonably achievable).162,264
A Age 75 years or above Age is an independent determinant of ischaemic stroke risk.265 Age-related risk is a continuum, 2
but for reasons of practicality, two points are given for age ≥75 years.
D Diabetes mellitus Diabetes mellitus (type 1 or type 2), as defined by currently accepted criteria,266 or treatment 1
with glucose lowering therapy.
S Prior stroke, TIA, or arterial Previous thromboembolism is associated with highly elevated risk of recurrence and therefore 2
thromboembolism weighted 2 points.
V Vascular disease Coronary artery disease, including prior myocardial infarction, angina, history of coronary 1
revascularization (surgical or percutaneous), and significant CAD on angiography or cardiac
imaging.267
OR
Peripheral vascular disease, including: intermittent claudication, previous revascularization for PVD,
© ESC 2024

percutaneous or surgical intervention on the abdominal aorta, and complex aortic plaque on
imaging (defined as features of mobility, ulceration, pedunculation, or thickness ≥4 mm).268,269
A Age 65–74 years 1 point is given for age between 65 and 74 years. 1

BP, blood pressure; CAD, coronary artery disease; CHA2DS2-VA, chronic heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, prior stroke/transient ischaemic attack/
arterial thromboembolism (2 points), vascular disease, age 65–74 years; HFmrEF, heart failure with mildly reduced ejection fraction; HFpEF, heart failure with preserved ejection
fraction; HFrEF, heart failure with reduced ejection fraction; LVEF, left ventricular ejection fraction; PVD, peripheral vascular disease.
a
In addition to these factors, other markers that modify an individual’s risk for stroke and thromboembolism should be considered, including cancer, chronic kidney disease, ethnicity (black,
Hispanic, Asian), biomarkers (troponin and BNP), and in specific groups, atrial enlargement, hyperlipidaemia, smoking, and obesity.
30 ESC Guidelines

6.2. Oral anticoagulants number of factor XI inhibitors in various stages of clinical evaluation. A
Vitamin K antagonists (VKA), predominantly warfarin but also other phase 2 trial of abelacimab in patients with AF has shown lower rates
coumarin and indandione derivatives, have been the principal drugs to of bleeding compared with rivaroxaban286; however, a phase 3 trial of
prevent thromboembolic events in the context of AF. As with any asundexian was terminated early due to lack of efficacy against apixaban
anticoagulant, a balance must be reached between preventing thrombo­ (NCT05643573), despite favourable phase 2 results.287 Regardless of the
embolism and preserving physiological haemostasis, with VKA-associated type of OAC prescribed, healthcare teams should be aware of the poten­
intracranial and other major haemorrhage the most critical limitation for tial for interactions with other drugs, foods, and supplements, and in­
acceptance of OAC. The global switch to DOACs as first-line therapy corporate this information into the education provided to patients and

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has changed this risk–benefit balance, allowing more widespread pre­ their carers. The list of potential interactions with VKA is broad,288,289
scription with no need for routine monitoring (see Supplementary but there are also some common cardiovascular and non-cardiovascular
data online, Additional Evidence Tables S5–S7). This component of AF drugs that interact with DOACs.290,291 Figure 9 highlights common and
management may see substantive changes in the coming years, with a major interactions to consider for VKAs and DOACs.

Vitamin K antagonist Direct oral anticoagulants

oral anticoagulants
Apixaban Dabigatran Edoxaban Rivaroxaban

Avoid where Avoid where Avoid where Avoid where Avoid where
possible possible possible possible possible
NSAIDs Carbamazepine Dronedarone Carbamazepine Dronedarone
Fluconazole Phenytoin Carbamazepine Phenytoin Carbamazepine
Voriconazole Phenobarbital Phenytoin Phenobarbital Phenytoin
Fluoxetine Rifampicin Rifampicin Rifampicin Phenobarbital
Ritonavir Ritonavir Ritonavir Itraconazole
Itraconazole Itraconazole Ketoconazole
Ketoconazole Ketoconazole Posaconazole
Cyclosporin Voriconazole
Glecaprevir/pibrentasvir Rifampicin
Tacrolimus Ritonavir

Reduce warfarin Avoid or reduce Delay timing of Avoid or reduce Avoid if another
dose apixaban dose if drugs and/or edoxaban dose interacting drug
Amiodarone another interacting adjust dose therapy
Metronidazole drug therapy Amiodarone Dronedarone Protease inhibitors
Sulphonamides Posaconazole Ticagrelor Tyrosine kinase
Allopurinol Voriconazole Verapamil inhibitors
Fluvastatin Avoid or reduce
Protease inhibitors Quinidine
Gemfibrozil Clarithromycin edoxaban dose if Caution if renal
Apalutamide
Fluorouracil Posaconazole another interacting function impaired
Enzalutamide
Tyrosine kinase drug therapy
Verapamil
Increase warfarin inhibitors Cyclosporin Cyclosporin
dose Itraconazole Clarithromycin
Carbamazepine Ketoconazole Erythromycin
Erythromycin Fluconazole
Monitor INR carefully
Dronedarone
Limit consumption Limit consumption Limit consumption Limit consumption
Statins
Penicillin antibiotics Grapefruit juice Grapefruit juice Grapefruit juice Grapefruit juice
Macrolide antibiotics St John’s wort St John’s wort St John’s wort St John’s wort
Quinolone antibiotics
Rifampicin
Methotrexate
Ritonavir
Phenytoin
Sodium valproate
Tamoxifen
Chemotherapies

Limit consumption
Alcohol
Grapefruit/cranberry juice
St John’s wort

Figure 9 Common drug interactions with oral anticoagulants. INR, international normalized ratio of prothrombin time; NSAID, non-steroidal anti-
inflammatory drug. This figure depicts only common or major interactions and is not an exhaustive list of all potential interactions. Please see the
European Medicines Agency website or your local formulary for more information.
ESC Guidelines 31

Recommendation Table 7 — Recommendations for (risk ratio, 0.42; 95% CI, 0.21–0.86; P = .017), with no heterogeneity be­
oral anticoagulation in AF (see also Evidence Table 7) tween trials and no significant difference in major bleeding.293
Specific patient subgroups show consistent benefit with DOACs vs.
Recommendations Classa Levelb VKAs. For heart failure, major thromboembolic events were lower in
Direct oral anticoagulants are recommended in DOAC-treated patients vs. warfarin in subgroup analysis of landmark
preference to VKAs to prevent ischaemic stroke and RCTs,322 confirmed in large-scale real-world data.323 In a retrospective
thromboembolism, except in patients with I A
cohort of patients aged over 80 years, DOAC use was associated with a
lower risk of ischaemic stroke, dementia, mortality, and major bleeding
mechanical heart valves or moderate-to-severe
than warfarin,324 but this may be confounded by prescription bias.

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mitral stenosis.25–28,292–294
Direct oral anticoagulants retain their efficacy and safety over VKAs
A target INR of 2.0–3.0 is recommended for patients
in patients with mild-to-moderate CKD (creatinine clearance
with AF prescribed a VKA for stroke prevention to I B
[CrCl] >30 mL/min),325 although specific dosing adjustments
ensure safety and effectiveness.295–298 apply.25–28,326 In Europe, reduced doses of rivaroxaban, apixaban, and
Switching to a DOAC is recommended for eligible edoxaban are approved in patients with severe CKD (CrCl 15–29 mL/
patients that have failed to maintain an adequate time min), although limited numbers of patients were included in the major
in therapeutic range on a VKA (TTR <70%) to I B RCTs against VKA.327 Dabigatran is more dependent on renal elimination
prevent thromboembolism and intracranial and so is contraindicated with an estimated glomerular filtration rate
haemorrhage.299–303 <30 mL/min/1.73 m2. Small trials have been performed in patients on
Keeping the time in therapeutic range above 70% haemodialysis, with two finding no difference between apixaban 2.5 mg
should be considered in patients taking a VKA to twice daily and VKA for efficacy or safety outcomes,328,329 and one trial
ensure safety and effectiveness, with INR checks at IIa A showing that rivaroxaban 10 mg led to significantly lower rates of cardiovas­
appropriate frequency and patient-directed cular events and major bleeding compared with VKA.330 Careful institution
education and counselling.304–308 and regular follow-up are advised when instituting anticoagulants in any pa­
tient with impaired renal function (See Supplementary data online,
Maintaining VKA treatment rather than switching to
Additional Evidence Table 8).326
a DOAC may be considered in patients aged ≥75
IIb B Direct oral anticoagulants as a class should be avoided in specific pa­
years on clinically stable therapeutic VKA with
tient groups, such as those with mechanical heart valves or
polypharmacy to prevent excess bleeding risk.309
moderate-to-severe mitral stenosis. In patients with mechanical heart
A reduced dose of DOAC therapy is not valves, an excess of thromboembolic and major bleeding events among
© ESC 2024

recommended, unless patients meet DOAC-specific patients on dabigatran therapy vs. VKA was observed, with an RCT ter­
III B
criteria,c to prevent underdosing and avoidable minated prematurely.331 A trial of apixaban vs. VKA after implantation
thromboembolic events.310–312 of a mechanical aortic valve was also stopped due to excess thrombo­
AF, atrial fibrillation; DOAC, direct oral anticoagulant; INR, international normalized ratio embolic events in the apixaban group.332 The restriction on DOAC use
of prothrombin time; TTR, time in therapeutic range; VKA, vitamin K antagonist. does not apply to bioprosthetic heart valves (including mitral) or after
a
Class of recommendation. transcatheter aortic valve implantation, where DOACs can be used and
b
Level of evidence.
c trial data show non-inferiority for clinical events compared with
See Table 11.
VKAs.304,333,334 With regards to mitral stenosis, the DOAC vs. VKA
trials excluded patients with moderate-to-severe disease. In 4531 ran­
domized patients with rheumatic heart disease and AF, VKAs led to a
6.2.1. Direct oral anticoagulants lower rate of composite cardiovascular events and death than rivarox­
The DOACs (apixaban, dabigatran, edoxaban, and rivaroxaban) have all aban, without a higher rate of bleeding.294 Eighty-two per cent of the
demonstrated at least non-inferior efficacy compared with warfarin for patients included had a mitral valve area ≤2 cm, supporting the restric­
the prevention of thromboembolism, but with the added benefit of a tion of DOAC use in patients with moderate-to-severe mitral stenosis.
50% reduction in intracranial haemorrhage (ICH).25–28 Meta-analyses of Note that patients with other types of valve disease (mitral regurgita­
individual data from 71 683 RCT patients showed that standard, full-dose tion and others) should preferentially be prescribed a DOAC, and
DOAC treatment compared with warfarin reduces the risk of stroke or the term ‘valvular’ AF is obsolete and should be avoided.
systemic embolism (HR, 0.81; 95% CI, 0.73–0.91), all-cause mortality (HR, Inappropriate dose reductions for DOACs are frequent in clinical
0.90; 95% CI, 0.85–0.95), and intracranial bleeding (HR, 0.48; 95% CI, practice,311 but need to be avoided as they increase the risk of stroke with­
0.39–0.59), with no significant difference in other major bleeding (HR, out decreasing bleeding risk.310 Hence, DOAC therapy should be instituted
0.86; 95% CI, 0.73–1.00) and little or no between-trial heterogeneity.292 according to the standard full dose as tested in phase 3 RCTs and approved
Post-marketing observational data on the effectiveness and safety of by regulators (Table 11). The prescribed dosage should consider the individ­
dabigatran,313,314 rivaroxaban,315,316 apixaban,317 and edoxaban318 vs. ual patient’s profile.335 Drug interactions need to be considered in all pa­
warfarin show general consistency with the respective phase 3 RCTs. tients taking or planned for DOACs (see Figure 9 for common drug
For patients undergoing cardioversion, three underpowered trials interactions).336 There is insufficient evidence currently to advise on routine
showed non-significantly lower rates of cardiovascular events with laboratory testing for DOAC levels. However, in certain situations, meas­
DOACs compared with warfarin.319–321 In meta-analysis of these urement of DOAC levels (where available) may be helpful, such as severe
5203 patients predominantly undergoing electrical cardioversion, the bleeding, the need for urgent surgery, or thromboembolic events despite
composite of stroke, systemic embolism, myocardial infarction (MI), apparent DOAC compliance.337,338 Patients should always be involved in
and cardiovascular death was significantly lower at 0.42% in decision-making on anticoagulation,339 leading to better alignment with per­
patients randomized to a DOAC vs. 0.98% in those allocated VKA sonal preferences that can help to increase understanding and adherence.
32 ESC Guidelines

Table 11 Recommended doses for direct oral anticoagulant therapy

DOAC Standard full dose Criteria for dose reduction Reduced dose only
if criteria met

Apixaban 5 mg twice daily Two out of three needed for dose reduction: 2.5 mg twice daily
(i) age ≥80 years
(ii) body weight ≤60 kg
(iii) serum creatinine ≥133 mmol/L.

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Dabigatran 150 mg twice daily Dose reduction recommended if any apply: 110 mg twice daily
(i) age ≥80 years
(ii) receiving concomitant verapamil.
Dose reduction considered on an individual basis if any apply:
(i) age 75–80
(ii) moderate renal impairment (creatinine clearance 30–50 mL/min)
(iii) patients with gastritis, oesophagitis, or gastro-oesophageal reflux
(iv) others at increased risk of bleeding.
Edoxaban 60 mg once daily Dose reduction if any apply: 30 mg once daily
(i) moderate or severe renal impairment (creatinine clearance 15–50 mL/min)

© ESC 2024
(ii) body weight ≤60 kg
(iii) concomitant use of ciclosporin, dronedarone, erythromycin, or ketoconazole.
Rivaroxaban 20 mg once daily Creatinine clearance 15–49 mL/min. 15 mg once daily

DOAC, direct oral anticoagulant.

Dose and dose adjustments are taken from the European Medicines Association Summary of Product Characteristics for each DOAC. There may be other patient-specific reasons
for providing a reduced dose, but, in general, the standard full dose should be used to provide optimal prevention of thromboembolism related to AF. Note that antiplatelet agents
should be stopped in most patients when commencing a DOAC (see Section 6.3). A number of drug interactions exist with each DOAC and should be taken into consideration
(see Figure 9).

6.2.2. Vitamin K antagonists VKA (17.8 vs. 10.5 per 100 patient-years, driven by non-major bleeds).309
Vitamin K antagonist therapy reduces stroke risk by 64% and mortality Hence, in such patients who are clinically stable with good TTR, VKAs
by 26% in patients with AF at elevated thromboembolic risk (mostly may be continued rather than switching to a DOAC after an open discus­
warfarin in trials, compared with placebo or no treatment).239 sion with the patient and shared decision-making.
Vitamin K antagonists are still used in many patients worldwide, but
prescriptions have declined sharply since the introduction of
DOACs.340,341 Vitamin K antagonists are currently the only treatment 6.2.3. Clinical vs. device-detected subclinical AF
option in AF patients with mechanical heart valves or moderate-to- The known benefit of anticoagulation applies to clinical AF. Two RCTs
severe mitral valve stenosis.294,331 The use of VKAs is not only limited have been published assessing the value of DOAC therapy in device-
by numerous drug and food interactions (Figure 9), but also a narrow detected subclinical AF. The ARTESiA trial (Apixaban for the
therapeutic range. This requires frequent monitoring and dose adjust­ Reduction of Thromboembolism in Patients With Device-Detected
ment according to the prothrombin time expressed as the international Sub-Clinical Atrial Fibrillation) was completed with 4012 patients
normalized ratio (INR).342 If the time in therapeutic range (TTR) is with device-detected subclinical AF and a mean follow-up of 3.5
maintained for long periods (e.g. >70% with INR 2.0–3.0), then VKA years.282 The primary efficacy outcome of stroke or systemic embolism
can be effective for thromboembolic protection with an acceptable was significantly less in those randomized to apixaban compared with
safety profile.295–297,343 However, VKAs are associated with higher aspirin (HR, 0.63; 95% CI, 0.45–0.88; P = .007). In the intention-to-treat
rates of intracranial bleeding,299,300 and also higher rates of other types analysis, the primary safety outcome of major bleeding was higher with
of bleeding compared with DOACs.83 apixaban (HR, 1.36; 95% CI, 1.01–1.82; P = .04). The NOAH trial (Non-
In view of the potential safety benefits, switching from VKAs to a vitamin K Antagonist Oral Anticoagulants in Patients With Atrial High
DOAC is justified where there are concerns about intracranial bleeding Rate Episodes) was stopped prematurely due to safety concerns and
or for patient-choice reasons, and a switch is recommended where pa­ futility for the efficacy of edoxaban, and hence provides limited informa­
tients have failed to maintain an adequate TTR (<70%). This depends tion.281 The analysis of 2536 patients with device-detected atrial high-
on patients fulfilling eligibility criteria for DOACs and should take into ac­ rate episodes and a median follow-up of 21 months identified no differ­
count other correctable reasons for poor INR control. There is limited ence in a composite of cardiovascular death, stroke, or embolism com­
data on switching OAC in older patients (≥75 years) with polypharmacy paring edoxaban and placebo (HR, 0.81; 95% CI, 0.60–1.08;
or other markers of frailty. A recent trial in this patient group premature­ P = .15). Those randomized to edoxaban had a higher rate of the
ly stopped for futility showed that switching from VKAs to DOACs led composite of death or major bleeding than placebo (HR, 1.31;
to a higher primary outcome rate of major or clinically relevant non- 95% CI, 1.02–1.67; P = .03). Patients had a low burden of device-
major bleeding events compared with continuing with INR-guided detected subclinical AF in both trials (median duration 1.5 h and
ESC Guidelines 33

2.8 h, respectively), with lower rates of thromboembolism (around 1% 6.4. Residual ischaemic stroke risk despite
per patient-year) than would be expected for an equivalent cohort of
patients with clinical AF and a CHA2DS2-VASc score of 4.
anticoagulation
Although OAC significantly reduces the risk of ischaemic stroke in pa­
Considering the trade-off between potential benefit and the risk of
tients with AF, there remains a residual risk.252,354 One-third of patients
major bleeding, this task force concludes that DOAC therapy may be
with AF presenting with an ischaemic stroke are already on anticoagu­
considered in subgroups of patients with asymptomatic device-
lation,355 with heterogeneous aetiology.356 This may include non-AF-
detected subclinical AF who have high estimated stroke risk and an ab­
related competing stroke mechanisms (such as large artery and small
sence of major bleeding risk factors (see Section 6.7). The duration and
vessel diseases), non-adherence to therapy, an inappropriately low

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burden of subclinical AF that could indicate potential benefit from OAC
dose of anticoagulant, or thromboembolism despite sufficient anticoa­
remains uncertain.344 Regardless of the initial decision on OAC, pa­
gulation.357 Laboratory measurement of INR or DOAC levels may con­
tients with subclinical AF should receive management and follow-up
tribute to revealing an amenable cause of the stroke. Regardless of
for all aspects of AF-CARE as the risk of developing clinical AF is high
anticoagulation status, patients with ischaemic stroke are more likely
(6%–9% per year).
to have cardiovascular risk factors.358 Many clinicians managing patients
with an incident stroke despite taking anticoagulation will be tempted
6.3. Antiplatelet drugs and combinations to switch their anticoagulant regimen. While there may be some advan­
with anticoagulants tage in switching from VKAs to DOACs for protection against future
recurrent ischaemic or haemorrhagic stroke, this task force does not
Antiplatelet drugs, such as aspirin and clopidogrel, are not an alternative
recommend routinely switching from one DOAC to another, or
to OAC. They should not be used for stroke prevention, and can lead
from a DOAC to a VKA, since this has no proven efficacy.252,356,359
to potential harm (especially among elderly patients with AF).345–347 In
There may be individual reasons for switching, including potential inter­
ACTIVE W (Atrial fibrillation Clopidogrel Trial with Irbesartan for
actions with new drugs; however, there is no consistent data across
prevention of Vascular Events), dual antiplatelet therapy (DAPT) with
countries that adherence or efficacy differs between once- and twice-
aspirin and clopidogrel was less effective than warfarin for the preven­
daily approaches.360,361 Emerging, but observational evidence suggests
tion of stroke, systemic embolism, MI, or vascular death (annual risk of
that switching provides limited reduction in the risk of recurrent ischae­
events 5.6% vs. 3.9%, respectively; P = .0003), with similar rates of
mic stroke.252,356,359 The alternative strategy of adding antiplatelet
major bleeding.348 The AVERROES (Apixaban Versus Acetylsalicylic
therapy to OAC may lead to an increased risk of bleeding.356,359
Acid to Prevent Stroke in Atrial Fibrillation Patients Who Have Failed
Aside from thorough attention to underlying risk factors and co­
or Are Unsuitable for Vitamin K Antagonist Treatment) trial demon­
morbidities, the approach to management of patients with a stroke des­
strated a lower rate of stroke or systemic embolism with apixaban
pite OAC remains a distinct challenge.
compared with aspirin (HR, 0.45; 95% CI, 0.32–0.62; P < .001), with
no significant difference in major bleeding (there were 11 cases of intra­
cranial bleeding with apixaban and 13 with aspirin).242 Recommendation Table 9 — Recommendations for
The combination of OAC with antiplatelet agents (especially aspirin) thromboembolism despite anticoagulation (see also
without an adequate indication occurs frequently in clinical practice Evidence Table 9)
(see Supplementary data online, Additional Evidence Table S9).349,350
Recommendation Classa Levelb
Bleeding events are more common when antithrombotic agents are
combined, and no clear benefit has been observed in terms of preven­ A thorough diagnostic work-up should be
tion of stroke or death.349 In general, combining antiplatelet drugs with considered in patients taking an oral anticoagulant
anticoagulants (DOACs or VKAs) should only occur in selected pa­ and presenting with ischaemic stroke or
tients with acute vascular disease (e.g. acute coronary syndromes; see IIa B
thromboembolism to prevent recurrent events,
Section 9.2). The combination of low-dose rivaroxaban (2.5 mg) with including assessment of non-cardioembolic causes,
aspirin reduced the risk of stroke in patients with chronic vascular dis­ vascular risk factors, dosage, and adherence.356,357
ease in a subanalysis of the COMPASS (Cardiovascular Outcomes for
Adding antiplatelet treatment to anticoagulation is
People Using Anticoagulation Strategies) trial,351,352 but this cannot
not recommended in patients with AF to prevent III B
be generalized to AF patients because those with an indication for full-
recurrent embolic stroke.356,359
dose anticoagulants were excluded.
Switching from one DOAC to another, or from a
© ESC 2024

DOAC to a VKA, without a clear indication is not

III B
Recommendation Table 8 — Recommendations for recommended in patients with AF to prevent
combining antiplatelet drugs with anticoagulants for recurrent embolic stroke.252,356,359
stroke prevention (see also Evidence Table 8)
AF, atrial fibrillation; DOAC, direct oral anticoagulant; VKA, vitamin K antagonist.
a
Recommendation Classa Levelb Class of recommendation.
b
Level of evidence.
Adding antiplatelet treatment to oral anticoagulation
© ESC 2024

is not recommended in AF patients for the goal of

preventing ischaemic stroke or
III B 6.5. Percutaneous left atrial appendage
thromboembolism.345,347,353 occlusion
Percutaneous left atrial appendage occlusion (LAAO) is a device-based
AF, atrial fibrillation.
a
Class of recommendation. therapy that aims to prevent ischaemic stroke in patients with AF.362,363
b
Level of evidence. In the VKA era, two RCTs compared warfarin with LAAO using the
34 ESC Guidelines

Watchman device. The 5-year pooled outcomes demonstrated a simi­ been associated with higher thromboembolic and bleeding events
lar rate of the composite endpoint (cardiovascular or unexplained during 1 year follow-up in a large observational registry of one par­
death, systemic embolism, and stroke) between the LAAO and war­ ticular device.398
farin arms. Those randomized to LAAO had significantly lower rates
of haemorrhagic stroke and all-cause death, but also a 71% non-
significant increase in ischaemic stroke and systemic embolism.364 Recommendation Table 10 — Recommendations for
With DOACs demonstrating similar rates of major bleeding to as­ percutaneous left atrial appendage occlusion (see also
pirin,242 warfarin in the control arms in these trials is no longer standard Evidence Table 10)

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of care and hence the place of LAAO in current practice is unclear. The
Amulet occluder is an alternative LAAO device which was non-inferior Recommendation Classa Levelb
in an RCT to the Watchman device for safety events Percutaneous LAA occlusion may be considered in
(procedure-related complications, death, or major bleeding) and

© ESC 2024
patients with AF and contraindications for long-term
thromboembolism.365 In the PRAGUE-17 trial, 402 AF patients were IIb C
anticoagulant treatment to prevent ischaemic stroke
randomized to DOAC or LAAO (Watchman or Amulet), with non- and thromboembolism.372,376,386,387
inferiority reported for a broad composite primary endpoint of stroke,
TIA, systemic embolism, cardiovascular death, major or non-major clin­ AF, atrial fibrillation; LAA, left atrial appendage.
a
Class of recommendation.
ically relevant bleeding, and procedure/device-related complica­ b
Level of evidence.
tions.366,367 Larger trials368,369 are expected to provide more
comprehensive data that can add to the current evidence base (see
Supplementary data online, Additional Evidence Table S10). 6.6. Surgical left atrial appendage occlusion
Pending further RCTs (see Supplementary data online, Table S4), pa­ Surgical occlusion or exclusion of the left atrial appendage (LAA) can
tients with a contraindication to all of the OAC options (the four contribute to stroke prevention in patients with AF undergoing
DOACs and VKAs) have the most appropriate rationale for LAAO im­ cardiac surgery.399,400 The Left Atrial Appendage Occlusion Study
plantation, despite the paradox that the need for post-procedure (LAAOS III) randomized 4811 patients with AF to undergo or not
antithrombotic treatment exposes the patient to a bleeding risk that undergo LAAO at the time of cardiac surgery for another indication.
may be equivalent to that of DOACs. Regulatory approvals based on During a mean of 3.8 years follow-up, ischaemic stroke or systemic em­
RCT protocols suggest the need for 45 days of VKA plus aspirin after bolism occurred in 114 patients (4.8%) in the occlusion group and 168
implantation, followed by 6 months of DAPT in patients with no major (7.0%) in the control arm (HR, 0.67; 95% CI, 0.53–0.85; P = .001).401
peri-device leaks, and then ongoing aspirin (see Supplementary data The LAAOS III trial did not compare appendage occlusion with anticoa­
online, Figure S2).370–372 However, real-world practice is markedly dif­ gulation (77% of participants continued to receive OAC), and there­
ferent and also varied. Direct oral anticoagulant administration at full fore, surgical LAA closure should be considered as an adjunct
or reduced dose has been proposed as a treatment alternative to therapy to prevent thromboembolism in addition to anticoagulation
warfarin.373 Observational studies have also supported the use of anti­ in patients with AF.
platelet therapy without associated increases in device-related throm­ There are no RCT data showing a beneficial effect on ischaemic
bosis or stroke.374–376 In a propensity-matched comparison of patients stroke or systemic embolism in patients with AF undergoing LAAO
receiving limited early OAC vs. antiplatelet treatment post-Watchman during endoscopic or hybrid AF ablation. A meta-analysis of RCT and
implantation, thromboembolic event rates and bleeding complications observational data showed no differences in stroke prevention or all-
were similar.377 While waiting for solid RCT data (NCT03445949, cause mortality when comparing LAA clipping during thoracoscopic
NCT03568890),378 pertinent decisions on antithrombotic treatment AF ablation with percutaneous LAAO and catheter ablation.402
are usually made on an individualized basis.379–381 Prevention of recur­ While the percutaneous LAAO/catheter ablation group showed a high­
rent stroke, in addition to OAC, is another potential indication for er acute success rate, it was also associated with a higher risk of haem­
LAAO. Only limited data are so far available from registries,382 with on­ orrhage during the peri-operative period. In an observational study
going trials expected to provide more insight (NCT03642509, evaluating 222 AF patients undergoing LAA closure using a clipping de­
NCT05963698). vice as a part of endoscopic or hybrid AF ablation, complete closure
Left atrial appendage occlusion device implantation is associated was achieved in 95% of patients.403 There were no intra-operative
with procedural risk including stroke, major bleeding, device- complications, and freedom from a combined endpoint of ischaemic
related thrombus, pericardial effusion, vascular complications, and stroke, haemorrhagic stroke, or TIA was 99.1% over 369 patient-years
death.362,383–385 Voluntary registries enrolling patients considered of follow-up. Trials evaluating the beneficial effect of surgical LAA clos­
ineligible for OAC have reported low peri-procedural ure in patients undergoing cardiac surgery but without a known history
risk,372,376,386,387 although national registries report in-hospital ma­ of AF are ongoing (NCT03724318, NCT02701062).404
jor adverse event rates of 9.5% in centres performing 5–15 LAAO There is a potential advantage for stand-alone epicardial over
cases per year, and 5.6% performing 32–211 cases per year percutaneous LAA closure in patients with a contraindication for
(P < .001).388 Registries with new-generation devices report a low­ OAC, as there is no need for post-procedure anticoagulation after epi­
er complication rate compared with RCT data.389,390 Device- cardial closure. Observational data show that stand-alone LAA closure
related thrombi occur with an incidence of 1.7%–7.2% and are using an epicardial clip is feasible and safe.405 A multidisciplinary team
associated with a higher risk of ischaemic stroke.386,391–397 Their approach can facilitate the choice between epicardial or percutaneous
detection can be documented as late as 1 year post-implantation LAA closure in such patients.406 The majority of safety data and experi­
in one-fifth of patients, thus mandating a late ‘rule-out’ imaging ap­ ence in epicardial LAA closure originate from a single clipping device
proach.391 Likewise, follow-up screening for peri-device leaks is (AtriClip)403,407,408 (see Supplementary data online, Additional
relevant, as small leaks (0–5 mm) are present in ∼25% and have Evidence Table S11).
ESC Guidelines 35

Recommendation Table 11 — Recommendations for OAC that are at high risk of gastrointestinal bleeding. However, the evi­
surgical left atrial appendage occlusion (see also dence base is limited and not specifically in patients with AF. Whereas
Evidence Table 11) observational studies have shown potential benefit from proton pump
inhibitors,437 a large RCT in patients receiving low-dose anticoagulation
Recommendations Classa Levelb
and/or aspirin for stable cardiovascular disease found that pantoprazole
Surgical closure of the left atrial appendage is had no significant impact on upper gastrointestinal bleeding events
recommended as an adjunct to oral anticoagulation compared with placebo (HR, 0.88; 95% CI, 0.67–1.15).438 Hence, the
in patients with AF undergoing cardiac surgery to I B use of gastric protection should be individualized for each patient

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prevent ischaemic stroke and according to the totality of their perceived bleeding risk.
thromboembolism.400,401,408–412
Surgical closure of the left atrial appendage should be Recommendation Table 12 — Recommendations for
considered as an adjunct to oral anticoagulation in assessment of bleeding risk (see also Evidence Table 12)
patients with AF undergoing endoscopic or hybrid IIa C
Recommendations Classa Levelb
AF ablation to prevent ischaemic stroke and
thromboembolism.402,403 Assessment and management of modifiable bleeding
Stand-alone endoscopic surgical closure of the left risk factors is recommended in all patients eligible for
atrial appendage may be considered in patients with oral anticoagulation, as part of shared I B

© ESC 2024
AF and contraindications for long-term anticoagulant IIb C decision-making to ensure safety and prevent
treatment to prevent ischaemic stroke and bleeding.439–444
thromboembolism.399,405,406,413 Use of bleeding risk scores to decide on starting or

© ESC 2024
AF, atrial fibrillation.
withdrawing oral anticoagulation is not
III B
a
Class of recommendation. recommended in patients with AF to avoid
b
Level of evidence. under-use of anticoagulation.431,445,446

AF, atrial fibrillation.

a
Class of recommendation.
b
Level of evidence.
6.7. Bleeding risk
6.7.1. Assessment of bleeding risk
When initiating antithrombotic therapy, modifiable bleeding risk factors 6.7.2. Management of bleeding on anticoagulant
should be managed to improve safety (Figure 10).414–418 This includes therapy
strict control of hypertension, advice to reduce excess alcohol intake, General management of bleeding in patients receiving OAC is outlined
avoidance of unnecessary antiplatelet or anti-inflammatory agents, in Figure 11. Cause-specific management is beyond the scope of these
and attention to OAC therapy (adherence, control of TTR if on guidelines, and will depend on the individual circumstances of the pa­
VKAs, and review of interacting medications). Clinicians should con­ tient and the healthcare environment.447 Assessment of patients with
sider the balance between stroke and bleeding risk—as factors for active bleeding should include confirmation of the bleeding site,
both are dynamic and overlapping, they should be re-assessed at bleeding severity, type/dose/timepoint of last anticoagulant intake,
each review depending on the individual patient.419–421 Bleeding risk concomitant use of other antithrombotic agents, and other factors in­
factors are rarely a reason to withdraw or withhold OAC in eligible fluencing bleeding risk (renal function, platelet count, and medications
patients, as the risk of stroke without anticoagulation often outweighs such as non-steroidal anti-inflammatories). INR testing and information
the risk of major bleeding.422,423 Patients with non-modifiable risk on recent results are invaluable for patients taking VKAs. Specific
factors should be reviewed more often, and where appropriate, coagulation tests for DOACs include diluted thrombin time, ecarin
a multidisciplinary team approach should be instituted to guide clotting time, ecarin chromogenic assay for dabigatran, and chro­
management. mogenic anti-factor Xa assay for rivaroxaban, apixaban, and edoxa­
Several bleeding risk scores have been developed to account for a ban.447–449 Diagnostic and treatment interventions to identify and
wide range of clinical factors (see Supplementary data online, manage the cause of bleeding (e.g. gastroscopy) should be performed
Table S5 and Additional Evidence Tables S12 and S13).424 Systematic re­ promptly.
views and validation studies in external cohorts have shown contrasting In cases of minor bleeding, temporary withdrawal of OAC while the
results and only modest predictive ability.244,425–434 This task force cause is managed is usually sufficient, noting that the reduction in anti­
does not recommend a specific bleeding risk score given the uncer­ coagulant effect is dependent on the INR level for VKAs or the half-life
tainty in accuracy and potential adverse implications of not providing of the particular DOAC.
appropriate OAC to those at thromboembolic risk. There are very For major bleeding events in patients taking VKAs, administration
few absolute contraindications to OAC (especially DOAC therapy). of fresh frozen plasma restores coagulation more rapidly than
Whereas primary intracranial tumours435 or an intracerebral bleed re­ vitamin K, but prothrombin complex concentrates achieve even
lated to cerebral amyloid angiopathy436 are examples where OAC faster blood coagulation with fewer complications, and so are
should be avoided, many other contraindications are relative or tem­ preferrable to achieve haemostasis.450 In DOAC-treated patients
porary. For example, a DOAC can often be safely initiated or re- where the last DOAC dose was taken within 2–4 h, charcoal
initiated after acute bleeding has stopped, as long as the source has administration and/or gastric lavage may reduce further exposure.
been fully investigated and managed. Co-prescription of proton If the patient is taking dabigatran, idarucizumab can fully reverse its anti­
pump inhibitors is common in clinical practice for patients receiving coagulant effect and help to achieve haemostasis within 2–4 h in
36 ESC Guidelines

Comprehensive medical history to determine all bleeding risk factors at OAC initiation/follow-up
(Class I)

Do not use bleeding risk scores to decide starting or withdrawing OAC

(Class III)

Manage all modifiable bleeding risk factors with shared decision-making

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(Class I)
Hypertension Antiplatelet drugs Alcohol intake Unstable/variable INR
Optimize blood Do not use antiplatelet Reduce alcohol to <3 Keep INR 2.0–3.0
pressure lowering therapy beyond 12 months standard drinks (Class I)
treatment in stable OAC-treated per week and TTR >70%
(Class I) patients with chronic (Class I) (Class IIa)
coronary/vascular disease
(Class III) Switch to DOAC if eligible
NSAIDs Other factors and failed to maintain
Do not add antiplatelet TTR on VKA
Offer alternative analgesia Consider drug interactions (Class I)
or disease-modifying therapy therapy to OAC to prevent Reduce corticosteroid use
thromboembolic events if possible
(Class III) Minimize duration of
Offer proton pump inhibitors heparin-bridging therapy
or recurrent stroke if high GI bleeding risk
(Class III) Advise restricting hazardous
hobbies/occupations
DOAC instead of VKA
when antiplatelet treatment
is needed
(Class I)

Address all potentially modifiable bleeding risk factors with shared decision-making

Anaemia Work with multidisciplinary team on each element

Reduced platelet count or Ensure correct OAC dose and monitoring
function
Renal impairment Manage heart failure and achieve euvolaemia
(Class I)
Risk of falls
Diabetes mellitus
Effective glycaemic control for patients with diabetes
Congestive heart failure (Class I)

Consider the impact of non-modifiable bleeding risk factors with shared decision-making

Age
Previous major bleeding Review patient more regularly
Severe renal impairment, dialysis or renal transplant Work with multidisciplinary team
Severe hepatic dysfunction or cirrhosis to monitor risk factors
Malignancy
Genetic factors (e.g. CYP2C9 polymorphisms) If clear contraindications for OACa, consider
Previous stroke left atrial appendage occlusion
Cognitive impairment or dementia (Class IIb)
Intracerebral pathology

Re-assess at next interaction with patient

Figure 10 Modifying the risk of bleeding associated with OAC. DOAC, direct oral anticoagulant; GI, gastrointestinal; INR, international normalized
ratio of prothrombin time; NSAID, non-steroidal anti-inflammatory drug; OAC, oral anticoagulant; TTR, time in therapeutic range; VKA, vitamin K
antagonist. aAbsolute contraindications for OAC therapy are rare, and include primary intracranial tumours and intracerebral bleeds related to amyloid
angiopathy. In most cases, contraindications may be relative or temporary. Left atrial appendage occlusion can be performed through a percutaneous or
endoscopic approach.
ESC Guidelines 37

Patient with active bleeding

Compress bleeding sites mechanically, if accessible

Assess haemodynamic status, basic coagulation parameters, blood count and kidney function

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Determine dose and time of last OAC and all co-medications

VKA DOAC

Non-life- Life-threatening Non-life- Life-threatening

Minor Minor
threatening or bleeding into threatening or bleeding into
bleeding bleeding
major bleeding a critical site major bleeding a critical site

Interrupt anticoagulation and perform diagnostic Interrupt anticoagulation and perform diagnostic
or treatment interventions or treatment interventions
(Class I) (Class I)

Multidisciplinary team approach Multidisciplinary team approach

Delay VKA Fluid Fluid Delay DOAC Fluid Fluid

until INR <2 replacement replacement for 1–2 doses replacement replacement
Blood Blood (or more Blood Blood
transfusion transfusion depending transfusion transfusion
Consider need PCC on recovery) Consider oral Specific
for vitamin K, (Class IIa) charcoal or antidotes
FFP, PCC gastric lavage (Class IIa)
FFP if PCC not if DOAC taken
available PCC if no
within 2–4 antidotes
Replacement hours available
of platelets Consider need
where Replacement
for PCC of platelets
appropriate
where
appropriate
Monitoring of
DOAC levels

Management after the bleeding episode

Discuss benefits and risk of restarting OAC (shared decision-making approach)
Aim to re-initiate anticoagulation in the absence of contraindications or if source of bleeding has been addressed
Assess risk of repeat bleeding
Intensify efforts to modify bleeding risk factors
Review choice and dose of OAC
Institute close and ongoing monitoring

Figure 11 Management of oral anticoagulant-related bleeding in patients with AF. DOAC, direct oral anticoagulant; FFP, fresh frozen plasma; INR,
international normalized ratio of prothrombin time; OAC, oral anticoagulant; PCC, prothrombin complex concentrate; VKA, vitamin K antagonist.
38 ESC Guidelines

uncontrolled bleeding.451 Dialysis can also be effective in reducing dabiga­ 7.1. Management of heart rate in patients
tran concentration. Andexanet alfa rapidly reverses the activity of factor
Xa inhibitors (apixaban, edoxaban, rivaroxaban) (see Supplementary data
with AF
Limiting tachycardia is an integral part of AF management and is often
online, Additional evidence Table S14). An open-label RCT comparing
sufficient to improve AF-related symptoms. Rate control is indicated as
andexanet alfa to usual care in patients presenting with acute ICH within
initial therapy in the acute setting, in combination with rhythm control
6 h of symptom onset was stopped early due to improved control of
therapies, or as the sole treatment strategy to control heart rate and
bleeding after 450 patients had been randomized.452 As DOAC-specific
reduce symptoms. Limited evidence exists to inform the best type
antidotes are not yet available in all institutions, prothrombin complex
and intensity of rate control treatment.457 The approach to heart

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concentrates are often used in cases of serious bleeding on factor Xa in­
rate control presented in Figure 7 can be used for all types of AF, includ­
hibitors, with evidence limited to observational studies.453
ing paroxysmal, persistent, and permanent AF.
Due to the complexities of managing bleeding in patients taking
OAC, it is advisable that each institution develop specific policies involv­
ing a multidisciplinary team that includes cardiologists, haematologists, Recommendation Table 14 — Recommendations for
emergency physicians/intensive care specialists, surgeons, and others. heart rate control in patients with AF (see also
It is also important to educate patients taking anticoagulants on the Evidence Table 14)
signs and symptoms of bleeding events and to alert their healthcare
Recommendations Classa Levelb
provider when such events occur.335
The decision to reinstate OAC will be determined by the severity, Rate control therapy is recommended in patients
cause, and subsequent management of bleeding, preferably by a multidis­ with AF, as initial therapy in the acute setting, an
ciplinary team and with close monitoring. Failure to reinstitute OAC after adjunct to rhythm control therapies, or as a sole I B
a bleed significantly increases the risk of MI, stroke, and death.454 treatment strategy to control heart rate and reduce
However, if the cause of severe or life-threatening bleeds cannot be trea­ symptoms.458–460
ted or reversed, the risk of ongoing bleeding may outweigh the benefit of Beta-blockers, diltiazem, verapamil, or digoxin are
thromboembolic protection.335 recommended as first-choice drugs in patients with
I B
AF and LVEF >40% to control heart rate and reduce
Recommendation Table 13 — Recommendations for symptoms.48,461,462
management of bleeding in anticoagulated patients Beta-blockers and/or digoxin are recommended in
(see also Evidence Table 13)
patients with AF and LVEF ≤40% to control heart I B
40,185,463–465
Recommendations Class a
Level b rate and reduce symptoms.
Combination rate control therapy should be
Interrupting anticoagulation and performing considered if a single drug does not control
diagnostic or treatment interventions is symptoms or heart rate in patients with AF, IIa C
I C
recommended in AF patients with active bleeding providing that bradycardia can be avoided, to control
until the cause of bleeding is identified and resolved. heart rate and reduce symptoms.
Prothrombin complex concentrates should be Lenient rate control with a resting heart rate of
considered in AF patients on VKAs who develop a < 110 b.p.m. should be considered as the initial
IIa C
life-threatening bleed, or bleed into a critical site, to target for patients with AF, with stricter control IIa B
reverse the antithrombotic effect.450 reserved for those with continuing AF-related
Specific antidotes should be considered in AF symptoms.459,460,466
© ESC 2024

patients on a DOAC who develop a life-threatening Atrioventricular node ablation in combination with
IIa B
bleed, or bleed into a critical site, to reverse the pacemaker implantation should be considered in
antithrombotic effect.451,455,456 patients unresponsive to, or ineligible for, intensive IIa B
AF, atrial fibrillation; DOAC, direct oral anticoagulant; VKA, vitamin K antagonist. rate and rhythm control therapy to control heart
a
Class of recommendation. rate and reduce symptoms.467–469
b
Level of evidence.
Atrioventricular node ablation combined with
cardiac resynchronization therapy should be
7. [R] Reduce symptoms by rate considered in severely symptomatic patients with
IIa B
permanent AF and at least one hospitalization for HF
and rhythm control to reduce symptoms, physical limitations, recurrent
Most patients diagnosed with AF will need therapies and/or interven­ HF hospitalization, and mortality.470,471
tions to control heart rate, revert to sinus rhythm, or maintain sinus Intravenous amiodarone, digoxin, esmolol, or
© ESC 2024

rhythm to limit symptoms or improve outcomes. While the concept landiolol may be considered in patients with AF who
IIb B
of choosing between rate and rhythm control is often discussed, in real­ have haemodynamic instability or severely depressed
ity most patients require a combination approach which should be con­ LVEF to achieve acute control of heart rate.472,473
sciously re-evaluated during follow-up. Within a patient-centred and
AF, atrial fibrillation; b.p.m., beats per minute; HF, heart failure; LVEF, left ventricular
shared-management approach, rhythm control should be a consider­
ejection fraction.
ation in all suitable AF patients, with explicit discussion of benefits a
Class of recommendation.
and risks. b
Level of evidence.
ESC Guidelines 39

7.1.1. Indications and target heart rate The choice of rate control drugs depends on symptoms, comorbid­
The optimal heart rate target in AF patients depends on the setting, ities, and the potential for side effects and interactions. Combination
symptom burden, presence of heart failure, and whether rate control therapy of different rate-controlling drugs should be considered only
is combined with a rhythm control strategy. In the RACE II (Rate when needed to achieve the target heart rate, and careful follow-up
Control Efficacy in Permanent Atrial Fibrillation) RCT of patients to avoid bradycardia is advised. Combining beta-blockers with verap­
with permanent AF, lenient rate control (target heart rate <110 [beats amil or diltiazem should only be performed in secondary care
per minute] b.p.m.) was non-inferior to a strict approach (<80 b.p.m. at with regular monitoring of heart rate by 24 h ECG to check for
rest; <110 b.p.m. during exercise; Holter for safety) for a composite of bradycardia.459 Some antiarrhythmic drugs (AADs) also have rate-

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clinical events, NYHA class, or hospitalization.186,459 Similar results limiting properties (e.g. amiodarone, sotalol), but they should generally
were found in a post-hoc combined analysis from the AFFIRM (Atrial be used only for rhythm control. Dronedarone should not be instituted
Fibrillation Follow-up Investigation of Rhythm Management) and the for rate control since it increases rates of heart failure, stroke, and
RACE (Rate Control versus Electrical cardioversion) studies.474 cardiovascular death in permanent AF.481
Therefore, lenient rate control is an acceptable initial approach, unless Beta-blockers, specifically beta-1 selective adrenoreceptor an­
there are ongoing symptoms or suspicion of tachycardia-induced car­ tagonists, are often first-line rate-controlling agents largely based on
diomyopathy, where stricter targets may be indicated. their acute effect on heart rate and the beneficial effects demonstrated
in patients with chronic HFrEF. However, the prognostic benefit of
beta-blockers seen in HFrEF patients with sinus rhythm may not be pre­
7.1.2. Heart rate control in the acute setting sent in patients with AF.133,482
In acute settings, physicians should always evaluate and manage under­ Verapamil and diltiazem are non-dihydropyridine calcium channel
lying causes for the initiation of AF prior to, or in parallel to, instituting blockers. They provide rate control461 and have a different adverse effect
acute rate and/or rhythm control. These include treating sepsis, addres­ profile, making verapamil or diltiazem useful for those experiencing side
sing fluid overload, or managing cardiogenic shock. The choice of drug effects from beta-blockers.483 In a 60 patient crossover RCT, verapamil
(Table 12) will depend on the patient’s characteristics, presence of heart and diltiazem did not lead to the same reduction in exercise capacity as
failure and LVEF, and haemodynamic profile (Figure 7). In general for seen with beta-blockers, and had a beneficial impact on BNP.480
acute rate control, beta-blockers (for all LVEF) and diltiazem/verapamil Digoxin and digitoxin are cardiac glycosides that inhibit the
(for LVEF >40%) are preferred over digoxin because of their more sodium–potassium adenosine triphosphatase and augment parasympa­
rapid onset of action and dose-dependent effects.462,475,476 More se­ thetic tone. In RCTs, there is no association between the use of digoxin
lective beta-1 receptor blockers have a better efficacy and safety profile and any increase in all-cause mortality.185,484 Lower doses of digoxin
than unselective beta-blockers.477 Combination therapy with digoxin may be associated with better prognosis.185 Serum digoxin concentra­
may be required in acute settings (combination of beta-blockers with tions can be monitored to avoid toxicity,485 especially in patients at
diltiazem/verapamil should be avoided except in closely monitored higher risk due to older age, renal dysfunction, or use of interacting
situations).177,478 In selected patients who are haemodynamically medications. In RATE-AF (RAte control Therapy Evaluation in perman­
unstable or with severely impaired LVEF, intravenous amiodarone, ent Atrial Fibrillation), a trial in patients with symptomatic permanent
landiolol, or digoxin can be used.472,473,479 AF, there was no difference between low-dose digoxin and bisoprolol
for patient-reported quality of life outcomes at 6 months. However,
those randomized to digoxin demonstrated fewer adverse effects, a
7.1.3. Long-term heart rate control greater improvement in mEHRA and NYHA scores, and a reduction
Pharmacological rate control can be achieved with beta-blockers, in BNP.48 Two ongoing RCTs are addressing digoxin and digitoxin
diltiazem, verapamil, digoxin, or combination therapy (Table 12) (see use in patients with HFrEF with and without AF (EudraCT-
Supplementary data online, Additional Evidence Table S15).480 2013-005326-38, NCT03783429).486

Table 12 Drugs for rate control in AF

Agenta Intravenous administration Usual range for oral maintenance Contraindicated

dose

Beta-blockersb
Metoprolol 2.5–5 mg bolus over 2 mins; up to 15 mg 25–100 mg twice daily In case of asthma, non-selective
tartrate maximal cumulative dose beta-blockers should be avoided.
Metoprolol XL N/A 50–200 mg once daily Contraindicated in acute HF and history of
(succinate) severe bronchospasm.
Bisoprolol N/A 1.25–20 mg once daily
Atenololc N/A 25–100 mg once daily
Esmolol 500 µg/kg i.v. bolus over 1 min; followed by N/A
50–300 µg/kg/min
Landiolol 100 µg/kg i.v. bolus over 1 min; followed by N/A
10–40 µg/kg/min
Nebivolol N/A 2.5–10 mg once daily
Carvedilol N/A 3.125–50 mg twice daily
Continued
40 ESC Guidelines

Non-dihydropyridine calcium channel antagonists

Verapamil 2.5–10 mg i.v. bolus over 5 min 40 mg twice daily to 480 mg (extended Contraindicated if LVEF ≤40%.
release) once daily Adapt doses in hepatic and renal
Diltiazem 0.25 mg/kg i.v. bolus over 5 min, then 60 mg three times daily to 360 mg impairment.
5–15 mg/h (extended release) once daily
Digitalis glycosides
Digoxin 0.5 mg i.v. bolus (0.75–1.5 mg over 24 h in 0.0625–0.25 mg once daily High plasma levels associated with adverse
divided doses) events.

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Digitoxin 0.4–0.6 mg 0.05–0.1 mg once daily Check renal function before starting
digoxin and adapt dose in CKD patients.
Other
Amiodaroned 300 mg i.v. diluted in 250 mL 5% dextrose over 200 mg once daily after loading Contraindicated in iodine sensitivity.
30–60 min (preferably via central venous Loading: 200 mg three times daily for 4 Serious potential adverse effects (including

© ESC 2024
cannula), followed by 900–1200 mg i.v. over 24 weeks, then 200 mg daily or less as pulmonary, ophthalmic, hepatic, and
h diluted in 500–1000 mL via a central venous appropriate (reduce other rate control thyroid). Consider numerous drug
cannula drugs according to heart rate) interactions.

AF, atrial fibrillation; CKD, chronic kidney disease; HF, heart failure; i.v., intravenous; min, minutes; N/A, not available or not widely available. Maximum doses have been defined based on the
summary of product characteristic of each drug.
a
All rate control drugs are contraindicated in Wolff–Parkinson–White syndrome; also intravenous amiodarone.
b
Other beta-blockers are available but not recommended as specific rate control therapy in AF and therefore not mentioned here (e.g. propranolol and labetalol).
c
No data on atenolol; should not be used in heart failure with reduced ejection fraction or in pregnancy.
d
Loading regimen may vary; i.v. dosage should be considered when calculating total load.

Due to its broad extracardiac adverse effect profile, amiodarone is 7.2. Rhythm control strategies in patients
reserved as a last option when heart rate cannot be controlled even
with maximal tolerated combination therapy, or in patients who do not
with AF
qualify for atrioventricular node ablation and pacing. Many of the adverse 7.2.1. General principles and anticoagulation
effects from amiodarone have a direct relationship with cumulative dose, Rhythm control refers to therapies dedicated to restoring and main­
restricting the long-term value of amiodarone for rate control.487 taining sinus rhythm. These treatments include cardioversion, AADs,
percutaneous catheter ablation, endoscopic and hybrid ablation, and
7.1.4. Atrioventricular node ablation and pacemaker open surgical approaches (see Supplementary data online, Additional
implantation Evidence Table S17). Rhythm control is never a strategy on its own; in­
Ablation of the atrioventricular node and pacemaker implantation (‘ablate stead, it should always be part of the AF-CARE approach.
and pace’) can lower and regularize heart rate in patients with AF (see In patients with acute or worsening haemodynamic instability thought to
Supplementary data online, Additional Evidence Table S16). The procedure be caused by AF, rapid electrical cardioversion is recommended. For other
has a low complication rate and a low long-term mortality risk.468,488 The patients, a wait-and-see approach should be considered as an alternative to
pacemaker should be implanted a few weeks before the atrioventricular immediate cardioversion (Figure 12). The Rate Control versus Electrical
node ablation, with the initial pacing rate after ablation set at 70– Cardioversion Trial 7–Acute Cardioversion versus Wait and See (RACE
90 b.p.m.489,490 This strategy does not worsen LV function,491 and may 7 ACWAS) trial in patients with recent-onset symptomatic AF without
even improve LVEF in selected patients.492,493 The evidence base has typ­ haemodynamic compromise showed a wait-and-see approach for spon­
ically included older patients. For younger patients, ablate and pace should taneous conversion until 48 h after the onset of AF symptoms was non-
only be considered if heart rate remains uncontrolled despite consideration inferior as compared with immediate cardioversion at 4 weeks follow-up.10
of other pharmacological and non-pharmacological treatment options. The Since the publication of landmark trials more than 20 years ago, the
choice of pacing therapy (right ventricular or biventricular pacing) depends main reason to consider longer-term rhythm control therapy has been
on patient characteristics, presence of heart failure, and LVEF.187,494 the reduction in symptoms from AF.497–500 Older studies have shown
In severely symptomatic patients with permanent AF and at least one that the institution of a rhythm control strategy using AADs does not re­
hospitalization for heart failure, atrioventricular node ablation combined duce mortality and morbidity when compared with a rate control-only
with CRT should be considered. In the APAF-CRT (Ablate and Pace for strategy,497–500 and may increase hospitalization.457 In contrast, multiple
Atrial Fibrillation-cardiac resynchronization therapy) trial in a population studies have shown that rhythm control strategies have a positive effect
with narrow QRS complexes, atrioventricular node ablation combined on quality of life once sinus rhythm is maintained.501,502 Therefore, in the
with CRT was superior to rate control drugs for the primary outcomes case of uncertainty of the presence of symptoms associated with AF, an
(all-cause mortality, and death or hospitalization for heart failure), and sec­ attempt to restore sinus rhythm is a rational first step. In patients with
ondary outcomes (symptom burden and physical limitation).470,471 symptoms, patient factors that favour an attempt at rhythm control
Conduction system pacing may become a potentially useful alternate pa­ should be considered, including suspected tachycardiomyopathy, a brief
cing mode when implementing a pace and ablate strategy, once safety and AF history, non-dilated left atrium, or patient preference.
efficacy have been confirmed in larger RCTs.495,496 In CRT recipients, the Rhythm control strategies have significantly evolved due to an increas­
presence (or occurrence) of AF is one of the main reasons for suboptimal ing experience in the safe use of antiarrhythmic drugs,17 consistent use of
biventricular pacing.187 Improvement of biventricular pacing is indicated OAC, improvements in ablation technology,503–509 and identification and
and can be reached by intensification of rate control drug regimens, atrio­ management of risk factors and comorbidities.39,510,511 In the ATHENA
ventricular node ablation, or rhythm control, depending on patient and AF trial (A Placebo-Controlled, Double-Blind, Parallel Arm Trial to Assess
characteristics.187 the Efficacy of Dronedarone 400 mg twice daily for the Prevention of
ESC Guidelines 41

Cardioversion for atrial fibrillation

Y Haemodynamically stable N

Emergency electrical cardioversion

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(Class I)

Check OAC status as soon as

possible and proceed to last step

Check OAC status

Already on therapeutic OAC

Not already on OAC
for minimum 3 weeks

Suitable for
wait-and-see Cardioversion
approach cannot wait
(Class IIa)

Therapeutic OAC
Initiation of DOAC
for at least 3 weeks
Wait-and-see (or VKA, LMWH,
Pharmacological before scheduled
approach for or UFH) for
or electrical cardioversion
spontaneous unscheduled
cardioversion (adherence to
conversion cardioversion as
(Class IIa) DOACs or
(Class IIa) soon as possible
INR ≥2.0 for VKAs)
(Class IIa)
(Class I)

Elective electrical
Check current AF
cardioversion,
episode duration
if needed

AF onset <24 h AF onset ≥24 h or unknown

Pharmacological or TOE guided cardioversion

electrical cardioversion (Class I)

Decide on continued OAC post-cardioversion

Short-term OAC after cardioversion (4 weeks) for all patients, even if CHA2DS2-VA = 0
(optional if AF onset definitely <24 h and low thromboembolic risk)
Long-term OAC for all patients according to thromboembolic risk assessment

Figure 12 Approaches for cardioversion in patients with AF. AF, atrial fibrillation; CHA2DS2-VA, congestive heart failure, hypertension, age ≥75 years
(2 points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial thromboembolism (2 points), vascular disease, age 65–74 years; h, hour;
LMWH, low molecular weight heparin; DOAC, direct oral anticoagulant; OAC, oral anticoagulant; TOE, transoesophageal echocardiography; UFH,
unfractionated heparin; VKA, vitamin K antagonist. Flowchart for decision-making on cardioversion of AF depending on clinical presentation, AF onset,
oral anticoagulation intake, and risk factors for stroke. aSee Section 6.
42 ESC Guidelines

Cardiovascular Hospitalization or Death from Any Cause in Patients with Recommendation Table 15 — Recommendations for
Atrial Fibrillation/Atrial Flutter), dronedarone significantly reduced the general concepts in rhythm control (see also Evidence
risk of hospitalization due to cardiovascular events or death as compared Table 15)
with placebo in patients with paroxysmal or persistent AF.512 The
Recommendations Classa Levelb
CASTLE-AF trial (Catheter Ablation versus Standard Conventional
Treatment in Patients With Left Ventricle Dysfunction and AF) demon­ Electrical cardioversion is recommended in AF patients
strated that a rhythm control strategy with catheter ablation can improve with acute or worsening haemodynamic instability to I C
mortality and morbidity in selected patients with HFrEF and an implanted improve immediate patient outcomes.520
cardiac device.4 In end-stage HFrEF, the CASTLE-HTx trial (Catheter

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Direct oral anticoagulants are recommended in
Ablation for Atrial Fibrillation in Patients With End-Stage Heart Failure
preference to VKAs in eligible patients with AF
and Eligibility for Heart Transplantation) found, in a single centre, that I A
undergoing cardioversion for thromboembolic risk
catheter ablation combined with guideline-directed medical therapy sig­ 293,319–321,521
reduction.
nificantly reduced the composite of death from any cause, implantation
Therapeutic oral anticoagulation for at least 3 weeks
of left ventricular assist device, or urgent heart transplantation compared
with medical treatment.513 At the same time, however, the CABANA (adherence to DOACs or INR ≥2.0 for VKAs) is
trial (Catheter Ablation versus Anti-arrhythmic Drug Therapy for recommended before scheduled cardioversion of AF I B
Atrial Fibrillation) could not demonstrate a significant difference in mor­ and atrial flutter to prevent procedure-related
tality and morbidity between catheter ablation and standard rhythm and/ thromboembolism.319–321
or rate control drugs in symptomatic AF patients older than 64 years, or Transoesophageal echocardiography is recommended
younger than 65 years with risk factors for stroke.3 EAST-AFNET 4 if 3 weeks of therapeutic oral anticoagulation has not
I B
(Early treatment of Atrial fibrillation for Stroke prevention Trial) re­ been provided, for exclusion of cardiac thrombus to
ported that implementation of a rhythm control strategy within 1 year enable early cardioversion.319–321,522
compared with usual care significantly reduced the risk of cardiovascular Oral anticoagulation is recommended to continue
death, stroke, or hospitalization for heart failure or acute coronary syn­ for at least 4 weeks in all patients after cardioversion
drome in patients older than 75 years or with cardiovascular condi­ and long-term in patients with thromboembolic risk I B
tions.17 Of note, rhythm control was predominantly pursued with factor(s) irrespective of whether sinus rhythm is
antiarrhythmic drugs (80% of patients in the intervention arm). Usual achieved, to prevent thromboembolism.239,319,320,523,524
care consisted of rate control therapy; only when uncontrolled
Cardioversion of AF (either electrical or
AF-related symptoms occurred was rhythm control considered.
pharmacological) should be considered in
Patients in the EAST-AFNET 4 trial all had cardiovascular risk factors IIa B
symptomatic patients with persistent AF as part of a
but were at an early stage of AF, with more than 50% being in sinus 52,525,526
rhythm control approach.
rhythm and 30% being asymptomatic at the start of the study.
Based on all of these studies, this task force concludes that implementa­ A wait-and-see approach for spontaneous
tion of a rhythm control strategy can be safely instituted and confers ameli­ conversion to sinus rhythm within 48 h of AF onset
oration of AF-related symptoms. Beyond control of symptoms, sinus should be considered in patients without IIa B
rhythm maintenance should also be pursued to reduce morbidity and mor­ haemodynamic compromise as an alternative to
tality in selected groups of patients.4,17,502,513,514 immediate cardioversion.10,525
Any rhythm control procedure has an inherent risk of thrombo­ Implementation of a rhythm control strategy should
embolism. Patients undergoing cardioversion require at least 3 weeks be considered within 12 months of diagnosis in
of therapeutic anticoagulation (adherence to DOACs or INR >2 if selected patients with AF at risk of thromboembolic IIa B
VKA) prior to the electrical or pharmacological procedure. In acute set­ events to reduce the risk of cardiovascular death or
tings or when early cardioversion is needed, transoesophageal echocar­ hospitalization.17,527
diography (TOE) can be performed to exclude cardiac thrombus prior Initiation of therapeutic anticoagulation should
to cardioversion. These approaches have been tested in multiple
be considered as soon as possible in the setting
RCTs.319–321 In the case of thrombus detection, therapeutic anticoagu­
of unscheduled cardioversion for AF or atrial IIa B
lation should be instituted for a minimum of 4 weeks followed by repeat
flutter to prevent procedure-related
TOE to ensure thrombus resolution. When the definite duration of AF
thromboembolism.319–321,528
is less than 48 hours, cardioversion has typically been considered with­
out the need for pre-procedure OAC or TOE for thrombus exclusion. Repeat transoesophageal echocardiography should be
However, the ‘definite’ onset of AF is often not known, and observa­ considered before cardioversion if thrombus has been
tional data suggest that stroke/thromboembolism risk is lowest within identified on initial imaging to ensure thrombus IIa C
a much shorter time period.515–519 This task force reached consensus resolution and prevent peri-procedural
that safety should come first. Cardioversion is not recommended if AF thromboembolism.529
duration is longer than 24 hours, unless the patient has already received Early cardioversion is not recommended without
© ESC 2024

at least 3 weeks of therapeutic anticoagulation or a TOE is performed appropriate anticoagulation or transoesophageal

III C
to exclude intracardiac thrombus. Most patients should continue OAC echocardiography if AF duration is longer than 24 h, or
for at least 4 weeks post-cardioversion. Only for those without there is scope to wait for spontaneous cardioversion.522
thromboembolic risk factors and sinus rhythm restoration within 24
AF, atrial fibrillation; DOAC, direct oral anticoagulant; INR, international normalized ratio
h of AF onset is post-cardioversion OAC optional. In the presence of of prothrombin time; VKA, vitamin K antagonist.
any thromboembolic risk factors, long-term OAC should be instituted a
Class of recommendation.
b
irrespective of the rhythm outcome. Level of evidence.
ESC Guidelines 43

7.2.2. Electrical cardioversion rhythm in 76%–83% of patients with recent-onset AF (10%–18% within
Electrical cardioversion (ECV) can be safely applied in the elective and the first 3 h, 55%–66% within 24 h, and 69% within 48 h).10,119,445,551–555
acute setting (see Supplementary data online, Additional Evidence The choice of a specific drug is based on the type and severity of con­
Table S18) with sedation by intravenous midazolam, propofol, or comitant heart disease (Table 13). A meta-analysis demonstrated that
etomidate.530 Structured and integrated care for patients with acute- intravenous vernakalant and flecainide have the highest conversion rate
onset AF at the emergency department is associated with better out­ within 4 h, possibly allowing discharge from the emergency department
comes without compromising safety.531 Rates of major adverse clinical and reducing hospital admissions. Intravenous and oral formulations of
events after cardioversion are significantly lower with DOACs com­ Class IC antiarrhythmics (flecainide more so than propafenone)

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pared with warfarin.293 are superior regarding conversion rates within 12 h, while amiodarone
Blood pressure monitoring and oximetry should be used routinely. efficacy is exhibited in a delayed fashion (within 24 h).556
Intravenous atropine or isoproterenol, or temporary transcutaneous Pharmacological cardioversion does not require fasting, sedation, or an­
pacing, should be available in case of post-cardioversion bradycardia. aesthesia. Anticoagulation should be started or continued according to a
Biphasic defibrillators are standard because of their superior efficacy formal (re-)assessment of thromboembolic risk.554,557–559
compared with monophasic defibrillators.532–534 There is no single op­ A single self-administered oral dose of flecainide or propafenone
timal position for electrodes, with a meta-analysis of 10 RCTs showing (pill-in-the-pocket) is effective in symptomatic patients with infre­
no difference in sinus rhythm restoration comparing anterior-posterior quent and recent-onset paroxysmal AF. Safe implementation of this
with antero-lateral electrode positioning.535 Applying active compres­ strategy requires patient screening to exclude sinus node dysfunction,
sion to the defibrillation pads is associated with lower defibrillation atrioventricular conduction defects, or Brugada syndrome, as well as
thresholds, lower total energy delivery, fewer shocks for successful prior in-hospital validation of its efficacy and safety.560 An atrioven­
ECV, and higher success rates.536 A randomized trial showed that max­ tricular node-blocking drug should be instituted in patients treated
imum fixed-energy shocks were more effective than low-escalating en­ with Class IC AADs to avoid 1:1 conduction if the rhythm transforms
ergy for ECV.537 to AFL.561
Immediate administration of vernakalant,538 or pre-treatment
for 3–4 days with flecainide,539,540 ibutilide,541,542 propafenone,543 or
Recommendation Table 17 — Recommendations for
amiodarone544–546 improves the rate of successful ECV and can pharmacological cardioversion of AF (see also Evidence
facilitate long-term maintenance of sinus rhythm by preventing Table 17)
early recurrent AF.547 A meta-analysis demonstrated that pre-
treatment with amiodarone (200–800 mg/day for 1–6 weeks pre- Recommendations Classa Levelb
cardioversion) and post-treatment (200 mg/day) significantly improved
Intravenous flecainide or propafenone is
the restoration and maintenance of sinus rhythm after ECV of AF.546
recommended when pharmacological cardioversion
In some cases of persistent AF there is no clear relationship between
of recent-onset AF is desired, excluding patients with I A
the arrhythmia and symptoms. In these cases, restoring sinus rhythm by
ECV might serve to confirm the impact of arrhythmia on symptoms severe left ventricular hypertrophy, HFrEF, or
and/or on heart failure symptoms and signs. Such an approach might coronary artery disease.562–566
be useful to identify truly asymptomatic individuals, to assess the impact Intravenous vernakalant is recommended when
of AF on LV function in patients with HFrEF, and to distinguish pharmacological cardioversion of recent-onset AF is
I A
AF-related symptoms from heart failure symptoms. desired, excluding patients with recent ACS, HFrEF,
or severe aortic stenosis.562–568
Recommendation Table 16 — Recommendations for Intravenous amiodarone is recommended when
electrical cardioversion of AF (see also Evidence cardioversion of AF in patients with severe left
Table 16)
ventricular hypertrophy, HFrEF, or coronary artery I A

Recommendations Class a
Level b disease is desired, accepting there may be a delay in
cardioversion.473,569,570
Electrical cardioversion as a diagnostic tool should be A single self-administered oral dose of flecainide or
considered in patients with persistent AF where propafenone (pill-in-the-pocket) should be
© ESC 2024

there is uncertainty about the value of sinus rhythm IIa C considered for patient-led cardioversion in selected
restoration on symptoms, or to assess improvement patients with infrequent paroxysmal AF, after efficacy IIa B
in left ventricular function.548 and safety assessment and excluding those with
AF, atrial fibrillation. severe left ventricular hypertrophy, HFrEF, or
a
Class of recommendation. coronary artery disease.560,571–573
b
Level of evidence.
Pharmacological cardioversion is not recommended
for patients with sinus node dysfunction,
7.2.3. Pharmacological cardioversion
© ESC 2024

atrioventricular conduction disturbances, or III C

Pharmacological cardioversion to sinus rhythm is an elective procedure prolonged QTc (>500 ms), unless risks for
in haemodynamically stable patients. It is less effective than electrical car­ proarrhythmia and bradycardia have been considered.
dioversion for restoration of sinus rhythm,549 with timing of cardiover­
ACS, acute coronary syndromes; AF, atrial fibrillation; HFrEF, heart failure with reduced
sion being a significant determinant of success.550 There are limited
ejection fraction.
contemporary data on the true efficacy of pharmacological cardiover­ a
Class of recommendation.
sion, which are likely biased by the spontaneous restoration of sinus b
Level of evidence.
44 ESC Guidelines

Table 13 Antiarrhythmic drugs for sinus rhythm restoration

Drug Administration Initial dosing Subsequent Acute success Contraindications and precautions
route dosing [long- rate and time
term approach] to sinus
rhythm

Flecainide Oral 200–300 mg [long-term 50%–60% at 3 h • Should not be used in patients with severe
50−150 mg twice and 75%–85% at structural or coronary artery disease, Brugada

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daily] 6–8 h (3–8 h) syndrome, or severe renal failure (CrCl
Intravenous 1–2 mg/kg over 52%–95% <35 mL/min/1.73 m2).
10 min (Up to 6 h) • Prior documentation of safety and efficacy in
Propafenone Oral 450–600 mg [long-term 45%–55% at 3 h, an inpatient setting is recommended prior to
150-300 mg three 69%–78% at 8 h pill-in-the-pocket use.
times daily] (3–8 h) • An AVN-blocking agent should be
Intravenous 1.5–2 mg/kg over 43%–89% administered to avoid 1:1 conduction if
10 min (Up to 6 h) transformation to AFL.
• Drug infusion should be discontinued in case
of QRS widening >25% or bundle branch
block occurrence.
• Caution is needed in patients with sinus node
disease and AVN dysfunction.
• Do NOT use for conversion of atrial flutter.
Amiodarone Intravenous (/oral) 300 mg intravenous 900-1200 mg 44% (8–12 h to • May cause phlebitis (use a large peripheral
over 30–60 min intravenous over 24 several days) vein, avoid i.v. administration >24 h and use
hours (or 200 mg preferably volumetric pump).
oral three times • May cause hypotension, bradycardia/
daily for 4 weeks). atrioventricular block, QT prolongation.
[long-term 200 mg • Only if no other option in patients with
oral daily] hyperthyroidism (risk of thyrotoxicosis).
• Consider the broad range of drug
interactions.
Ibutilide Intravenous 1 mg over 10 min 1 mg over 10 min 31%–51% • Should be used in the setting of a cardiac care
(0.01 mg/kg if body (10–20 min after (30–90 min) unit as it may cause QT prolongation and
weight <60 kg) the initial dose) in AF torsades de pointes.
60–75% in AFL • ECG monitoring for at least 4 h after
(60 min) administration to detect any proarrhythmic
effects.
• Should not be used in patients with prolonged
QT, severe LVH, or low LVEF.
Vernakalant Intravenous 3 mg/kg over 10 min 2 mg/kg over 10 min 50% within • Should not be used in patients with arterial
(maximum 339 mg) (10–15 min after 10 min hypotension (SBP <100 mmHg), recent ACS
the initial dose) (within 1 month), NYHA III or IV HF, QT
(maximum 226 mg) prolongation or severe aortic stenosis.
© ESC 2024

• May cause arterial hypotension, QT

prolongation, QRS widening, or
non-sustained ventricular tachycardia.

ACS, acute coronary syndromes; AF, atrial fibrillation; AFL, atrial flutter; AVN, atrioventricular node; CrCl, creatinine clearance; ECG, electrocardiogram; HF, heart failure; LVEF, left
ventricular ejection fraction; LVH, left ventricular hypertrophy; NYHA, New York Heart Association; QT, QT interval; SBP, systolic blood pressure. Long-term dosage for maintenance
of sinus rhythm is indicated in [square brackets]. Long-term oral dosing for dronedarone is 400 mg twice daily, and for sotalol 80-160 mg twice daily.

7.2.4. Antiarrhythmic drugs failure if episodes are less frequent, briefer, or less symptomatic.
The aims of long-term rhythm control are to maintain sinus rhythm, im­ Antiarrhythmic drugs also have a role for long-term rhythm control in
prove quality of life, slow the progression of AF, and potentially reduce AF patients that are considered ineligible or unwilling to undergo cath­
morbidity related to AF episodes (see Supplementary data online, eter or surgical ablation.
Additional Evidence Table S19).17,445,574,575 Antiarrhythmic drugs do Before starting AAD treatment, reversible triggers should be identified
not eliminate recurrences of AF, but in patients with paroxysmal and underlying comorbidities treated to reduce the arrhythmogenic sub­
or persistent AF, a recurrence is not equivalent to treatment strate, prevent progression of AF, and facilitate maintenance of sinus
ESC Guidelines 45

rhythm.39,128 The RACE 3 trial, including patients with early persistent AF Sotalol may be considered in patients with AF
and mild-to-moderate heart failure (predominantly HFpEF and HFmrEF), requiring long-term rhythm control with normal
showed that targeted therapy of underlying conditions improved sinus LVEF or coronary artery disease to prevent
rhythm maintenance at 1 year (75% vs. 63% as compared with standard recurrence and progression of AF, but requires close IIb A
care).39 The selection of an AAD for long-term rhythm control requires monitoring of QT interval, serum potassium levels,
careful evaluation that takes into account AF type, patient parameters, renal function, and other proarrhythmia risk
and safety profile.445 It also includes shared decision-making, balancing factors.585,587
the benefit/risk ratio of AADs in comparison with other strategies.

© ESC 2024
Antiarrhythmic drug therapy is not recommended in

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Notably, recent evidence has shown that careful institution of AADs
patients with advanced conduction disturbances III C
can be performed safely.17
unless antibradycardia pacing is provided.
The long-term effectiveness of AADs is limited. In a meta-analysis of
59 RCTs, AADs reduced AF recurrences by 20%–50% compared with AF, atrial fibrillation; HFmrEF, heart failure with mildly reduced ejection fraction; HFpEF,
no treatment, placebo, or drugs for rate control.576,577 When one AAD heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection
fraction; LVEF, left ventricular ejection fraction.
fails to reduce AF recurrences, a clinically acceptable response may be a
Class of recommendation.
achieved with another drug, particularly if from a different class.578 b
Level of evidence.
Combinations of AADs are not recommended. The data available sug­
gest that AADs do not produce an appreciable effect on mortality or
other cardiovascular complications with the exception of increased 7.2.5. Catheter ablation
mortality signals for sotalol574,579,580 and amiodarone.581 In contrast,
Catheter ablation prevents AF recurrences, reduces AF burden, and
use of AADs within a rhythm control strategy can be associated with
improves quality of life in symptomatic paroxysmal or persistent AF
reduction of morbidity and mortality in selected patients.582
where the patient is intolerant or does not respond to AAD.503–509
All AADs may produce serious cardiac (proarrhythmia, negative in­
Multiple RCTs have provided evidence in favour of catheter ablation
otropism, hypotension) and extracardiac adverse effects (organ tox­
as a first-line approach for rhythm control in patients with paroxysmal
icity, predominantly amiodarone). Drug safety, rather than efficacy,
AF, with a similar risk of adverse events as compared with initial AAD
should determine the choice of drug. The risk of proarrhythmia in­
treatment (see Supplementary data online, Additional Evidence Table
creases in patients with structural heart disease. Suggested doses for
S20).15,16,591–594 In contrast, it is not clear whether first-line ablation
long-term oral AAD are presented in Table 13.577,583,584
is superior to drug therapy in persistent AF. Catheter ablation may
also have a role in patients with symptoms due to prolonged pauses
upon AF termination, where non-randomized data have shown im­
Recommendation Table 18 — Recommendations for
proved symptoms, and avoidance of pacemaker implantation.595–598
antiarrhythmic drugs for long-term maintenance of si­
nus rhythm (see also Evidence Table 18) Pulmonary vein isolation (PVI) remains the cornerstone of AF cath­
eter ablation,503,508,593,599 but the optimal ablation strategy has not
Recommendations Classa Levelb been clarified in the non-paroxysmal AF population.600 New technolo­
gies are emerging, such as pulsed field ablation, in which high-amplitude
Amiodarone is recommended in patients with AF electrical pulses are used to ablate the myocardium by electroporation
and HFrEF requiring long-term antiarrhythmic drug with high tissue specificity. In a single-blind RCT of 607 patients, pulsed
therapy to prevent recurrence and progression of I A field ablation was non-inferior for efficacy and safety endpoints com­
AF, with careful consideration and monitoring for pared with conventional radiofrequency or cryoballoon ablation.601
extracardiac toxicity.577,585–587 Regarding timing of ablation, a small RCT found that delaying catheter
Dronedarone is recommended in patients with AF ablation in patients with paroxysmal or persistent AF by 12 months
requiring long-term rhythm control, including those (while on optimized medical therapy) did not impact on arrhythmia-
with HFmrEF, HFpEF, ischaemic heart disease, or I A free survival compared with ablation within 1 month.602
valvular disease to prevent recurrence and As with any type of rhythm control, many patients in clinical practice
progression of AF.512,577,588,589 will not be suitable for catheter ablation due to factors that reduce the
Flecainide or propafenone is recommended in likelihood of a positive response, such as left atrial dilatation. Definitive
patients with AF requiring long-term rhythm control evidence that supports the prognostic benefit of catheter ablation is
to prevent recurrence and progression of AF,
needed before this invasive treatment can be considered for truly
I A asymptomatic patients. As previously noted, the CABANA trial did
excluding those with impaired left ventricular systolic
not confirm a benefit of catheter ablation compared with medical ther­
function, severe left ventricular hypertrophy, or
apy, although high crossover rates and low event rates may have diluted
coronary artery disease.526,577,585,590
the treatment effect.3 Therefore, only highly selected asymptomatic pa­
Concomitant use of a beta-blocker, diltiazem, or
tients could be candidates for catheter ablation, and only after detailed
verapamil should be considered in AF patients discussion of associated risks and potential benefit of delaying AF pro­
treated with flecainide or propafenone, to prevent IIa C gression.4,603 Randomized trials have shown that AF catheter ablation
1:1 conduction if their rhythm is transformed to atrial in patients with HFrEF significantly reduces arrhythmia recurrence
flutter. and increases ejection fraction, with improvement in clinical outcomes
Continued and mortality also observed in selected patients.4,513,514,604–612 Several
46 ESC Guidelines

characteristics, including but not limited to AF type, left atrial dilatation, Patients with heart failure
and the presence of atrial and/or ventricular fibrosis, could refine pa­
AF catheter ablation is recommended in patients
tient selection to maximize outcome benefit from AF catheter ablation
with AF and HFrEF with high probability of
in patients with HFrEF.604,608,613–617 The prognostic value of catheter I B
tachycardia-induced cardiomyopathy to reverse left
ablation in patients with HFpEF is less well established than for
ventricular dysfunction.604,611
HFrEF.617–626
Recent registries and trials report varying rates of peri-procedural AF catheter ablation should be considered in
serious adverse events associated with catheter ablation (2.9%–7.2%) selected AF patients with HFrEF to reduce HF IIa B
hospitalization and prolong survival.4,513,514,604,610,612

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with a very low 30 day mortality rate (<0.1%). Operator experience
and procedural volume at the ablation centre are critical, since they Sinus node disease/tachycardia–bradycardia syndrome
are associated with complication rates and 30 day mortality.627–631 AF catheter ablation should be considered in patients
Intermittent rhythm monitoring has typically been used to detect AF
with AF-related bradycardia or sinus pauses on AF
relapses following catheter ablation. Recent technology developments IIa C
termination to improve symptoms and avoid
such as smartwatch or smartphone photoplethysmography and wear­
pacemaker implantation.595–598
able patches may have an emerging role in post-ablation monitor­
ing.632,633 In addition, implantable loop recorders have been used to Recurrence after catheter ablation
quantify AF burden before and after ablation as an additional endpoint Repeat AF catheter ablation should be considered in
beyond binary AF elimination.634 Management of arrhythmia recur­ patients with AF recurrence after initial catheter
rence post-ablation is an informed, shared decision-making process dri­ ablation, provided the patient’s symptoms were
IIa B

© ESC 2024
ven by available options for symptom control. In the post-AF ablation improved after the initial PVI or after failed initial PVI,
context, there is data supporting a role for AAD continuation or re- to reduce symptoms, recurrence, and progression of
initiation, even for previously ineffective drugs.635 A short-term AAD AF.643–645
treatment (2–3 months) following ablation reduces early recurrences
of AF,554,635–639 but does not affect late recurrences636,637,640–642 or AF, atrial fibrillation; HF, heart failure; HFrEF, heart failure with reduced ejection fraction;
PVI, pulmonary vein isolation.
1 year clinical outcomes.642 Repeat PVI should be offered in patients a
Class of recommendation.
with AF recurrence if symptom improvement was demonstrated after b
Level of evidence.
the first ablation, with shared decision-making and clear goals of treat­
ment.643–645
7.2.6. Anticoagulation in patients undergoing
catheter ablation
Recommendation Table 19 — Recommendations for
catheter ablation of AF (see also Evidence Table 19) The presence of left atrial thrombus is a contraindication to catheter-
based AF ablation due to the risk of thrombus dislodgement leading
Recommendations Classa Levelb to ischaemic stroke. Patients planned for catheter ablation of AF with
an increased risk of thromboembolism should be on OAC for at least
Shared decision-making 3 full weeks prior to the procedure.554,647
Shared decision-making is recommended when There is a wide range in practice for visualization of intra-atrial
considering catheter ablation for AF, taking into thrombi prior to catheter ablation, including TOE, intracardiac echo­
I C
account procedural risks, likely benefits, and risk cardiography, or delayed phase cardiac computed tomography
factors for AF recurrence.128,210,503,646 (CT).554,648 The prevalence of left atrial thrombus was 1.3% and
AF patients resistant or intolerant to antiarrhythmic drug
2.7% in two meta-analyses of observational studies in patients planned
for catheter ablation of AF on adequate OAC.649,650 The prevalence of
therapy
left atrial thrombus was higher in patients with elevated stroke risk
Catheter ablation is recommended in patients with scores, and in patients with non-paroxysmal compared with paroxys­
paroxysmal or persistent AF resistant or intolerant mal AF.650 In addition, several patient subgroups with AF have increased
I A
to antiarrhythmic drug therapy to reduce symptoms, risk of ischaemic stroke and intracardiac thrombus even if treated with
3,15,503,505,506,508
recurrence, and progression of AF. adequate anticoagulation, including those with cardiac amyloidosis,
First-line rhythm control therapy rheumatic heart disease, and hypertrophic cardiomyopathy (HCM).
Catheter ablation is recommended as a first-line Cardiac imaging before catheter ablation should be considered in these
option within a shared decision-making rhythm
high-risk patient groups regardless of preceding effective OAC.
I A
Observational studies suggest that patients with a low thromboembolic
control strategy in patients with paroxysmal AF, to
risk profile may be managed without visualization of the LAA,651–653
reduce symptoms, recurrence, and progression of
but no RCTs have been performed (see Supplementary data online,
AF.16,591–594
Additional Evidence Table S21).
Catheter ablation may be considered as a first-line
For patients who have been anticoagulated prior to the ablation pro­
option within a shared decision-making rhythm cedure it is recommended to avoid interruption of OAC (see
control strategy in selected patients with persistent IIb C Supplementary data online, Additional Evidence Table S22).654–656
AF to reduce symptoms, recurrence, and Patients with interrupted OAC showed an increase in silent stroke de­
progression of AF. tected by brain magnetic resonance imaging (MRI) as compared with
Continued those with uninterrupted OAC.657–659 In a true uninterrupted
ESC Guidelines 47

DOAC strategy for once-daily dosing, a pre-procedural shift to evening 7.2.7. Endoscopic and hybrid AF ablation
intake might be considered to mitigate bleeding risk. Randomized trials Minimally invasive surgical AF ablation can be performed via a thoraco­
show comparable safety and efficacy with minimally interrupted OAC scopic approach or a subxiphoid approach. The term endoscopic cov­
(withholding the morning DOAC dose on the day of the procedure) ers both strategies. Hybrid ablation approaches have been developed
and a totally uninterrupted peri-ablation OAC strategy.655 where endoscopic epicardial ablation on the beating heart is performed
Anticoagulation with heparin during AF ablation is common in combination with endocardial catheter ablation, either in a simultan­
practice.554 Post-ablation DOACs should be continued as per the eous or sequential procedure. The rationale for combining an endocar­
dosing regimen when haemostasis has been achieved.335,554,647 All dial with an epicardial approach is that a more effective transmural

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patients should be kept on an OAC for at least 2 months after an ablation strategy can be pursued.666,667
AF ablation procedure irrespective of estimated thromboembolic For paroxysmal AF, an endoscopic or hybrid ablation approach may
risk (see Supplementary data online, Additional Evidence be considered after a failed percutaneous catheter ablation strat­
Table S23).647 Meta-analyses of observational studies have tried to as­ egy.668–670 Long-term follow-up of the FAST RCT (mean of 7.0 years),
sess the safety of stopping OAC treatment after catheter ablation for which included patients with paroxysmal and persistent AF, found ar­
AF, but the results have been heterogenous.660–663 Until the comple­ rhythmia recurrence was common but substantially lower with thor­
tion of relevant RCTs (e.g. NCT02168829), it is recommended to acoscopic ablation than catheter ablation: 34/61 patients (56%)
continue OAC therapy post-AF ablation according to the patient’s compared with 55/63 patients (87%), with P < .001 for the compari­
CHA2DS2-VA score and not the perceived success of the ablation son.669 For persistent AF, endoscopic or hybrid ablation approaches
procedure.554 are suitable as a first procedure to maintain long-term sinus rhythm
in selected patients.667–672 A meta-analysis of three RCTs confirmed
a lower rate of atrial arrhythmia recurrence after thoracoscopic vs.
Recommendation Table 20 — Recommendations for catheter ablation (incidence rate ratio, 0.55; 95% CI, 0.38–0.78;
anticoagulation in patients undergoing catheter ablation with no heterogeneity between trials).669 An RCT with 12 month
(see also Evidence Table 20) follow-up published after the meta-analysis in patients with long-
standing persistent AF found no difference in arrhythmia freedom
Recommendations Classa Levelb comparing thoracoscopic with catheter ablation.673 Although overall
morbidity and mortality of both techniques is low, endoscopic and hy­
Initiation of oral anticoagulation is recommended at
brid ablation have higher complication rates than catheter ablation,
least 3 weeks prior to catheter-based ablation in AF
but similar long-term rates of the composite of mortality, MI, or
patients at elevated thromboembolic risk, to prevent I C
stroke.667,669
peri-procedural ischaemic stroke and More recent trials have assessed the efficacy and safety of the hybrid
thromboembolism.554,647 epicardial-plus-endocardial approach in persistent AF refractory to
Uninterrupted oral anticoagulation is recommended AAD therapy, including a single-centre RCT670 and two multicentre
in patients undergoing AF catheter ablation to
I A
RCTs.671,674 Across these trials, hybrid ablation was consistently super­
prevent peri-procedural ischaemic stroke and ior to catheter ablation alone for maintaining long-term sinus rhythm,
664,665
thromboembolism. without significant differences in major adverse events. Notably, these
Continuation of oral anticoagulation is studies were typically performed in highly experienced centres (see
recommended for at least 2 months after AF ablation Supplementary data online, Additional Evidence Table S24).
in all patients, irrespective of rhythm outcome or Similar to other rhythm control approaches, this task force recom­
I C mends that OAC are continued in all patients who have a risk of
CHA2DS2-VA score, to reduce the risk of
peri-procedural ischaemic stroke and thromboembolism, irrespective of rhythm outcome, and regardless
thromboembolism.554,663 of LAA exclusion performed as part of the surgical procedure.
Continuation of oral anticoagulation is
recommended after AF ablation according to the
patient’s CHA2DS2-VA score, and not the perceived I C
success of the ablation procedure, to prevent Recommendation Table 21 — Recommendations for
ischaemic stroke and thromboembolism. 554 endoscopic and hybrid AF ablation (see also Evidence
Table 21)
Cardiac imaging should be considered prior to
catheter ablation of AF in patients at high risk of Recommendations Classa Levelb
© ESC 2024

ischaemic stroke and thromboembolism despite IIa B

Continuation of oral anticoagulation is
taking oral anticoagulation to exclude
recommended in patients with AF at elevated
thrombus.649,650
thromboembolic risk after concomitant, endoscopic,
AF, atrial fibrillation; CHA2DS2-VA, congestive heart failure, hypertension, age ≥75 years (2
I C
or hybrid AF ablation, independent of rhythm
points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial
thromboembolism (2 points), vascular disease, age 65–74 years. outcome or LAA exclusion, to prevent ischaemic
a
Class of recommendation. stroke and thromboembolism.
b
Level of evidence.
Continued
48 ESC Guidelines

Endoscopic and hybrid ablation procedures should Recommendation Table 22 — Recommendations for
be considered in patients with symptomatic AF ablation during cardiac surgery (see also Evidence
Table 22)
persistent AF refractory to AAD therapy to
prevent symptoms, recurrence, and progression of IIa A
Recommendations Classa Levelb
AF, within a shared decision-making rhythm
control team of electrophysiologists and Concomitant surgical ablation is recommended in
surgeons.667–671,674 patients undergoing mitral valve surgery and AF
Endoscopic and hybrid ablation procedures may suitable for a rhythm control strategy to prevent

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be considered in patients with symptomatic symptoms and recurrence of AF, with shared I A
paroxysmal AF refractory to AAD therapy and decision-making supported by an experienced team
failed percutaneous catheter ablation strategy to of electrophysiologists and arrhythmia surgeons.683–
IIb B 685,701
prevent symptoms, recurrence, and progression of

© ESC 2024
AF, within a shared decision-making rhythm Intraprocedural imaging for detection of left atrial
control team of electrophysiologists and thrombus in patients undergoing surgical ablation is
surgeons.668,669 recommended to guide surgical strategy,
I C
independent of oral anticoagulant use, to prevent
AAD, antiarrhythmic drugs; AF, atrial fibrillation; LAA, left atrial appendage.
a peri-procedural ischaemic stroke and
Class of recommendation.
b
Level of evidence. thromboembolism.
Concomitant surgical ablation should be considered
in patients undergoing non-mitral valve cardiac
7.2.8. AF ablation during cardiac surgery surgery and AF suitable for a rhythm control strategy
Atrial fibrillation is a significant risk factor for early mortality, late mor­ to prevent symptoms and recurrence of AF, with IIa B
tality, and stroke in patients referred for cardiac surgery.675–677 The

© ESC 2024
shared decision-making supported by an
best validated method of surgical ablation is the Maze procedure, experienced team of electrophysiologists and
consisting of a pattern of transmural lesions including PVI, with arrhythmia surgeons.701,703–707
subsequent modifications using bipolar radiofrequency and/or
cryothermy ablation with LAA amputation (see Supplementary data AF, atrial fibrillation.
a
Class of recommendation.
online, Additional Evidence Table S25).678–681 Education and training, b
Level of evidence.
close co-operation within a multidisciplinary team, and shared
decision-making can improve the quality and outcomes of surgical
ablation.682
A number of RCTs have shown that surgical AF ablation during 7.2.9. Atrial tachycardia after pulmonary vein
cardiac surgery increases freedom from arrhythmia recur­ isolation
rence.683–688 Performing surgical AF ablation, mainly targeting After any ablation for AF, recurrent arrhythmias may manifest as AF,
those patients needing mitral valve surgery, is not associated with but also as atrial tachycardia (AT). Although AT may be perceived as
increased morbidity or mortality.678,683–685 Observational data, a step in the right direction by the treating physician, this view is often
including large registries, have supported the potential value of not shared by the patient because AT can be equally or more symptom­
surgical AF ablation,689–700 but further RCTs are needed to evaluate atic than the original AF. Conventionally, an early arrhythmia recur­
which patients should be selected, and whether this approach rence post-PVI (whether AT, AF, or flutter) is considered potentially
contributes to the prevention of stroke, thromboembolism, and transitory.708 Recent trials using continuous implantable loop recorders
death. for peri-procedural monitoring have provided insight into the incidence
Data on pacemaker implantation rates after surgical AF ablation and significance of early arrhythmia recurrences, and have confirmed a
are variable and are likely influenced by centre experience and the link between early and later recurrence.709 Discussion of management
patients treated (e.g. underlying sinus node disease). In a systematic options for AT post-ablation should ideally involve a multidisciplinary
review of 22 RCTs (1726 patients), permanent pacemaker implant­ team with experience in interventional management of complex ar­
ation rates were higher with surgical AF ablation than without con­ rhythmias, considering technical challenges, procedural efficacy, and
comitant AF surgery (6.0% vs. 4.1%; RR, 1.69; 95% CI, 1.12–2.54).701 safety, in the context of patient preferences.
Observational registry data from contemporary cohorts (2011–
2020) suggest an overall pacemaker rate post-operatively of 2.1%
in patients selected for surgical AF ablation, with no discernible 8. [E] Evaluation and dynamic
impact of surgical ablation on the need for a pacemaker, but
higher rates in those needing multivalve surgery.702 With a safety-
reassessment
first approach in mind, imaging is advised during surgical AF ablation The development and progression of AF results from continuous
to exclude thrombus and help to plan the surgical approach interactions between underlying mechanisms (electrical, cellular,
(e.g. with TOE), regardless of effective pre-procedural anticoagulant neurohormonal, and haemodynamic), coupled with a broad range of
use. clinical factors and associated comorbidities. Each individual factor
ESC Guidelines 49

has considerable variability over time, affecting its contribution to the RACE 4 (IntegRAted Chronic Care Program at Specialized AF Clinic
AF-promoting substrate. The risk profile of each patient is also far Versus Usual CarE in Patients with Atrial Fibrillation) trial, which in­
from static, and requires a dynamic mode of care to ensure optimal cluded 1375 patients, failed to demonstrate superiority of nurse-led
AF management.710,711 Patients with AF require periodic reassessment over usual care.79 New studies of the components and optimal models
of therapy based on this changing risk status if we are to improve the for delivery for integrated care approaches in routine practice are on­
overall quality of care. Timely attention to modifiable factors and going (ACTRN12616001109493, NCT03924739).
underpinning comorbidities has the potential to slow or reverse the
progression of AF, increase quality of life, and prevent adverse out­

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comes such as heart failure, thromboembolism, and major bleeding. 8.2. Improving treatment adherence
The [E] in AF-CARE encompasses the range of activity needed by
Advances in the care of patients with AF can only be effective if appro­
healthcare professionals and patients to: (i) thoroughly evaluate asso­
priate tools are available to support the implementation of the treat­
ciated comorbidities and risk factors that can guide treatment; and
ment regimen.719 A number of factors are related to the optimal
(ii) provide the dynamic assessment needed to ensure that treatment
implementation of care at the level of: (i) the individual patient (culture,
plans remain suited to that particular patient. This task force recom­
cognitive impairment, and psychological status); (ii) the treatment
mends an adaptive strategy that not only reacts to changes notified
(complexity, side effects, polypharmacy, impact on daily life, and
by a patient, but also proactively seeks out issues where altering man­
cost); (iii) the healthcare system (access to treatment and multidiscip­
agement could impact on patient wellbeing. Avoidance of unnecessary
linary approach); and (iv) the healthcare professional (knowledge,
and costly follow-up is also inherent in this framework, with educated
awareness of guidelines, expertise, and communication skills). A collab­
and empowered patients contributing to identifying the need for access
orative approach to patient care, based upon shared decision-making
to specialist care or an escalation of management. The patient-centred,
and goals tailored to individual patient needs, is crucial in promoting on­
shared decision philosophy is embedded to improve efficiency in mod­
going patient adherence to the agreed treatment regimen.720 Even
els of care and to address the needs of patients with AF.
when treatment seems feasible for the individual, patients often lack ac­
Medical history and the results of any tests should be regularly re-
cess to reliable and up-to-date information about risks and benefits of
evaluated to address the dynamic nature of comorbidities and risk fac­
various treatment options, and consequently are not empowered to
tors.712 This may have impact on therapeutic decisions; e.g. resumption
engage in their own management. A sense of ownership that promotes
of full-dose DOAC therapy after improvement in the patient’s renal
the achievement of joint goals can be encouraged through the use of
function. The timing of review of the AF-CARE pathway is patient spe­
educational programmes, websites (such as https://afibmatters.org),
cific and should respond to changes in clinical status. In most cases, this
app-based tools, and individually tailored treatment protocols which
task force advises re-evaluation 6 months after initial presentation, and
take into account gender, ethnic, socioeconomic, environmental, and
then at least annually by a healthcare professional in primary or second­
work factors. In addition, practical tools (e.g. schedules, apps, bro­
ary care (see Figure 3).
chures, reminders, pillboxes) can help to implement treatment in daily
life.721,722 Regular review by members of the multidisciplinary team en­
8.1. Implementation of dynamic care ables the evolution of a flexible and responsive management regimen
that the patient will find easier to follow.
A multidisciplinary-based approach is advocated to improve implemen­
tation of dynamic AF-CARE (see Figure 2); although potentially re­
source intensive, this is preferred to more simplistic or opportunistic
methods. For example, in a pragmatic trial of 47 333 AF patients iden­ 8.3. Cardiac imaging
tified through health insurance claims, there was no difference in OAC A TTE is a valuable asset across all four AF-CARE domains when
initiation at 1 year in those randomized to a single mailout of patient and there are changes in the clinical status of an individual patient
clinician education, compared with those in the usual care group.713 For (Figure 13).723–725 The key findings to consider from an echocardiogram
co-ordination of care there is a core role for cardiologists, general prac­ are any structural heart disease (e.g. valvular disease or left ventricular
titioners, specialized nurses, and pharmacists.714 If needed, and depend­ hypertrophy), impairment of left ventricular function (systolic and/or
ing on local resources, others may also be involved (cardiac surgeons, diastolic to classify heart failure subtype), left atrial dilatation, and right
physiotherapists, neurologists, psychologists, and other allied health heart dysfunction.59,67,726 To counter irregularity when in AF, obtaining
professionals). It is strongly advocated that one core team member co- measurements in cardiac cycles that follow two similar RR intervals can
ordinates care, and that additional team members become involved ac­ improve the value of parameters compared with sequential averaging of
cording to the needs of the individual patient throughout their AF cardiac cycles.723,727 Contrast TTE or alternative imaging modalities
trajectory. may be required where image quality is poor, and quantification of
Several organizational models of integrated care for AF have been left ventricular systolic function is needed for decisions on rate or
evaluated, but which components are most useful remains unclear. rhythm control. Other cardiac imaging techniques, such as cardiac mag­
Some models include a multidisciplinary team,715,716 while others are netic resonance (CMR), CT, TOE, and nuclear imaging can be valuable
nurse-led79,122,124,717 or cardiologist-led.79,122,124,717 Several published when: (i) TTE quality is suboptimal for diagnostic purposes; (ii) addition­
models used computerized decision support systems or electronic al information is needed on structure, substrate, or function; and (iii) to
health applications.79,122,715,718 Evaluation within RCTs has demon­ support decisions on interventional procedures (see Supplementary
strated mixed results due to the variety of methods tested and differ­ data online, Figure S1).59,724,725,728 As with TTE, other types of cardiac
ences in regional care. Several studies report significant improvements imaging can be challenging in the context of AF irregularity or with rapid
with respect to adherence to anticoagulation, cardiovascular mortality, heart rate, requiring technique-specific modifications when acquiring
and hospitalization relative to standard of care.121–123 However, the ECG-gated sequences.729–731
50 ESC Guidelines

AF-CARE Objective for Example of

Assessment
pathway imaging pathology

Left ventricular ejection fraction,

wall motion abnormalities, diastolic
Cardiac amyloid

C To identify indices, right ventricular function and

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comorbidities which left ventricular hypertrophy to
determine subtype and aetiology of
are associated with
heart failure
recurrence and
Comorbidity and risk progression of AF Detection of pericardial fluid or
factor management pericardial disease
Detection of valvular disease

Detection of heart failure for Clot in LAA

CHA2DS2-VA score

A
To determine
stroke risk, choice Detection of moderate-severe
of anticoagulant mitral stenosis to determine choice
drug and ensure of anticoagulation
Avoid stroke and safety for Transoesophageal echocardiogram
cardioversion for left atrial appendage assessment
thromboembolism to exclude thrombus prior to
cardioversion

Left ventricular ejection fraction to Severe LV

R
determine choice of rate control impairment
To determine optimal Severity of valvular disease to
choice of rate and determine choice of rhythm control
rhythm control Left ventricular size and function to
Reduce symptoms strategy and likely determine choice of rhythm control
by rate and success of ablation Left atrial size and function to
rhythm control determine risk of arrhythmia
recurrence following ablation

Mixed mitral

E
valve disease
To detect changes in Reassess known valve disease for
the patient's heart increase in severity
structure and function Reassess left ventricular size and
Evaluation and which would affect function if there is a change in the
dynamic their management plan patient’s clinical status or symptoms
reassessment

Figure 13 Relevance of echocardiography in the AF-CARE pathway. AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk fac­
tor management, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment;
CHA2DS2-VA, congestive heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial
thromboembolism (2 points), vascular disease, age 65–74 years; LAA, left atrial appendage; LV, left ventricle.

8.4. Patient-reported outcome measures with AF over time.55,733–735 Patient-reported outcome measures are
Patients with AF have a lower quality of life compared with the general playing an increasing role in clinical trials to assess the success of treat­
population.732 Improvement in quality of life and functional status should ment; however, they remain under-utilized.736,737 They can be divided
play a key role in assessing and reassessing treatment decisions (see into generic or disease-specific tools, with the latter helping to provide
Supplementary data online, Additional Evidence Table S26).36 insight into AF-related impacts.738 However, multimorbidity can still con­
Patient-reported outcome measures are valuable to measure quality of found the sensitivity of all PROMs, impacting on association with other
life, functional status, symptoms, and treatment burden for patients established metrics of treatment performance such as mEHRA symptom
ESC Guidelines 51

class and natriuretic peptides.48 Intervention studies have demonstrated rate control in intensive care patients, and superior to digoxin and cal­
an association between improvement in PROM scores and reduction in cium channel blockers.749 The ultra-short acting and highly selective beta-
AF burden and symptoms.48,738 blocker landiolol can safely control rapid AF in patients with low ejection
Atrial fibrillation-specific questionnaires include the AF 6 (AF6),739 fraction and acutely decompensated heart failure, with a limited impact
Atrial Fibrillation Effect on QualiTy-of-Life (AFEQT),740 the Atrial on myocardial contractility or blood pressure.477,750,751
Fibrillation Quality of Life Questionnaire (AFQLQ),741 the Atrial
Fibrillation Quality of Life (AF-QoL),742 and the Quality of Life in 9.2. AF-CARE in acute and chronic
Atrial Fibrillation (QLAF).743 The measurement properties of most of
these tools lack sufficient validation.49 The International Consortium
coronary syndromes

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for Health Outcomes Measurement (ICHOM) working group recom­ The incidence of AF in acute coronary syndromes (ACS) ranges from
mends the use of the AFEQT PROM or a symptom questionnaire called 2% to 23%.752 The risk of new-onset AF is increased by 60%–77% in
the Atrial Fibrillation Severity Scale (AFSS) for measuring exercise tol­ patients suffering an MI,753 and AF may be associated with an increased
erance and the impact of symptoms in AF.744 Through wider use of pa­ risk of ST-segment elevation myocardial infarction (STEMI) or
tient experience measures, there is an opportunity at the institutional non-STEMI ACS.754 Overall, 10%–15% of AF patients undergo percu­
level to improve the quality of care delivered to patients with AF.49–55 taneous intervention (PCI) for CAD.755 In addition, AF is a common
precipitant for type 2 MI.756 Observational studies show that patients
with both ACS and AF are less likely to receive appropriate antithrom­
Recommendation Table 23 — Recommendations to
improve patient experience (see also Evidence Table 23) botic therapy757 and more likely to experience adverse outcomes.758
Peri-procedural management of patients with ACS or chronic coronary
Recommendations Classa Levelb syndromes (CCS) are detailed in the 2023 ESC Guidelines for the man­
agement of acute coronary syndromes and 2024 ESC Guidelines for the
Evaluating quality of care and identifying © ESC 2024
management of chronic coronary syndromes.759,760
opportunities for improved treatment of AF should The combination of AF with ACS is the area where use of multiple
IIa B
be considered by practitioners and institutions to antithrombotic drugs is most frequently indicated, consisting of antiplate­
improve patient experiences.49–55 let agents plus OAC (Figure 14) (see Supplementary data online,
AF, atrial fibrillation. Additional Evidence Table S27). There is a general trend to decrease the
a
Class of recommendation. duration of DAPT to reduce bleeding; however, this may increase ischae­
mic events and stent thrombosis.761,762 In ACS there is a high risk of pre­
b
Level of evidence.
dominantly platelet-driven atherothrombosis and thus of coronary
9. The AF-CARE pathway in specific ischaemic events. Acute coronary syndromes treated by PCI require
DAPT for improved short- and long-term prognosis. Therefore, a peri-
clinical settings procedural triple antithrombotic regimen including an OAC, aspirin, and
The following sections detail specific clinical settings where approaches a P2Y12 inhibitor should be the default strategy for most patients. Major
to AF-CARE may vary. Unless specially discussed, measures for [C] co­ thrombotic events vs. major bleeding risk need to be balanced when pre­
morbidity and risk factor management, [A] avoidance of stroke and scribing antiplatelet therapy and OAC after the acute phase and/or after
thromboembolism, [R] rate and rhythm control, and [E] evaluation PCI. The combination of OAC (preferably a DOAC) and a P2Y12 inhibi­
and dynamic reassessment should follow the standard pathways intro­ tor results in less major bleeding than triple therapy that includes aspirin.
duced in Section 4. Clopidogrel is the preferred P2Y12 inhibitor, as the evidence for ticagre­
lor and prasugrel is less clear with higher bleeding risk.763–769 Ongoing
trials will add to our knowledge about safely combining DOACs with
9.1. AF-CARE in unstable patients antiplatelet agents (NCT04981041, NCT04436978). When using
Unstable patients with AF include those with haemodynamic instability VKAs with antiplatelet agents, there is consensus opinion to use an
caused by the arrhythmia or acute cardiac conditions, and severely ill INR range of 2.0–2.5 to mitigate excess bleeding risk.
patients who develop AF (sepsis, trauma, surgery, and particularly Short–term triple therapy (≤1 week) is recommended for all pa­
cancer-related surgery). Conditions such as sepsis, adrenergic over­ tients without diabetes after ACS or PCI. In pooled analyses of
stimulation, and electrolyte disturbances contribute to onset and recur­ RCTs, omitting aspirin in patients with ACS undergoing PCI has
rence of AF in these patients. Spontaneous restoration of sinus rhythm the potential for higher rates of ischaemic/stent thrombosis, without
has been reported in up to 83% during the first 48 h after appropriate impact on incident stroke.761,762,770–772 None of the trials were
treatment of the underlying cause.551,745 powered for ischaemic events. All patients in AUGUSTUS (an open–
Emergency electrical cardioversion is still considered the first-choice label, 2 × 2 factorial, randomized controlled clinical trial to evaluate
treatment if sinus rhythm is thought to be beneficial, despite the limita­ the safety of apixaban vs. vitamin k antagonist and aspirin vs. aspirin pla­
tion of having a high rate of immediate relapse.746 Amiodarone is a cebo in patients with AF and ACS or PCI) received aspirin plus a P2Y12
second-line option because of its delayed activity; however, it may be inhibitor for a median time of 6 days.773 At the end of the trial, apixaban
an appropriate alternative in the acute setting.747,748 In a multicentre co­ and a P2Y12 inhibitor without aspirin was the optimal treatment regi­
hort study carried out in the United Kingdom and the United States of men for most patients with AF and ACS and/or PCI, irrespective of
America, amiodarone and beta-blockers were similarly effective for the patient’s baseline bleeding and stroke risk.774,775
52 ESC Guidelines

Prolonged triple therapy up to 1 month after ACS/PCI should patients with ACS or CCS and diabetes mellitus undergoing
be considered in patients at high ischaemic risk, e.g. STEMI, coronary stent implantation, prolonging triple therapy with low-
prior stent thrombosis, complex coronary procedures, and pro­ dose aspirin, clopidogrel, and an OAC up to 3 months may be
longed cardiac instability, even though these patients were not of benefit if thrombotic risk outweighs bleeding risk in the individ­
adequately represented in the RCTs so far available.776 In AF ual patient.207

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DOACs rather than VKA are recommended in eligible patients when combining with antiplatelet therapy
(Class I)

Use the appropriate DOAC dosea. A reduced dose is not recommended unless the patient meets DOAC-specific criteriaa
(Class III)

When using VKA in combination with antiplatelet therapy, keep INR 2.0–2.5 and TTR >70% VKA: INR 2.0–3.0
(Class IIa) (Class I)

Clopidogrel is the preferred P2Y12i when combining with any OAC

ACS, PCI or CCS Up to 1 week 1 month 6 months 12 months

ACS OAC + P2Y12i

undergoing + aspirin OAC + P2Y12i (Class I) OAC only (Class I)
PCI (Class I)

ACS high OAC + P2Y12i

ischaemic + aspirin OAC + P2Y12i (Class I) OAC only (Class I)
riskb (Class IIa)

ACS
medically OAC + P2Y12i OAC only
managed

CCS OAC + P2Y12i

uncomplicated + aspirin OAC + P2Y12i (Class I) OAC only (Class I)
PCI (Class I)

CCS high OAC + P2Y12i

ischaemic + aspirin OAC + P2Y12i (Class I) OAC only (Class I)
riskb (Class IIa)

OAC only
Stable CCS

Figure 14 Antithrombotic therapy in patients with AF and acute or chronic coronary syndromes. ACS, acute coronary syndromes; CCS, chronic
coronary syndrome; DOAC, direct oral anticoagulant; INR, international normalized ratio of prothrombin time; OAC, oral anticoagulant; P2Y12i,
P2Y12-receptor inhibitor antiplatelet agents (clopidogrel, prasugrel, ticagrelor); PCI, percutaneous intervention; TTR, time in therapeutic range;
VKA, vitamin K antagonist. The flowchart applies to those patients with an indication for oral anticoagulant therapy. aThe full standard dose of
DOACs should be used unless the patient fulfils dose-reduction criteria (Table 11). When rivaroxaban or dabigatran are used as the DOAC and con­
cerns about bleeding risk prevail over stent thrombosis or ischaemic stroke, the reduced dose should be considered (15 mg and 110 mg respectively;
Class IIa). bIn patients with diabetes mellitus undergoing coronary stent implantation, prolonging triple antithrombotic therapy for up to 3 months may
be of value if thrombotic risk outweighs the bleeding risk.
ESC Guidelines 53

The evidence for ACS treated without revascularization is Recommendations for AF patients undergoing PCI
limited. Six to 12 months of a single antiplatelet agent in addition to a
After uncomplicated PCI, early cessation (≤1 week)
long-term DOAC is usually sufficient and can minimize bleeding
of aspirin and continuation of an oral anticoagulant
risk.760,764,774 Although there are no head-to-head comparisons be­
and a P2Y12 inhibitor (preferably clopidogrel) for up I A
tween aspirin and clopidogrel, studies have typically used clopidogrel.
to 6 months is recommended to avoid major
In patients with stable CCS for more than 12 months, sole
therapy with a DOAC is sufficient and no additional antiplatelet therapy bleeding, if ischaemic risk is low.763–766,776,780
is required.353 In patients at potential risk of gastrointestinal bleeding, Triple therapy with aspirin, clopidogrel, and an oral

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use of proton pump inhibitors is reasonable during combined anticoagulant for longer than 1 week should be
antithrombotic therapy, although evidence in AF patients is considered after PCI when the risk of stent
IIa B
limited.437,777–779 Multimorbid patients with ACS or CCS need careful thrombosis outweighs the bleeding risk, with the total
assessment of ischaemic risk and management of modifiable bleeding duration (≤1 month) decided according to
risk factors, with a comprehensive work-up to individually adapt assessment of these risks and clear documentation.776
antithrombotic therapy. Recommendations for AF patients with chronic coronary or
vascular disease
Antiplatelet therapy beyond 12 months is not
Recommendation Table 24 — Recommendations for
patients with acute coronary syndromes or undergoing recommended in stable patients with chronic

© ESC 2024
percutaneous intervention (see also Evidence Table 24) coronary or vascular disease treated with oral III B
anticoagulation, due to lack of efficacy and to avoid
Recommendations Classa Levelb major bleeding.353,781,782

General recommendations for patients with AF and an ACS, acute coronary syndromes; AF, atrial fibrillation; DOAC, direct oral anticoagulant;
INR, international normalized ratio of prothrombin time; PCI, percutaneous
indication for concomitant antiplatelet therapy
intervention; TTR, time in therapeutic range; VKA, vitamin K antagonist.
a
For combinations with antiplatelet therapy, a DOAC Class of recommendation.
b
is recommended in eligible patients in preference to a Level of evidence.
I A
VKA to mitigate bleeding risk and prevent
thromboembolism.764,766
9.3. AF-CARE in vascular disease
Rivaroxaban 15 mg once daily should be considered
Peripheral arterial disease (PAD) is common in patients with AF, ran­
in preference to rivaroxaban 20 mg once daily when
ging from 6.7% to 14% of patients.783,784 Manifest PAD is associated
combined with antiplatelet therapy in patients where IIa B
with incident AF.785 PAD predicts a higher mortality in patients with
concerns about bleeding risk prevail over concerns AF and is an independent predictor of stroke in those not on
about stent thrombosis or ischaemic stroke.765 OAC.783,786 Patients with lower extremity artery disease and AF
Dabigatran 110 mg twice daily should be considered also have a higher overall mortality and risk of major cardiac
in preference to dabigatran 150 mg twice daily when events.784,787,788 A public health database of >40 000 patients
combined with antiplatelet therapy in patients where IIa B hospitalized for PAD or critical limb ischaemia showed AF to be an
concerns about bleeding risk prevail over concerns independent predictor for mortality (HR, 1.46; 95% CI, 1.39–1.52)
about stent thrombosis or ischaemic stroke.766 and ischaemic stroke (HR, 1.63; 95% CI, 1.44–1.85) as compared
Carefully regulated VKA dosing with a target INR of with propensity-matched controls.784 Similarly, in patients undergoing
2.0–2.5 and TTR >70% should be considered when carotid endarterectomy or stenting, the presence of AF is associated
IIa C with higher mortality (OR, 1.59; 95% CI, 1.11–2.26).789
combined with antiplatelet therapy in AF patients to
mitigate bleeding risk. Anticoagulation alone is usually sufficient in the chronic disease
phase, with DOACs being the preferred agents despite one RCT sub­
Recommendations for AF patients with ACS
analysis showing a higher risk of bleeding as compared with warfarin.790
Early cessation (≤1 week) of aspirin and continuation In the case of recent endovascular revascularization, a period of com­
of an oral anticoagulant (preferably DOAC) with a bination with single antiplatelet therapy should be considered, weighing
P2Y12 inhibitor (preferably clopidogrel) for up to 12 bleeding and thrombotic risks and keeping the period of combination
months is recommended in AF patients with ACS I A antithrombotic therapy as brief as possible (ranging between 1 month
undergoing an uncomplicated PCI to avoid major for peripheral791 and 90 days for neuro-interventional procedures).792
bleeding, if the risk of thrombosis is low or bleeding
risk is high.764–767
Triple therapy with aspirin, clopidogrel, and oral 9.4. AF-CARE in acute stroke or
anticoagulation for longer than 1 week after an ACS intracranial haemorrhage
should be considered in patients with AF when 9.4.1. Management of acute ischaemic stroke
ischaemic risk outweighs the bleeding risk, with the IIa C
Management of acute stroke in patients with AF is beyond the scope of
total duration (≤1 month) decided according to these guidelines. In AF patients presenting with acute ischaemic stroke
assessment of these risks and clear documentation of while taking OAC, acute therapy depends on the treatment regimen
the discharge treatment plan.776 and intensity of OAC. Management should be co-ordinated by a spe­
Continued cialist neurologist team according to relevant guidelines.793
54 ESC Guidelines

9.4.2. Introduction or re-introduction of always underlying factors in individual patients that can benefit from full
anticoagulation after ischaemic stroke consideration of the AF-CARE pathway. The most common precipitant
The optimal time for administering OAC in patients with acute cardio­ unmasking a tendency to AF is acute sepsis, where AF prevalence is
embolic stroke and AF remains unclear. Randomized control trials have between 9% and 20% and has been associated with a worse
been unable to provide any evidence to support the administration of prognosis.11–14 The degree of inflammation correlates with the incidence
anticoagulants or heparin in patients with acute ischaemic stroke within of AF,799 which may partly explain the wide variability across studies in
48 h from stroke onset. This suggests that low-dose aspirin should be prevalence, as well as recurrence of AF. Longer-term data suggest that
administered to all patients during this timeframe.794 AF triggered by sepsis recurs after discharge in between a third to a half
of patients.12,800–807 In addition to other acute triggers which may be causal

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Two trials have examined the use of DOAC therapy early after
stroke, with no difference in clinical outcomes compared with delayed (such as alcohol808,809 and illicit drug use810), numerous conditions are also
DOAC prescription. The ELAN (Early versus Late initiation of direct associated with chronic inflammation leading to subacute stimuli for AF
oral Anticoagulants in post-ischaemic stroke patients with atrial (Table 14). The specific trigger of an operative procedure is discussed in
fibrillatioN) trial randomized 2013 patients with acute ischaemic stroke Section 9.6.
and AF to open-label early use of DOACs (<48 h after minor/moderate After meeting the diagnostic criteria for AF (see Section 3.2), the
stroke; day 6–7 after major stroke) vs. later DOAC prescription (day management of trigger-induced AF is recommended to follow the
3–4 after minor stroke; day 6–7 after moderate stroke; day 12–14 after AF-CARE principles, with critical consideration of underlying risk factors
major stroke). There was no significant difference in the composite and comorbidities. Based on retrospective and observational data, patients
thromboembolic, bleeding, and vascular death outcome at 30 days with AF and trigger-induced AF seem to carry the same thromboembolic
(risk difference early vs. late, −1.18%; 95% CI, −2.84 to 0.47).795 The risk as patients with primary AF.811,812 In the acute phase of sepsis, patients
TIMING (Timing of Oral Anticoagulant Therapy in Acute Ischemic show an unclear risk–benefit profile with anticoagulation therapy.813,814
Stroke With Atrial Fibrillation) trial, a registry-based, non-inferiority, Prospective studies on anticoagulation in patients with triggered AF epi­
open-label, blinded endpoint trial randomized 888 patients within sodes are lacking.802,812,815 Acknowledging that there are no RCTs specif­
72 h of ischaemic stroke onset to early (≤4 days) or delayed (5–10 days) ically available in this population to assess trigger-induced AF, long-term
DOAC initiation. Early DOAC use was non-inferior to the delayed OAC therapy should be considered in suitable patients with trigger-
strategy for the composite of thromboembolism, bleeding and all-cause induced AF who are at elevated risk of thromboembolism, starting
mortality at 90 days (risk difference, −1.79%; 95% CI, −5.31% to OAC after the acute trigger has been corrected and considering the antici­
1.74%).796 Two ongoing trials will provide further guidance on the pated net clinical benefit and informed patient preferences. As with any de­
most appropriate timing of DOAC therapy after ischaemic stroke cision on OAC, not all patients will be suitable for OAC, depending on
(NCT03759938, NCT03021928). relative and absolute contraindications and the risk of major bleeding.
The approach to rate and rhythm control will depend on subsequent re­
currence of AF or any associated symptoms, and re-evaluation should be
9.4.3. Introduction or re-introduction of
individualized to take account of the often high AF recurrence rate.
anticoagulation after haemorrhagic stroke
There is insufficient evidence currently to recommend whether OAC
should be started or re-started after ICH to protect against the high
Table 14 Non-cardiac conditions associated with
risk of ischaemic stroke in these patients (see Supplementary data trigger-induced AF
online, Additional Evidence Table S28). Data from two pilot trials are avail­
able. The APACHE-AF (Apixaban After Anticoagulation-associated Acute conditions
Intracerebral Haemorrhage in Patients With Atrial Fibrillation) trial
was a prospective, randomized, open-label trial with masked endpoint as­ Infections (bacterial and viral)
sessment; 101 patients who survived 7–90 days after anticoagulation- Pericarditis, myocarditis
associated ICH were randomized to apixaban or no OAC. During a Emergency conditions (burn injury, severe trauma, shock)
median of 1.9 years follow-up (222 person-years), there was no differ­ Binge alcohol consumption
ence in non-fatal stroke or vascular death, with an annual event rate of Drug use, including methamphetamines, cocaine, opiates, and cannabis
12.6% with apixaban and 11.9% with no OAC (adjusted HR, 1.05; 95% Acute interventions, procedures, and surgery
CI, 0.48–2.31; P = .90).797 SoSTART (Start or STop Anticoagulants
Endocrine disorders (thyroid, adrenal, pituitary, others)
Randomised Trial) was an open-label RCT in 203 patients with AF after
symptomatic spontaneous ICH. Starting OAC was not non-inferior to Chronic conditions with inflammation and enhanced AF
avoiding long-term (≥1 year) OAC, with ICH recurrence in 8/101 substrate
(8%) vs. 4/102 (4%) patients (adjusted HR, 2.42; 95% CI, 0.72–8.09). Immune-mediated diseases (rheumatoid arthritis, systemic lupus
Mortality occurred in 22/101 (22%) patients in the OAC group vs. erythematosus, inflammatory bowel disease, coeliac disease, psoriasis,
11/102 (11%) patients where OAC were avoided.798 others)
Until additional trials report on the clinical challenge of post-ICH an­ Obesity
ticoagulation (NCT03950076, NCT03996772), an individualized multi­
Chronic obstructive airways disease
disciplinary approach is advised led by an expert neurology team.
Obstructive sleep apnoea
Cancer
9.5. AF-CARE for trigger-induced AF
Fatty liver disease
© ESC 2024

Trigger-induced AF is defined as new AF in the immediate association of a

Stress
precipitating and potentially reversible factor. Also known as ‘secondary’
AF, this task force prefer the term trigger-induced as there are almost Endocrine disorders (see Section 9.10)
ESC Guidelines 55

Recommendation Table 25 — Recommendations for bleeding risk soon after cardiac surgery or major non-cardiac inter­
trigger-induced AF (see also Evidence Table 25) ventions.827 Conversely, meta-analyses of observational cohort stud­
ies suggest a possible protective impact of OAC in POAF for all-cause
Recommendation Classa Levelb mortality848 and a lower risk of thromboembolic events following car­
Long-term oral anticoagulation should be considered diac surgery, accompanied by higher rates of bleeding.849 This task
force recommends to treat post-operative AF according to the

© ESC 2024
in suitable patients with trigger-induced AF at
IIa C AF-CARE pathway as discussed for trigger-induced AF (with the [R]
elevated thromboembolic risk to prevent ischaemic
pathway the same as for first-diagnosed AF). Ongoing RCTs in cardiac
stroke and systemic thromboembolism.13,800,806,807,815

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surgery (NCT04045665) and non-cardiac surgery (NCT03968393)
AF, atrial fibrillation. will inform optimal long-term OAC use among patients with POAF.
a
Class of recommendation.
b
While awaiting the results of these trials, this task force recommends
Level of evidence.
that after acute bleeding risk has settled, long-term OAC should be
considered in patients with POAF according to their thromboembolic
risk factors.

9.6. AF-CARE in post-operative patients

Recommendation Table 26 — Recommendations for
Peri-operative AF describes the onset of the arrhythmia during an
management of post-operative AF (see also Evidence
ongoing intervention. Post-operative AF (POAF), defined as new- Table 26)
onset AF in the immediate post-operative period, is a common com­
plication with clinical impact that occurs in 30%–50% of patients Recommendations Classa Levelb
undergoing cardiac surgery,816–818 and in 5%–30% of patients under­
going non-cardiac surgery. Intra- and post-operative changes and Peri-operative amiodarone therapy is recommended
specific AF triggers (including peri-operative complications) and where drug therapy is desired to prevent I A
pre-existing AF-related risk factors and comorbidities increase the post-operative AF after cardiac surgery.838,839,850,851
susceptibility to POAF.819 Although POAF episodes may be self- Concomitant posterior peri-cardiotomy should be
terminating, POAF is associated with 4–5 times increase in recurrent considered in patients undergoing cardiac surgery to IIa B
AF during the next 5 years,820,821 and is a risk factor for stroke, MI, prevent post-operative AF.845,846
heart failure, and death.822–827 Other adverse events associated Long-term oral anticoagulation should be considered
with POAF include haemodynamic instability, prolonged hospital in patients with post-operative AF after cardiac and
stay, infections, renal complications, bleeding, increased in-hospital non-cardiac surgery at elevated thromboembolic IIa B
death, and greater healthcare cost.828–830 risk, to prevent ischaemic stroke and
While multiple strategies to prevent POAF with pre-treatment or acute thromboembolism.811,852–854
drug treatment have been described, there is a lack of evidence from large

© ESC 2024
Routine use of beta-blockers is not recommended in
RCTs. Pre-operative use of propranolol or carvedilol plus N-acetyl
patients undergoing non-cardiac surgery for the III B
cysteine in cardiac and non-cardiac surgery is associated with a reduced
prevention of post-operative AF.836,855
incidence of POAF,831–834 but not major adverse events.835 An umbrella
review of 89 RCTs from 23 meta-analyses (19 211 patients, but not neces­ AF, atrial fibrillation.
a
sarily in AF) showed no benefit from beta-blockers in cardiac surgery for Class of recommendation.
b
Level of evidence.
mortality, MI, or stroke. In non-cardiac surgery, beta-blockers were asso­
ciated with reduced rates of MI after surgery (RR range, 0.08–0.92), but
higher mortality (RR range, 1.03–1.31), and increased risk of stroke (RR
range, 1.33–7.72).836 Prevention of peri-operative AF can also be achieved
9.7. AF-CARE in embolic stroke of
with amiodarone. In a meta-analyses, amiodarone (oral or intravenous unknown source
[i.v.]) and beta-blockers were equally effective in reducing post-operative The term ‘embolic stroke of undetermined source’ (ESUS) was introduced
AF,837 but their combination was better than beta-blockers alone.838 to identify non-lacunar strokes whose mechanism is likely to be embolic,
Lower cumulative doses of amiodarone (<3000 mg during the but the source remains unidentified.856 Of note, these patients have a re­
loading phase) could be effective, with fewer adverse events.837,839,840 current risk of stroke of 4%–5% per year.856 The main embolic sources as­
Withdrawal of beta-blockers should be avoided due to increased risk sociated with ESUS are concealed AF, atrial cardiomyopathy, left
of POAF.841 Other treatment strategies (steroids, magnesium, sotalol, ventricular disease, atherosclerotic plaques, patent foramen ovale (PFO),
(bi)atrial pacing, and botulium injection into the epicardial fat pad) lack valvular diseases, and cancer. Atrial cardiomyopathy and left ventricular dis­
scientific evidence for the prevention of peri-operative AF.842,843 ease are the most prevalent causes.856 AF is reported to be the underlying
Peri-operative posterior pericardiotomy, due to the reduction of post- mechanism in 30% of ESUS patients.857–859 The detection of AF among
operative pericardial effusion, showed a significant decrease in POAF ESUS patients increases the longer cardiac monitoring is provided (see
in patients undergoing cardiac surgery (OR, 0.44; 95% CI, 0.27–0.70; Supplementary data online, Additional Evidence Table S29).857,860–864 This
P = .0005).844–846 In 3209 patients undergoing non-cardiac thoracic sur­ also holds for the duration of implantable cardiac monitoring, with prob­
gery, colchicine did not lead to any significant reduction in AF compared ability of AF detection ranging from 2% with 1 week to over 20% by 3
with placebo (HR, 0.85; 95% CI, 0.65–1.10; P = .22).847 years.865 In patients with ESUS, factors associated with an increased detec­
The evidence for prevention of ischaemic stroke in POAF by OAC tion of AF are increasing age,866,867 left atrial enlargement,866 cortical loca­
is limited.822,827 Oral anticoagulant therapy is associated with a high tion of stroke,868 large or small vessel disease,863 an increased number of
56 ESC Guidelines

atrial premature beats per 24 h,868 rhythm irregularity,859 and risk stratifi­ (verapamil should be avoided in the first trimester). Rhythm control is
cation scores (such as CHA2DS2-VASc,869 Brown ESUS-AF,870 the preferred strategy during pregnancy. Electrical cardioversion is re­
HAVOC,871 and C2HEST872). This task force recommends prolonged commended if there is haemodynamic instability, considerable risk to
monitoring depending on the presence of the above-mentioned risk mother or foetus, or with concomitant HCM. Electrical cardioversion
markers.865,873,874 can be performed safely without compromising foetal blood flow,
Currently available evidence, including two completed RCTs and one and the consequent risk for foetal arrhythmias or pre-term labour is
stopped for futility, do not support the use of DOACs compared with low. The foetal heart rate should be closely monitored throughout
aspirin in patients with acute ESUS without documented AF.875–877 and after cardioversion, which should generally be preceded by anticoa­
gulation.885 In haemodynamically stable women without structural

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Ongoing trials will provide further guidance (NCT05134454,
NCT05293080, NCT04371055). heart disease, intravenous ibutilide or flecainide may be considered
for termination of AF, but experience is limited.890 Catheter ablation
is normally avoided during pregnancy,883 but is technically feasible with­
Recommendation Table 27 — Recommendations for out radiation in refractory symptomatic cases with a minimal/zero
patients with embolic stroke of unknown source (see fluoroscopy approach.883
also Evidence Table 27) Counselling is important in women of childbearing potential prior to
pregnancy, highlighting the potential risks of anticoagulation and rate or
Recommendations Classa Levelb rhythm control drugs (including teratogenic risk, where relevant).
Prolonged monitoring for AF is recommended in Contraception and timely switch to safe drugs should be proactively
patients with ESUS to inform on AF treatment I B discussed.
decisions.861–863
Initiation of oral anticoagulation in ESUS patients Recommendation Table 28 — Recommendations for
patients with AF during pregnancy (see also Evidence
© ESC 2024

without documented AF is not recommended due to

III A Table 28)
lack of efficacy in preventing ischaemic stroke and
thromboembolism.875,876 Recommendations Classa Levelb
AF, atrial fibrillation; ESUS, embolic stroke of undetermined source.
a Immediate electrical cardioversion is recommended
Class of recommendation.
b
Level of evidence. in patients with AF during pregnancy and
I C
haemodynamic instability or pre-excited AF to
improve maternal and foetal outcomes.885,891–893
9.8. AF-CARE during pregnancy Therapeutic anticoagulation with LMWHs or VKAs
Atrial fibrillation is one of the most common arrhythmias during preg­ (except VKAs for the first trimester or beyond
nancy, with prevalence increasing due to higher maternal age and Week 36) is recommended for pregnant patients I C
changes in lifestyle, and because more women with congenital heart dis­ with AF at elevated thromboembolic risk to prevent
ease survive to childbearing age.878–881 Rapid atrioventricular conduc­ ischaemic stroke and thromboembolism.885
tion of AF may have serious haemodynamic consequences for Beta-1 selective blockers are recommended for
mother and foetus. AF during pregnancy is associated with an increased heart rate control of AF in pregnancy to reduce
I C
risk of death.882 A multidisciplinary approach is essential to prevent ma­ symptoms and improve maternal and foetal
ternal and foetal complications, bringing together gynaecologists, neo­ outcomes, excluding atenolol.888
natologists, anaesthesiologists, and cardiologists experienced in Electrical cardioversion should be considered for
maternal medicine.883 persistent AF in pregnant women with HCM to IIa C
Pregnancy is associated with a hypercoagulable state and increased improve maternal and foetal outcomes.885,894
thromboembolic risk.884 The same rules for risk assessment of
Digoxin should be considered for heart rate control
thromboembolism should be used as in non-pregnant women, as de­
of AF in pregnancy, if beta-blockers are ineffective or
tailed in the 2018 ESC Guidelines for the management of cardiovascular IIa C
not tolerated, to reduce symptoms and improve
diseases during pregnancy.885 The preferred agents for anticoagulation
maternal and foetal outcomes.885
of AF during pregnancy are unfractionated or low molecular weight he­
parins (LMWHs), which do not cross the placenta. Vitamin K antago­ Intravenous ibutilide or flecainide may be considered
nists should be avoided in the first trimester (risk of miscarriage, for termination of AF in stable pregnant patients with
IIb C
teratogenicity) and from week 36 onwards (risk of foetal intracranial a structurally normal heart to improve maternal and
bleeding if early unexpected delivery). Direct oral anticoagulants are foetal outcomes.895,896
not recommended during pregnancy due to concerns about safety.886 Flecainide or propafenone may be considered for
However, an accidental exposure during pregnancy should not lead to a longer-term rhythm control in pregnancy, if rate
recommendation for termination of the pregnancy.887 Vaginal delivery
© ESC 2024

controlling drugs are ineffective or not tolerated, to IIb C

should be advised for most women, but is contraindicated during VKA reduce symptoms and improve maternal and foetal
treatment because of the risk of foetal intracranial bleeding.885 outcomes.885
Intravenous selective beta-1 receptor blockers are recommended as
AF, atrial fibrillation; HCM, hypertrophic cardiomyopathy; LMWH, low molecular weight
first choice for acute heart rate control of AF.888 This does not include
heparin; VKA, vitamin K antagonist.
atenolol, which can lead to intrauterine growth retardation.889 If beta- a
Class of recommendation.
blockers fail, digoxin and verapamil can be considered for rate control b
Level of evidence.
ESC Guidelines 57

9.9. AF-CARE in congenital heart disease in vulnerable patients, including the elderly and those with structural
Survival of patients with congenital heart disease has increased over atrial diseases,914,915 as well as cancer patients on immune checkpoint
time, but robust data on the management of AF are missing and avail­ inhibitors.916,917 In hyperthyroidism, and even in the euthyroid range,
able evidence is derived mainly from observational studies. Oral anti­ the risk of AF increases according to the reduction in TSH and elevated
coagulants are recommended for all patients with AF and intracardiac levels of thyroxine.918,919 Moreover, the risk of stroke is higher in
repair, cyanotic congenital heart disease, Fontan palliation, or systemic patients with hyperthyroidism, which can be mitigated by treating the
right ventricle irrespective of the individuals’ thromboembolic risk thyroid disorder.920,921 Amiodarone induces thyroid dysfunction in
factors.897 Patients with AF and other congenital heart diseases should 15%–20% of treated patients, leading to both hypo- and hyperthyroid­
ism,922,923 which warrants referral to an endocrinologist (see

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follow the general risk stratification for OAC use in AF (i.e. depending
on the thromboembolic risk or CHA2DS2-VA score). Direct oral Supplementary data online for further details).
anticoagulants are contraindicated in patients with mechanical heart Hypercalcaemia may also induce arrhythmias, but the role of primary
valves,331 but appear safe in patients with congenital heart dis­ hyperparathyroidism in incident AF is poorly studied. Surgical para­
ease,898,899 or those with a valvular bioprosthesis.900,901 thyroidectomy has been found to reduce both supraventricular and ven­
Rate control drugs such as selective beta-1 receptor blockers, tricular premature beats.924–926 Primary aldosteronism is related to an
verapamil, diltiazem, and digoxin can be used with caution, with moni­ increased risk of AF through direct actions and vascular effects,927,928
toring for bradycardia and hypotension. Rhythm control strategies such with a three-fold higher rate of incident AF compared with patients
as amiodarone may be effective, but warrant monitoring for bradycar­ with essential hypertension.929 Increases in genetically predicted plasma
dia. When cardioversion is planned, both 3 weeks of OAC and TOE cortisol are associated with greater risk of AF, and patients with adrenal
should be considered because thrombi are common in patients with incidentalomas with subclinical cortisol secretion have a higher preva­
congenital heart disease and atrial arrhythmias.902,903 Ablation ap­ lence of AF.930,931 Acromegaly may predispose to an increased sub­
proaches can be successful in patients with congenital heart disease, strate for AF, with incident AF rates significantly higher than controls
but AF recurrence rates may be high (see Supplementary data online, in long-term follow-up, even after adjusting for AF risk factors.932
Additional Evidence Table S30). The association between type 2 diabetes and AF is discussed in
In patients with atrial septal defect, closure may be performed be­ Sections 5.3 (AF recurrence) and Section 10.5 (incident AF). In addition
fore the fourth decade of life to decrease the risk of AF or AFL.904 to insulin-resistance mechanisms typical of type 2 diabetes, the loss of
Patients with stroke who underwent closure of their PFO may have insulin signalling has recently been associated with electrical changes
an increased risk of AF,905 but in patients with PFO and AF, PFO clos­ that can lead to AF. Type 1 diabetes is associated with an increased
ure is not recommended for stroke prevention. AF surgery or cath­ risk of several cardiovascular diseases including AF.933–937
eter ablation can be considered at the time of closure of the atrial
septal defect within a multidisciplinary team.906–908 AF catheter 9.11. AF-CARE in inherited
ablation of late atrial arrhythmias is likely to be effective after surgical cardiomyopathies and primary
atrial septal closure.909
arrhythmia syndromes
A higher incidence and prevalence of AF have been described in pa­
Recommendation Table 29 — Recommendations for tients with inherited cardiomyopathies and primary arrhythmia syn­
patients with AF and congenital heart disease (see also dromes.271,938–970 AF can be the presenting or only clinically overt
Evidence Table 29) feature.969,971–975 AF in these patients is associated with adverse clinical
outcomes,947,954,959,963,965,976–978 and has important implications on
Recommendation Classa Levelb management (see Supplementary data online, Additional Evidence
Table S31). When AF presents at a young age, there should be a careful
Oral anticoagulation should be considered in all adult
interrogation about family history and a search for underlying
congenital heart disease patients with AF/AFL and
disease.979
intracardiac repair, cyanosis, Fontan palliation, or
IIa C Rhythm control approaches may be challenging in patients with inher­
© ESC 2024

systemic right ventricle to prevent ischaemic stroke

ited cardiomyopathies and primary arrhythmia syndromes. For example,
and thromboembolism, regardless of other
many drugs have a higher risk of adverse events or may be contraindicated
thromboembolic risk factors.897
(e.g. amiodarone and sotalol in congenital long QT syndrome, and Class IC
AF, atrial fibrillation; AFL, atrial flutter. AADs in Brugada syndrome) (see Supplementary Data online, Table S6).
a
Class of recommendation. Owing to long-term adverse effects, chronic use of amiodarone is prob­
b
Level of evidence.
lematic in these typically young individuals. In patients with an implantable
cardioverter defibrillator, AF is a common cause of inappropriate
shocks.959,966,980,981 Programming a single high-rate ventricular fibrillation
9.10. AF-CARE in endocrine disorders zone ≥210–220 b.p.m. with long detection time is safe,950,953,982 and is
Endocrine dysfunction is closely related to AF, both as the direct action suggested in patients without documented slow monomorphic ventricu­
of endocrine hormones and as a consequence of treatments for endo­ lar tachycardia. Implantation of an atrial lead may be considered in the case
crine disease. Optimal management of endocrine disorders is therefore of significant bradycardia with beta-blocker treatment.
part of the AF-CARE pathway.910,911 Patients with Wolff–Parkinson–White syndrome and AF are at risk
Clinical and subclinical hyperthyroidism, as well as subclinical hypo­ of fast ventricular rates from rapid conduction of atrial electrical activity
thyroidism, are associated with an increased risk of AF.912,913 Patients to the ventricles via the accessory pathway, potentially leading to ven­
presenting with new-onset or recurrent AF should be tested for tricular fibrillation and sudden death.983,984 Immediate electrical cardi­
thyroid-stimulating hormone (TSH) levels. The risk of AF is enhanced oversion is needed for haemodynamically compromised patients with
58 ESC Guidelines

pre-excited AF, and atrioventricular node-modulating drugs should be multimorbid AF patients has improved since the introduction of
avoided.985,986 Pharmacological cardioversion can be attempted using DOACs, but is still lower in AF patients at older age (OR, 0.98 per
ibutilide987 or flecainide, while propafenone should be used with cau­ year; 95% CI, 0.98–0.98), with dementia (OR, 0.57; 95% CI,
tion due to effects on the atrioventricular node.988,989 Amiodarone 0.55–0.58), or frailty (OR, 0.74; 95% CI, 0.72–0.76).1021 The value of
should be avoided in pre-excited AF due to its delayed action. observational data which show potential benefit from OAC (in particu­
Further details on inherited cardiomyopathies can be found in the lar, DOACs) is limited due to prescription biases.1022–1027 Frail patients
2023 ESC Guidelines for the management of cardiomyopathies.990 aged ≥75 years with polypharmacy and stable on a VKA may remain on
the VKA rather than switching to a DOAC (Section 6.2).309

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9.12. AF-CARE in cancer
All types of cancer show an increased risk of AF, with prevalence vary­ 9.14. AF-CARE in atrial flutter
ing from 2% to 28%.991–995 The occurrence of AF may often be related Due to the association between AFL and thromboembolic outcomes,
to a pre-existing atrial substrate with vulnerability to AF. AF may be an and the frequent development of AF in patients with AFL, the manage­
indicator of an occult cancer, but also can appear in the context of con­ ment of comorbidities and risk factors in AFL should mirror that for AF
comitant surgery, chemotherapy, or radiotherapy.916,994,996 Risk of AF (see Section 5). Similarly, the approach to prevent thromboembolism in
is dependent on, among other factors, the cancer type and stage,997 and AFL includes peri-procedural and long-term OAC (see Section 6). Rate
is greater in older patients with pre-existing cardiovascular dis­ control can be difficult to achieve in AFL, despite combination therapy.
ease.991,993,994 Some procedures are associated with higher incidence Rhythm control is often the first-line approach,983 with small rando­
of AF, including lung surgery (from 6% to 32%) and non-thoracic sur­ mized trials showing that cavo-tricuspid isthmus (CTI) ablation is super­
gery such as a colectomy (4%–5%).994 ior to AADs.1028,1029 Recurrence of AFL is uncommon after achieving
Atrial fibrillation in the context of cancer is associated with a two- and confirming bidirectional block in typical CTI-dependent AFL.
fold higher risk of systemic thromboembolism and stroke, and six-fold However, the majority of patients (50%–70%) have manifested AF
increased risk of heart failure.991,994 On the other hand, the coexistence during long-term follow-up in observational studies after AFL
of cancer increases the risk of all-cause mortality and major bleeding in ablation.1030,1031 Hence the necessity for long-term dynamic re-
patients with AF.998 Bleeding in those receiving OAC can also unmask evaluation in all patients with AFL in keeping with the AF-CARE
the presence of cancer.999 approach. More detail on the management of AFL and other atrial ar­
Stroke risk scores may underestimate thromboembolic risk in cancer rhythmias is described in the 2019 ESC Guidelines for the management of
patients.1000 The association between cancer, AF, and ischaemic stroke patients with supraventricular tachycardia.983
also differs between cancer types. In some types of cancer, the risk of
bleeding seems to exceed the risk of thromboembolism.998 Risk strati­
fication is therefore complex in this population, and should be per­ Recommendation Table 30 — Recommendations for
formed on an individual basis considering cancer type, stage, prevention of thromboembolism in atrial flutter (see
also Evidence Table 30)
prognosis, bleeding risk, and other risk factors. These aspects can
change within a short period of time, requiring dynamic assessment Recommendation Classa Levelb
and management.
As with non-cancer patients, DOACs in those with cancer have simi­ Oral anticoagulation is recommended in patients

© ESC 2024
lar efficacy and better safety compared with VKAs.1001–1010 Low with atrial flutter at elevated thromboembolic risk to
I B
molecular weight heparin is a short-term anticoagulation option, mostly prevent ischaemic stroke and
during some cancer treatments, recent active bleeding, or thrombo­ thromboembolism.86,1032
cytopaenia.1011 Decision-making on AF management, including on
AF, atrial fibrillation; AFL, atrial flutter.
rhythm control, is best performed within a cardio-oncology multi­ a
Class of recommendation.
disciplinary team.916,1012 Attention is required on interactions with can­ b
Level of evidence.
cer treatments, in particular QT-interval prolongation with AADs.

9.13. AF-CARE in older, multimorbid, or

frail patients 10. Screening and prevention of AF
Atrial fibrillation increases with age, and older patients more frequently 10.1. Epidemiology of AF
have multimorbidity and frailty which are associated with worse clinical
Atrial fibrillation is the most common sustained arrhythmia worldwide,
outcomes.1013–1016 Multimorbidity is the coexistence of two or more
with an estimated global prevalence in 2019 of 59.7 million persons
medically diagnosed diseases in the same individual. Frailty is defined
with AF.1033 Incident cases of AF are doubling every few decades.1034
as a person more vulnerable and less able to respond to a stressor
Future increases are anticipated, in particular in middle-income coun­
or acute event, increasing the risk of adverse outcomes.1016,1017 The
prevalence of frailty in AF varies due to different methods of assess­ tries.1034 In community-based individuals, the prevalence of AF in a
ment from 4.4% to 75.4%, and AF prevalence in the frail population United States of America cohort was up to 5.9%.1035 The
ranges from 48.2% to 75.4%.1018 Frailty status is a strong independent age-standardized prevalence and incidence rates have remained con­
risk factor for new-onset AF among older adults with hypertension.1019 stant over time.1033,1036 The increase in overall prevalence is largely at­
Atrial fibrillation in frail patients is associated with less use of tributable to population growth, ageing, and survival from other cardiac
OAC and lower rates of management with a rhythm control conditions. In parallel, increases in risk factor burden, better awareness,
strategy.1015,1018,1020 Oral anticoagulation initiation in older, frail and improved detection of AF have been observed.1037 The lifetime risk
ESC Guidelines 59

of AF has been estimated to be as high as 1 in 3 for older individuals,1038 10.2. Screening tools for AF
with age-standardized incidence rates higher for men than women. In recent years, an abundance of novel devices that can monitor heart
Populations of European ancestry are typically found to have higher rhythm have come to the market, including fitness bands and smart­
AF prevalence, individuals of African ancestry have worse outcomes, watches. Although the evidence for clinical effectiveness of digital de­
and other groups may have less access to interventions.1039–1041 vices is limited, they may be useful in detecting AF, and their clinical,
Socioeconomic and other factors likely play a role in racial and ethnic economic, legal, and policy implications merit further investiga­
differences in AF, but studies are also limited due to differences in tion.1043,1044 Devices for AF detection can broadly be divided into those
how groups access healthcare. Greater deprivation in socioeconomic that provide an ECG, and those with non-ECG approaches such as

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and living status is associated with higher AF incidence.1042 photoplethysmography (Figure 15 and Table 15).

ECG-based methods

Diagnostic for AF if diagnosis is confirmed by a physician

(Class I)

No of leads 1 or 2 6 >6

Tracing

Non ECG-based methods

Not diagnostic (may be indicative for AF)

Pulse Mechano- Smart

Oscillometry PPG
palpation cardiography speaker
Method
Contact Contactless Contactless

Tracing

Figure 15 Non-invasive diagnostic methods for AF screening. AF, atrial fibrillation; BP, blood pressure; ECG, electrocardiogram; PPG,
photoplethysmography.
60 ESC Guidelines

Table 15 Tools for AF screening

Tools for AF screening

(i) Pulse palpation1045

(ii) Use of artificial intelligence algorithms to identify patients at risk1046
(iii) ECG-based devices
(a) Conventional ECG devices
(1) Classic 12-lead ECG 1047

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(2) Holter monitoring (from 24 h to a week or more)1048
(3) Mobile cardiac telemetry (during hospitalization)1049
(4) Handheld devices1050–1052
(5) Wearable patches (up to 14 days)1053–1067
(6) Biotextiles (up to 30 days)1068–1072
(7) Smart devices (30 s)1073–1091
(b) Implantable loop recorders (3–5 years)1092–1099
(iv) Non-ECG-based devices
(a) Photoplethysmography and automatic algorithms: contact (fingertip, smart device, band) and contactless (video)1100–1106
(b) Oscillometry (blood pressure monitors that derive heart rhythm regularity algorithmically)1107–1110

© ESC 2024
(c) Mechanocardiography (accelerometers and gyroscopes to sense the mechanical activity of the heart)1111
(d) Contactless video plethysmography (through video monitoring)1112–1115
(e) Smart speakers (through the identification of abnormal heart rate patterns)1116

ECG, electrocardiogram.

Most consumer-based devices use photoplethysmography, and 10.3. Screening strategies for AF
several large studies have been performed typically in low-risk indi­ Screening can be performed systematically, with an invitation issued to
viduals.633,1076,1117,1118 In an RCT of 5551 participants invited by a patient, or opportunistically, at the time of an ad hoc meeting with a
their health insurer, smartphone-based photoplethysmography in­ healthcare professional. Regardless of the mode of invitation, screening
creased the odds of OAC-treated new AF by 2.12 (95% CI,
should be part of a structured programme1128 and is not the same as
1.19–3.76; P = .01) compared with usual care.605 RCTs powered
identification of AF during a routine healthcare visit or secondary to ar­
for assessment of clinical outcomes are still lacking for consumer-
rhythmia symptoms.
based AF screening. Further head-to-head comparisons between
Screening can be done at a single timepoint (snapshot of the heart
novel digital devices and those commonly used in healthcare set­
rhythm), e.g. using pulse palpation or a 12-lead ECG. Screening can
tings are needed to establish their comparative effectiveness in
also be of an extended duration, i.e. prolonged, using either intermittent
the clinical setting and account for different populations and set­
or continuous monitoring of heart rhythm. Most studies using an oppor­
tings.1119 In a systematic review of smartphone-based photo­
tunistic strategy have screened for AF at a single timepoint with short
plethysmography compared with a reference ECG, unrealistically
duration (such as a single timepoint ECG), compared with systematic
high sensitivity and specificity were noted, likely due to small, low-
screening studies that have mainly used prolonged (repeated or continu­
quality studies with a high degree of patient selection bias.1120
Hence, when AF is suggested by a photoplethysmography device ous) rhythm assessment.1129 The optimal screening method will vary de­
or any other screening tool, a single-lead or continuous ECG tra­ pending on the population being studied (Figure 16) (see Supplementary
cing of >30 s or 12-lead ECG showing AF analysed by a physician data online, Additional Evidence Table S32). More sensitive methods will
with expertise in ECG rhythm interpretation is recommended to detect more AF but may lead to an increased risk of false positives and
establish a definitive diagnosis of AF.1091,1121–1125 an increased detection of low burden AF, whereas more specific meth­
The combination of big data and artificial intelligence (AI) is hav­ ods result in less false positives, at the risk of missing AF.
ing an increasing impact on the field of electrophysiology. Invasive monitoring of heart rhythm in high-risk populations ex­
Algorithms have been created to improve automated AF diagnosis tended for several years has been shown to result in device-detected
and several algorithms to aid diagnostics are being investigated.1046 AF prevalence of around 30%, albeit most of whom have a low burden
However, the clinical performance and broad applicability of these of AF.5,857,1130,1131 Pacemaker studies have shown that patients with a
solutions are not yet known. The use of AI may enable future low burden of device-detected subclinical AF have a lower risk of is­
treatment changes to be assessed with dynamic and continuous chaemic stroke.5,24,1131,1132 This has been confirmed in RCTs assessing
patient-directed monitoring using wearable devices.1126 There are DOAC use in patients with device-detected subclinical AF (see Section
still challenges in the field that need clarification, such as data acqui­ 6.1.1).5,281,282 The burden needed for device-detected subclinical AF to
sition, model performance, external validity, clinical implementation, translate into stroke risk is not known, and further studies are clearly
algorithm interpretation, and confidence, as well as the ethical needed.1133,1134 Benefit and cost-effectiveness of screening are dis­
aspects.1127 cussed in the Supplementary data online.
ESC Guidelines 61

Recommendation Table 31 — Recommendations for 10.3.1. Single timepoint screening ‘snapshot’

screening for AF (see also Evidence Table 31) Several cluster RCTs in primary care settings have explored whether
a b
screening performed as a snapshot of the heart rhythm at one time­
Recommendations Class Level
point can detect more AF compared with usual care in individuals
Review of an ECG (12-lead, single, or multiple leads) aged ≥65 years.1138–1140 No increased detection of AF was seen in
by a physician is recommended to provide a definite groups randomized to single timepoint screening.1138–1140 These find­
I B ings were confirmed in a meta-analysis of RCTs showing that screening
diagnosis of AF and commence appropriate
management.1091,1121–1123,1125 as a one-time event did not increase detection of AF compared with

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Routine heart rhythm assessment during healthcare
usual care.1135 Notably, these studies were performed in healthcare
settings where the detection of AF in the population might be high,
contact is recommended in all individuals aged ≥65 I C
hence the results might not be generalizable to healthcare settings
years for earlier detection of AF.
with a lower spontaneous AF detection. There are no RCTs addressing
Population-based screening for AF using a prolonged
clinical outcomes in patients with AF detected by single timepoint
non-invasive ECG-based approach should be
screening.1123,1135

© ESC 2024
considered in individuals aged ≥75 years, or ≥65 IIa B
years with additional CHA2DS2-VA risk factors to
10.3.2. Prolonged screening
ensure earlier detection of AF.6,1135–1137
Studies using prolonged screening have shown an increased detection
AF, atrial fibrillation; CHA2DS2-VA, congestive heart failure, hypertension, age ≥75 years of AF leading to initiation of OAC.1129,1135,1141 Two RCTs have inves­
(2 points), diabetes mellitus, prior stroke/transient ischaemic attack/arterial
tigated the effect on clinical outcomes in prolonged screening for AF.5,6
thromboembolism (2 points), vascular disease, age 65–74 years; ECG, electrocardiogram.
a
Class of recommendation. In the STROKESTOP trial (Systematic ECG Screening for Atrial
b
Level of evidence. Fibrillation Among 75 Year Old Subjects in the Region of Stockholm

Screening Population Setting for Type of Follow

approach example AF detection screening AF-CARE

Invasive or
After
thromboembolic
Patients with
embolic stroke of
Initiated after
non-invasive ECG
Prolonged
C
index event Comorbidity and risk
event unknown source monitoring
factor management
(Class I)

Patient
Any rhythm check,
A
informed Avoid stroke and
Age ≥65 years, At the time of confirmed by ECG
Ad-hoc to about thromboembolism
implications or risk of routine healthcare Routine heart
catch AF
thromboembolism contact
of AF
detection
rhythm assessment
(Class I) R
Reduce symptoms by
rate and rhythm control
Age ≥75 years, Population-based
In patients with
risk factors
or ≥65 years plus
other
Structured national
or regional
screening Non-invasive ECG
E
CHA2DS2-VA (Class IIa) Evaluation and
programmes
factors dynamic reassessment

Figure 16 Approaches to screening for AF. AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk factor management, [A] Avoid
stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; CHA2DS2-VA, congestive
heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, prior stroke/TIA/arterial thromboembolism (2 points), vascular disease, age 65–
74 years; ECG, electrocardiogram. See Figure 15 for non-invasive ECG methods.
62 ESC Guidelines

and Halland, Sweden), 75- and 76-year-olds were randomized to be in­

Comorbidities and risk Hypertension1149–1151
vited to prolonged screening for AF using single-lead ECGs twice daily
factors Heart failure178,1149–1151,1161
for 2 weeks, or to standard of care. After a median of 6.9 years there
was a small reduction in the primary combined endpoint of all-cause Valvular disease1149,1151,1162–1164
mortality, stroke, systematic embolism, and severe bleeding in favour Coronary artery disease1149,1151,1161,1165
of prolonged screening (HR, 0.96; 95% CI, 0.92–1.00; P = .045).6 In Peripheral arterial disease785
the LOOP (Atrial Fibrillation Detected by Continuous ECG Congenital heart disease1149,1166
Monitoring) trial, individuals at increased risk of stroke were rando­ Heart rate, heart rate variability1167,1168

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mized to receive an implantable loop recorder that monitored heart Total cholesterol1149,1150
rhythm for an average of 3.3 years, or to a control group receiving
Low-density lipoprotein cholesterol1150
standard of care. Although there was a higher detection of AF
High-density lipoprotein cholesterol1150
(31.8%) and subsequent initiation of OAC in the loop recorder
group compared with standard of care (12.2%), this was not accom­ Triglycerides1150
panied by a difference in the primary outcome of stroke or systemic Impaired glucose tolerance,1169–1172diabetes
embolism.5 In a meta-analysis of recent RCTs on the outcome of mellitus1149–1151,1169
stroke, a small but significant benefit was seen in favour of prolonged Renal dysfunction/CKD1149–1151,1173,1174
screening (RR, 0.91; 95% CI, 0.84–0.99).1136 This was not repeated Obesity1149–1151,1175,1176
in a second meta-analysis including older RCTs, where no risk reduc­ Body mass index, weight1149–1151
tion was seen with regard to mortality or stroke.1135 Notably, both
Height1150
these meta-analyses are likely underpowered to assess clinical
Sleep apnoea1149,1151,1177,1178
outcomes.
Chronic obstructive pulmonary disease1179
Subclinical Coronary artery calcification1149,1151,1180
atherosclerosis Carotid IMT and carotid plaque1149,1151,1181,1182
10.4. Factors associated with incident AF
ECG abnormalities PR interval prolongation1149,1151,1183
The most common risk predictors for incident (new-onset) AF are
Sick sinus syndrome1149,1184,1185
shown in Table 16. While the factors listed are robustly associated
with incident AF in observational studies, it is not known whether Wolff–Parkinson–White1149,1186
the relationships are causal. Studies using Mendelian randomization Genetic factors Family history of AF1149,1151,1187–1190
(genetic proxies for risk factors to estimate causal effects) robustly im­ AF-susceptible loci identified by
plicate systolic BP and higher BMI as causal risk factors for incident GWAS1149,1151,1191,1192
AF.1142 Short QT syndrome1149
A high degree of interaction occurs between all factors related to AF Genetic cardiomyopathies990,1193
development (see Supplementary data online, Additional Evidence
Biomarkers C-reactive protein1150,1151
Table S33).1038,1039,1143–1145 For ease of clinical application, risk predic­
Fibrinogen1150
tion tools have combined various factors, and have recently employed
machine learning algorithms for prediction.1146,1147 Classical risk scores Growth differentiation factor-151194
are also available with variable predictive ability and model performance Natriuretic peptides (atrial and B-type)1195–1200
(see Supplementary data online, Table S7).1148 Improved outcomes Cardiac troponins1199
when using these risk scores have yet to be demonstrated. Although Inflammatory biomarkers 1149,1151
knowledge is rapidly increasing about the genetic basis for AF in Others Thyroid dysfunction912,1149–1151
some patients, the value of genetic screening is limited at the present Autoimmune diseases1150
time (see Supplementary data online).
Air pollution1149,1201
Sepsis1149,1202 © ESC 2024

Psychological factors 1203,1204

Table 16 Factors associated with incident AF
AF, atrial fibrillation; CKD, chronic kidney disease; GWAS, genome-wide association
Demographic factors Age1149–1151 studies; HF, heart failure; IMT, intima-media thickness.
Male sex1149–1152
European ancestry1149,1150
Lower socioeconomic status1150
Lifestyle behaviours Smoking/tobacco use1149–1151 10.5. Primary prevention of AF
1149,1150
Alcohol intake Preventing the onset of AF before clinical manifestation has clear
Physical inactivity1149,1150 potential to improve the lives of the general population and reduce
Vigorous exercise1153–1156 the considerable health and social care costs associated with
development of AF. Whereas the [C] in AF-CARE is focused on the
Competitive or athlete-level endurance
effective management of risk factors and comorbidities to limit AF
sports1151,1157
recurrence and progression, there is also evidence they can be targeted
Caffeine1158–1160
to prevent AF. Available data are presented below for hypertension,
Continued heart failure, type 2 diabetes mellitus, obesity, sleep apnoea syndrome,
ESC Guidelines 63

physical activity, and alcohol, although many other risk markers can incident AF, several meta-analyses have demonstrated that there is
also be targeted. Further information on each factor’s attributable an 18%–37% reduction in incident AF.136,1210,1211,1237 However, treat­
risk for AF is provided in the Supplementary data online (see ment of HFrEF with sacubitril/valsartan has not yet been shown to con­
Supplementary data online, Evidence Table 32 and additional Evidence fer any adjunctive benefit in reducing new-onset AF when compared
Tables S34–S39). with ACE inhibitors/ARBs alone.1238 There is some evidence to suggest
that effective CRT in eligible patients with HFrEF reduces the risk of in­
cident AF.1239 To date, no treatments in HFpEF have been shown to
Recommendation Table 32 — Recommendations for reduce incident AF.
primary prevention of AF (see also Evidence Table 32)

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Recommendation Classa Levelb 10.5.3. Type 2 diabetes mellitus
The integrated care of type 2 diabetes, based on lifestyle and pharma­
Maintaining optimal blood pressure is recommended
cological treatments for comorbidities such as obesity, hypertension,
in the general population to prevent AF, with ACE I B
and dyslipidaemia, are useful steps in preventing atrial remodelling
inhibitors or ARBs as first-line therapy.1205–1207
and subsequent AF. Intensive glucose-lowering therapy targeting an
Appropriate medical HF therapy is recommended in HbA1c level of <6.0% (<42 mmol/mol) failed to show a protective ef­
I B
individuals with HFrEF to prevent AF.133,136,1208–1211 fect on incident AF.1240 More than glycaemic control per se, the class of
Maintaining normal weight (BMI 20–25 kg/m2) is glucose-lowering agent may influence the risk of AF.1240 Insulin pro­
recommended for the general population to prevent I B motes adipogenesis and cardiac fibrosis, and sulfonylureas have been
AF.208,1212,1213 consistently associated with an increased risk of AF.193 Observational
Maintaining an active lifestyle is recommended to studies have associated metformin with lower rates of incident
prevent AF, with the equivalent of 150–300 min AF.1224,1225,1241–1243 Various recent studies and meta-analyses point
per week of moderate intensity or 75–150 min per I B to the positive role of SGLT2 inhibitors to reduce the risk of incident
week of vigorous intensity aerobic physical AF in diabetic and non-diabetic patients.136,1226,1244–1246 Pooled
activity.1214–1219 data from 22 trials including 52 951 patients with type 2 diabetes and
heart failure showed that SGLT2 inhibitors compared with placebo
Avoidance of binge drinking and alcohol excess is
can significantly reduce the incidence of AF by 18% in studies on dia­
recommended in the general population to prevent I B
betes, and up to 37% in heart failure with or without type 2
AF.1220–1223
diabetes.1210,1211
Metformin or SGLT2 inhibitors should be considered
for individuals needing pharmacological management IIa B
10.5.4. Obesity
© ESC 2024

of diabetes mellitus to prevent AF.1210,1211,1224–1226

Weight reduction should be considered in obese Management of weight is important in the prevention of AF. In a large
IIa B population-based cohort study, normal weight was associated with a
individuals to prevent AF.1212,1227–1231
reduced risk of incident AF compared with those who were obese
ACE, angiotensin-converting enzyme; AF, atrial fibrillation; ARB, angiotensin receptor (4.7% increase in the risk of incident AF for each 1 kg/m2 increase of
blocker; BMI, body mass index; HF, heart failure; HFrEF, heart failure with reduced
BMI).208 In the Women’s Health Study, participants who became obese
ejection fraction; SGLT2, sodium-glucose cotransporter-2.
a
Class of recommendation. had a 41% increased risk of incident AF compared with those who
b
Level of evidence. maintained their BMI <30 kg/m2.1212 Similarly, observational studies
in populations using bariatric surgery for weight loss in morbidly obese
individuals (BMI ≥40 kg/m2) have observed a lower risk of incident
AF.1227–1231
10.5.1. Hypertension
Management of hypertension has been associated with a reduction in
incident AF.1205–1207,1232 In the LIFE (Losartan Intervention for End 10.5.5. Sleep apnoea syndrome
point reduction in hypertension) trial, a 10 mmHg reduction in systolic Although it would seem rational to optimize sleep habits, to date there
BP was associated with a 17% reduction in incident AF.1207 Secondary is no conclusive evidence to support this for the primary prevention of
analysis of RCTs and observational studies suggest that ACE inhibitors AF. The SAVE (Sleep Apnea cardioVascular Endpoints) trial failed to
or ARBs may be superior to beta-blockers, calcium channel blockers, or demonstrate a difference in clinical outcomes in those randomized to
diuretics for the prevention of incident AF.1233–1236 CPAP therapy or placebo.230 There was no difference in incident AF,
albeit the analysis of AF was not based on systematic screening but ra­
10.5.2. Heart failure ther on clinically documented AF.
Long-standing established pharmacological treatments for HFrEF have
been associated with a reduction in incident AF. The use of ACE inhi­ 10.5.6. Physical activity
bitors or ARBs in patients with known HFrEF was associated with a Several studies have demonstrated beneficial effects of moderate phys­
44% reduction in incidence of AF.1208 Similarly, beta-blockers in ical activity on cardiovascular health.1247 Moderate aerobic exercise
HFrEF led to a 33% reduction in the odds of incident AF.133 may also reduce the risk of new-onset AF.1214–1219 It should be noted
Mineralocorticoid receptor antagonists have also been shown to re­ that the incidence of AF appears to be increased among athletes, with a
duce the risk of new-onset AF by 42% in patients with HFrEF.1209 meta-analysis of observational studies showing a 2.5-fold increased risk
Although there have been variable effects of SGLT2 inhibitors on of AF compared with non-athlete controls.1248
64 ESC Guidelines

10.5.7. Alcohol intake (16) Rate control therapy: use beta-blockers (any ejection fraction), di­
The premise that reducing alcohol intake can prevent AF is based on goxin (any ejection fraction), or diltiazem/verapamil (LVEF >40%)
observational studies linking alcohol to an excess risk of incident AF as initial therapy in the acute setting, an adjunct to rhythm control
in a dose-dependent manner (see Supplementary data online).1220–1222 therapies, or as a sole treatment strategy to control heart rate and
In addition, a population cohort study of those with high alcohol con­ symptoms.
sumption (>60 g/day for men and >40 g/day for women) found that ab­ (17) Rhythm control: consider in all suitable AF patients, explicitly dis­
stinence from alcohol was associated with a lower incidence of AF cussing with patients all potential benefits and risks of cardiover­
compared with patients who continued heavy drinking.1223 sion, antiarrhythmic drugs, and catheter or surgical ablation to

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reduce symptoms and morbidity.
(18) Safety first: keep safety and anticoagulation in mind when consid­
11. Key messages ering rhythm control; e.g. delay cardioversion and provide at least
3 weeks of anticoagulation beforehand if AF duration >24 h, and
(1) General management: optimal treatment according to the consider toxicity and drug interactions for antiarrhythmic
AF-CARE pathway, which includes: [C] Comorbidity and risk fac­ therapy.
tor management; [A] Avoid stroke and thromboembolism; [R] (19) Cardioversion: use electrical cardioversion in cases of haemo­
Reduce symptoms by rate and rhythm control; and [E] dynamic instability; otherwise choose electrical or pharmacologic­
Evaluation and dynamic reassessment. al cardioversion based on patient characteristics and preferences.
(2) Shared care: patient-centred AF management with joint decision- (20) Indication for long-term rhythm control: the primary indication
making and a multidisciplinary team. should be reduction in AF-related symptoms and improvement
(3) Equal care: avoid health inequalities based on gender, ethnicity, in quality of life; for selected patient groups, sinus rhythm main­
disability, and socioeconomic factors. tenance can be pursued to reduce morbidity and mortality.
(4) Education: for patients, family members, caregivers, and health­ (21) Success or failure of rhythm control: continue anticoagulation ac­
care professionals to aid shared decision-making. cording to the patient’s individual risk of thromboembolism, irre­
(5) Diagnosis: clinical AF requires confirmation on an ECG device to spective of whether they are in AF or sinus rhythm.
initiate risk stratification and AF management. (22) Catheter ablation: consider as second-line option if antiarrhyth­
(6) Initial evaluation: medical history, assessment of symptoms and mic drugs fail to control AF, or first-line option in patients with
their impact, blood tests, echocardiography/other imaging, paroxysmal AF.
patient-reported outcome measures, and risk factors for (23) Endoscopic or hybrid ablation: consider if catheter ablation fails,
thromboembolism and bleeding. or an alternative to catheter ablation in persistent AF despite anti­
(7) Comorbidities and risk factors: thorough evaluation and manage­ arrhythmic drugs.
ment critical to all aspects of care for patients with AF to avoid (24) Atrial fibrillation ablation during cardiac surgery: perform in cen­
recurrence and progression of AF, improve success of AF treat­ tres with experienced teams, especially for patients undergoing
ments, and prevent AF-related adverse outcomes. mitral valve surgery.
(8) Focus on conditions associated with AF: including hypertension, (25) Dynamic evaluation: periodically reassess therapy and give atten­
heart failure, diabetes mellitus, obesity, obstructive sleep apnoea, tion to new modifiable risk factors that could slow/reverse the
physical inactivity, and high alcohol intake. progression of AF, increase quality of life, and prevent adverse
(9) Assessing the risk of thromboembolism: use locally validated risk outcomes.
tools or the CHA2DS2-VA score and assessment of other risk fac­
tors, with reassessment at periodic intervals to assist in decisions
on anticoagulant prescription. 12. Gaps in evidence
(10) Oral anticoagulants: recommended for all eligible patients, except
those at low risk of incident stroke or thromboembolism The following bullet list gives the most important gaps in evidence
(CHA2DS2-VA = 1 anticoagulation should be considered; where new clinical trials could substantially aid the patient pathway:
CHA2DS2-VA ≥2 anticoagulation recommended). Definition and clinical impact of AF
(11) Choice of anticoagulant: DOACs (apixaban, dabigatran, edoxa­
ban, and rivaroxaban) are preferred over VKAs (warfarin and • Paroxysmal AF is not one entity, and patterns of AF progression and
others), except in patients with mechanical heart valves and mitral regression are highly variable. It is uncertain what the relevance is for
stenosis. treatment strategies and management decisions.
(12) Dose/range of anticoagulant: use full standard doses for DOACs • Thirty seconds as definition for clinical AF needs validation and evalu­
unless the patient meets specific dose-reduction criteria; for ation whether it is related to AF-related outcomes.
VKAs, keep INR generally 2.0–3.0, and in range for >70% of the • Definition, clinical features, diagnosis, and implementation for treat­
time. ment choices of atrial cardiomyopathy in patients with AF is
(13) Switching anticoagulants: switch from a VKA to DOAC if risk of unsettled.
intracranial haemorrhage or poor control of INR levels. • Diversity in AF presentation, underlying pathophysiological mechan­
(14) Bleeding risk: modifiable bleeding risk factors should be managed isms, and associated comorbidities is incompletely understood with
to improve safety; bleeding risk scores should not be used to de­ regard to differences in sex, gender, race/ethnicity, socioeconomic
cide on starting or withdrawing anticoagulants. state, education, and differences between low-, moderate-, and high-
(15) Antiplatelet therapy: avoid combining anticoagulants and antipla­ income countries.
telet agents, unless the patient has an acute vascular event or • Personalized risk prediction for AF incidence, AF progression, and as­
needs interim treatment for procedures. sociated outcomes remains challenging.
ESC Guidelines 65

• Insights into psychosocial and environmental factors and risk of AF • The amount of AF reduction obtained by rhythm control to improve
and adverse outcomes in AF are understudied. outcomes is unknown.
• Large catheter ablation studies showed no improved outcome of
Patient-centred, multidisciplinary AF management patients with AF. Some small studies in specific subpopulations
• The benefit of additional education directed to patients, to family have observed an improved outcome. This warrants further inves­
members, and to healthcare professionals in order to optimize tigation to provide each patient with AF with personalized treat­
shared decision-making still needs to be proved. ment goals.
• Access to patient-centred management according to the AF-CARE • Uncertainty exists on the time of duration of AF and risk of stroke

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principles to ensure equality in healthcare provision and improve out­ when performing a cardioversion.
comes warrants evidence. • The value of diagnostic cardioversion for persistent AF in steering
• The place of remote monitoring and telemedicine for identification management of AF is unknown.
and follow-up of patients with AF, or its subgroups is non-established, • Decisions on continuation of OAC are completely based on stroke
though widely applied. risk scores and irrespective of having (episodes) of AF; whether
this holds for patients undergoing successful catheter ablation is
uncertain.
[C] Comorbidity and risk factor management • Large variability in ablation strategies and techniques exist for pa­
tients with persistent AF, or after first failed catheter ablation for par­
• Methods to achieve consistent and reproducible weight loss in pa­ oxysmal AF. The optimal catheter ablation strategy and techniques,
tients with AF requires substantial improvement. Despite some evi­ however, are unknown.
dence demonstrating the benefits of weight loss, widespread • Sham-controlled intervention studies are lacking to determine the ef­
adoption has been limited by the need for reproducible strategies. fects on AF symptoms, quality of life, and PROMS, accounting for the
• The importance of sleep apnoea syndrome and its treatment on placebo effect that is associated with interventions.
AF-related outcomes remains to be elucidated.

[A] Avoid stroke and thromboembolism The AF-CARE pathway in specific clinical settings

• Data are lacking on how to treat patients with low risk of stroke (with • The optimal duration of triple therapy in patients with AF at high risk
a CHA2DS2-VA score of 0 or 1), as these patients were excluded of recurrent coronary events after acute coronary syndrome is
from large RCTs. unclear.
• Not enough evidence is available for OAC in elderly patients, frail • The role of the coronary vessel involved and whether this should im­
polypharmacy patients, those with cognitive impairment/dementia, pact on the duration of combined OAC and antiplatelet treatment
recent bleeding, previous ICH, severe end-stage renal failure, liver im­ needs further study.
pairment, cancer, or severe obesity. • The role of antiplatelet therapy in patients with AF and peripheral ar­
• In elderly patients, routinely switching VKAs to DOACs is associated tery disease on OAC is uncertain.
with increased bleeding risk; however, the reasons why this happens • The use of DOACs in patients with congenital heart disease, particu­
are unclear. larly in patients with complex corrected congenital defects, is poorly
• The selection of which patients with asymptomatic device-detected studied.
subclinical AF benefit from OAC therapy needs to be defined. • Improved risk stratification for stroke in patients with AF and cancer,
• There is a lack of evidence whether and when to (re)start anticoagu­ or with post-operative or trigger-induced AF is needed to inform on
lation after intracranial haemorrhage. OAC treatment decisions.
• There is lack of evidence about optimal anticoagulation in patients
with ischaemic stroke or left atrial thrombus while being treated Screening and prevention of AF
with OAC.
• There are a lack of adequately powered randomized controlled stud­
• There is uncertainty about the place of LAA closure and how to man­
ies on ischaemic stroke rate in patients screened for AF, both in the
age antithrombotic post-procedural management when LAAO is
primary prevention setting and in secondary prevention (post-
performed.
stroke), and its cost-effectiveness.
• Balance of thromboembolism and bleeding is unclear in patients with
• Population selection that might benefit the most from screening, the
AF and incidental cerebral artery aneurysms identified on brain MRI.
optimal duration of screening, and the burden of AF that might in­
crease the risk for patients with screening-detected AF are uncertain.
[R] Reduce symptoms by rate and rhythm control
• Evaluation of strategies to support longer-term use of technologies
• In some patients, AF can be benign in terms of symptoms and out­ for AF detection are awaited.
comes. In which patients rhythm control is not needed warrants • The role of photoplethysmography technology for AF screening in an
investigation. effort to assess AF burden and reduce stroke is still unclear.
• Application of antiarrhythmic drugs has been hampered by poor ef­ • How new consumer devices and wearable technology can be used
fectiveness and side effects; however, new antiarrhythmic drugs are for diagnostic and monitoring purposes in routine clinical practice
needed to increase the therapeutic arsenal for AF patients. needs to be clarified.
66 ESC Guidelines

13. ‘What to do’ and ‘What not to do’ messages from the guidelines
Table 17 lists all Class I and Class III recommendations from the text alongside their level of evidence.

Table 17 ‘What to do’ and ‘what not to do’

Recommendations Classa Levelb

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Recommendations for the diagnosis of AF
Confirmation by an electrocardiogram (12-lead, multiple, or single leads) is recommended to establish the diagnosis of clinical AF and
I A
commence risk stratification and treatment.
Recommendations for symptom evaluation in patients with AF
Evaluating the impact of AF-related symptoms is recommended before and after major changes in treatment to inform shared
I B
decision-making and guide treatment choices.
Recommendations for diagnostic evaluation in patients with new AF
A transthoracic echocardiogram is recommended in patients with an AF diagnosis where this will guide treatment decisions. I C
Recommendations for patient-centred care and education
Education directed to patients, family members, caregivers, and healthcare professionals is recommended to optimize shared
I C
decision-making, facilitating open discussion of both the benefit and risk associated with each treatment option.
Access to patient-centred management according to the AF-CARE principles is recommended in all patients with AF, regardless of gender,
I C
ethnicity, and socioeconomic status, to ensure equality in healthcare provision and improve outcomes.
Recommendations for comorbidity and risk factor management in AF
Identification and management of risk factors and comorbidities is recommended as an integral part of AF care. I B
Blood pressure lowering treatment is recommended in patients with AF and hypertension to reduce recurrence and progression of AF and
I B
prevent adverse cardiovascular events.
Diuretics are recommended in patients with AF, HF, and congestion to alleviate symptoms and facilitate better AF management. I C
Appropriate medical therapy for HF is recommended in AF patients with HF and impaired LVEF to reduce symptoms and/or HF
I B
hospitalization and prevent AF recurrence.
Sodium-glucose cotransporter-2 inhibitors are recommended for patients with HF and AF regardless of left ventricular ejection fraction to
I A
reduce the risk of HF hospitalization and cardiovascular death.
Effective glycaemic control is recommended as part of comprehensive risk factor management in individuals with diabetes mellitus and AF,
I C
to reduce burden, recurrence, and progression of AF.
Weight loss is recommended as part of comprehensive risk factor management in overweight and obese individuals with AF to reduce
I B
symptoms and AF burden, with a target of 10% or more reduction in body weight.
A tailored exercise programme is recommended in individuals with paroxysmal or persistent AF to improve cardiorespiratory fitness and
I B
reduce AF recurrence.
Reducing alcohol consumption to ≤3 standard drinks (≤30 grams of alcohol) per week is recommended as part of comprehensive risk
I B
factor management to reduce AF recurrence.
When screening for obstructive sleep apnoea in individuals with AF, using only symptom-based questionnaires is not recommended. III B
Recommendations to assess and manage thromboembolic risk in AF
Oral anticoagulation is recommended in patients with clinical AF at elevated thromboembolic risk to prevent ischaemic stroke and
I A
thromboembolism.
A CHA2DS2-VA score of 2 or more is recommended as an indicator of elevated thromboembolic risk for decisions on initiating oral
I C
anticoagulation.
Oral anticoagulation is recommended in all patients with AF and hypertrophic cardiomyopathy or cardiac amyloidosis, regardless of
I B
CHA2DS2-VA score, to prevent ischaemic stroke and thromboembolism.
Individualized reassessment of thromboembolic risk is recommended at periodic intervals in patients with AF to ensure anticoagulation is
I B
started in appropriate patients.
Antiplatelet therapy is not recommended as an alternative to anticoagulation in patients with AF to prevent ischaemic stroke and
III A
thromboembolism.
Using the temporal pattern of clinical AF (paroxysmal, persistent, or permanent) is not recommended to determine the need for oral
III B
anticoagulation.
Continued
ESC Guidelines 67

Recommendations for oral anticoagulation in AF

Direct oral anticoagulants are recommended in preference to VKAs to prevent ischaemic stroke and thromboembolism, except in patients
I A
with mechanical heart valves or moderate-to-severe mitral stenosis.
A target INR of 2.0–3.0 is recommended for patients with AF prescribed a VKA for stroke prevention to ensure safety and effectiveness. I B
Switching to a DOAC is recommended for eligible patients that have failed to maintain an adequate time in therapeutic range on a VKA
I B
(TTR <70%) to prevent thromboembolism and intracranial haemorrhage.
A reduced dose of DOAC therapy is not recommended, unless patients meet DOAC-specific criteria, to prevent underdosing and
III B

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avoidable thromboembolic events.
Recommendations for combining antiplatelet drugs with anticoagulants for stroke prevention
Adding antiplatelet treatment to oral anticoagulation is not recommended in AF patients for the goal of preventing ischaemic stroke or
III B
thromboembolism.
Recommendations for thromboembolism despite anticoagulation
Adding antiplatelet treatment to anticoagulation is not recommended in patients with AF to prevent recurrent embolic stroke. III B
Switching from one DOAC to another, or from a DOAC to a VKA, without a clear indication is not recommended in patients with AF to
III B
prevent recurrent embolic stroke.
Recommendations for surgical left atrial appendage occlusion
Surgical closure of the left atrial appendage is recommended as an adjunct to oral anticoagulation in patients with AF undergoing cardiac
I B
surgery to prevent ischaemic stroke and thromboembolism.
Recommendations for assessment of bleeding risk
Assessment and management of modifiable bleeding risk factors is recommended in all patients eligible for oral anticoagulation, as part of
I B
shared decision-making to ensure safety and prevent bleeding.
Use of bleeding risk scores to decide on starting or withdrawing oral anticoagulation is not recommended in patients with AF to avoid
III B
under-use of anticoagulation.
Recommendations for management of bleeding in anticoagulated patients
Interrupting anticoagulation and performing diagnostic or treatment interventions is recommended in AF patients with active bleeding until
I C
the cause of bleeding is identified and resolved.
Recommendations for heart rate control in patients with AF
Rate control therapy is recommended in patients with AF, as initial therapy in the acute setting, an adjunct to rhythm control therapies, or as
I B
a sole treatment strategy to control heart rate and reduce symptoms.
Beta-blockers, diltiazem, verapamil, or digoxin are recommended as first-choice drugs in patients with AF and LVEF >40% to control heart
I B
rate and reduce symptoms.
Beta-blockers and/or digoxin are recommended in patients with AF and LVEF ≤40% to control heart rate and reduce symptoms. I B
Recommendations for general concepts in rhythm control
Electrical cardioversion is recommended in AF patients with acute or worsening haemodynamic instability to improve immediate patient
I C
outcomes.
Direct oral anticoagulants are recommended in preference to VKAs in eligible patients with AF undergoing cardioversion for
I A
thromboembolic risk reduction.
Therapeutic oral anticoagulation for at least 3 weeks (adherence to DOACs or INR ≥2.0 for VKAs) is recommended before scheduled
I B
cardioversion of AF and atrial flutter to prevent procedure-related thromboembolism.
Transoesophageal echocardiography is recommended if 3 weeks of therapeutic oral anticoagulation has not been provided, for exclusion of
I B
cardiac thrombus to enable early cardioversion.
Oral anticoagulation is recommended to continue for at least 4 weeks in all patients after cardioversion and long-term in patients with
I B
thromboembolic risk factor(s) irrespective of whether sinus rhythm is achieved, to prevent thromboembolism.
Early cardioversion is not recommended without appropriate anticoagulation or transoesophageal echocardiography if AF duration is
III C
longer than 24 h, or there is scope to wait for spontaneous cardioversion.
Recommendations for pharmacological cardioversion of AF
Intravenous flecainide or propafenone is recommended when pharmacological cardioversion of recent-onset AF is desired, excluding
I A
patients with severe left ventricular hypertrophy, HFrEF, or coronary artery disease.
Intravenous vernakalant is recommended when pharmacological cardioversion of recent-onset AF is desired, excluding patients with recent
I A
ACS, HFrEF, or severe aortic stenosis.
Intravenous amiodarone is recommended when cardioversion of AF in patients with severe left ventricular hypertrophy, HFrEF, or
I A
coronary artery disease is desired, accepting there may be a delay in cardioversion.
Pharmacological cardioversion is not recommended for patients with sinus node dysfunction, atrioventricular conduction disturbances, or
III C
prolonged QTc (>500 ms), unless risks for proarrhythmia and bradycardia have been considered.
Continued
68 ESC Guidelines

Recommendations for antiarrhythmic drugs for long-term maintenance of sinus rhythm

Amiodarone is recommended in patients with AF and HFrEF requiring long-term antiarrhythmic drug therapy to prevent recurrence and
I A
progression of AF, with careful consideration and monitoring for extracardiac toxicity.
Dronedarone is recommended in patients with AF requiring long-term rhythm control, including those with HFmrEF, HFpEF, ischaemic
I A
heart disease, or valvular disease to prevent recurrence and progression of AF.
Flecainide or propafenone is recommended in patients with AF requiring long-term rhythm control to prevent recurrence and progression
I A
of AF, excluding those with impaired left ventricular systolic function, severe left ventricular hypertrophy, or coronary artery disease.

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Antiarrhythmic drug therapy is not recommended in patients with advanced conduction disturbances unless antibradycardia pacing is
III C
provided.
Recommendations for catheter ablation of AF
Shared decision-making
Shared decision-making is recommended when considering catheter ablation for AF, taking into account procedural risks, likely benefits, and
I C
risk factors for AF recurrence.
Atrial fibrillation patients resistant or intolerant to antiarrhythmic drug therapy
Catheter ablation is recommended in patients with paroxysmal or persistent AF resistant or intolerant to antiarrhythmic drug therapy to
I A
reduce symptoms, recurrence, and progression of AF.
First-line rhythm control therapy
Catheter ablation is recommended as a first-line option within a shared decision-making rhythm control strategy in patients with
I A
paroxysmal AF, to reduce symptoms, recurrence, and progression of AF.
Patients with heart failure
Atrial fibrillation catheter ablation is recommended in patients with AF and HFrEF with high probability of tachycardia-induced
I B
cardiomyopathy to reverse left ventricular dysfunction.
Recommendations for anticoagulation in patients undergoing catheter ablation
Initiation of oral anticoagulation is recommended at least 3 weeks prior to catheter-based ablation in AF patients at elevated
I C
thromboembolic risk, to prevent peri-procedural ischaemic stroke and thromboembolism.
Uninterrupted oral anticoagulation is recommended in patients undergoing AF catheter ablation to prevent peri-procedural ischaemic
I A
stroke and thromboembolism.
Continuation of oral anticoagulation is recommended for at least 2 months after AF ablation in all patients, irrespective of rhythm outcome
I C
or CHA2DS2-VA score, to reduce the risk of peri-procedural ischaemic stroke and thromboembolism.
Continuation of oral anticoagulation is recommended after AF ablation according to the patient’s CHA2DS2-VA score, and not the
I C
perceived success of the ablation procedure, to prevent ischaemic stroke and thromboembolism.
Recommendations for endoscopic and hybrid AF ablation
Continuation of oral anticoagulation is recommended in patients with AF at elevated thromboembolic risk after concomitant, endoscopic,
I C
or hybrid AF ablation, independent of rhythm outcome or LAA exclusion, to prevent ischaemic stroke and thromboembolism.
Recommendations for AF ablation during cardiac surgery
Concomitant surgical ablation is recommended in patients undergoing mitral valve surgery and AF suitable for a rhythm control strategy to
prevent symptoms and recurrence of AF, with shared decision-making supported by an experienced team of electrophysiologists and I A
arrhythmia surgeons.
Intraprocedural imaging for detection of left atrial thrombus in patients undergoing surgical ablation is recommended to guide surgical
I C
strategy, independent of oral anticoagulant use, to prevent peri-procedural ischaemic stroke and thromboembolism.
Recommendations for patients with acute coronary syndromes or undergoing percutaneous intervention
General recommendations for patients with AF and an indication for concomitant antiplatelet therapy
For combinations with antiplatelet therapy, a DOAC is recommended in eligible patients in preference to a VKA to mitigate bleeding risk
I A
and prevent thromboembolism.
Recommendations for AF patients with ACS
Early cessation (≤1 week) of aspirin and continuation of an oral anticoagulant (preferably DOAC) with a P2Y12 inhibitor (preferably
clopidogrel) for up to 12 months is recommended in AF patients with ACS undergoing an uncomplicated PCI to avoid major bleeding, if the I A
risk of thrombosis is low or bleeding risk is high.
Recommendations for AF patients undergoing PCI
After uncomplicated PCI, early cessation (≤1 week) of aspirin and continuation of an oral anticoagulant and a P2Y12 inhibitor (preferably
I A
clopidogrel) for up to 6 months is recommended to avoid major bleeding, if ischaemic risk is low.
Continued
ESC Guidelines 69

Recommendations for AF patients with chronic coronary or vascular disease

Antiplatelet therapy beyond 12 months is not recommended in stable patients with chronic coronary or vascular disease treated with oral
III B
anticoagulation, due to lack of efficacy and to avoid major bleeding.
Recommendations for management of post-operative AF
Peri-operative amiodarone therapy is recommended where drug therapy is desired to prevent post-operative AF after cardiac surgery. I A
Routine use of beta-blockers is not recommended in patients undergoing non-cardiac surgery for the prevention of post-operative AF. III B
Recommendations for patients with embolic stroke of unknown source

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Prolonged monitoring for AF is recommended in patients with ESUS to inform on AF treatment decisions. I B
Initiation of oral anticoagulation in ESUS patients without documented AF is not recommended due to lack of efficacy in preventing
III A
ischaemic stroke and thromboembolism.
Recommendations for patients with AF during pregnancy
Immediate electrical cardioversion is recommended in patients with AF during pregnancy and haemodynamic instability or pre-excited AF
I C
to improve maternal and foetal outcomes.
Therapeutic anticoagulation with LMWHs or VKAs (except VKAs for the first trimester or beyond Week 36) is recommended for pregnant
I C
patients with AF at elevated thromboembolic risk to prevent ischaemic stroke and thromboembolism.
Beta-1 selective blockers are recommended for heart rate control of AF in pregnancy to reduce symptoms and improve maternal and foetal
I C
outcomes, excluding atenolol.
Recommendations for prevention of thromboembolism in atrial flutter
Oral anticoagulation is recommended in patients with atrial flutter at elevated thromboembolic risk to prevent ischaemic stroke and
I B
thromboembolism.
Recommendations for screening for AF
Review of an ECG (12-lead, single, or multiple leads) by a physician is recommended to provide a definite diagnosis of AF and commence
I B
appropriate management.
Routine heart rhythm assessment during healthcare contact is recommended in all individuals aged ≥65 years for earlier detection of AF. I C
Recommendations for primary prevention of AF
Maintaining optimal blood pressure is recommended in the general population to prevent AF, with ACE inhibitors or ARBs as first-line
I B
therapy.
Appropriate medical HF therapy is recommended in individuals with HFrEF to prevent AF. I B
2
Maintaining normal weight (BMI 20–25 kg/m ) is recommended for the general population to prevent AF. I B

© ESC 2024
Maintaining an active lifestyle is recommended to prevent AF, with the equivalent of 150–300 min per week of moderate intensity or 75–
I B
150 min per week of vigorous intensity aerobic physical activity.
Avoidance of binge drinking and alcohol excess is recommended in the general population to prevent AF. I B

AAD, antiarrhythmic drugs; ACEi, angiotensin-converting enzyme inhibitor; ACS, acute coronary syndromes; AF, atrial fibrillation; AF-CARE, atrial fibrillation—[C] Comorbidity and risk
factor management, [A] Avoid stroke and thromboembolism, [R] Reduce symptoms by rate and rhythm control, [E] Evaluation and dynamic reassessment; AFL, atrial flutter; ARB,
angiotensin receptor blocker; BMI, body mass index; CHA2DS2-VA, congestive heart failure, hypertension, age ≥75 years (2 points), diabetes mellitus, prior stroke/transient ischaemic
attack/arterial thromboembolism (2 points), vascular disease, age 65–74 years; DOAC, direct oral anticoagulant; ECG, electrocardiogram; ESUS, embolic stroke of undetermined source;
HF, heart failure; HFmrEF, heart failure with mildly reduced ejection fraction; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction;
INR, international normalized ratio of prothrombin time; LAA, left atrial appendage; LMWH, low molecular weight heparin; LVEF, left ventricular ejection fraction; PCI, percutaneous
intervention; SGLT2, sodium-glucose cotransporter-2; TTR, time in therapeutic range; VKA, vitamin K antagonist.
a
Class of recommendation.
b
Level of evidence.

14. Evidence tables Medical Center Groningen, Groningen, Netherlands; Karina

V. Bunting, Institute of Cardiovascular Sciences, University of
Evidence tables are available at European Heart Journal online. Birmingham, Birmingham, United Kingdom, Cardiology Department,
Queen Elizabeth Hospital, University Hospitals Birmingham NHS
Foundation Trust, Birmingham, United Kingdom; Ruben
15. Data availability statement Casado-Arroyo, Department of Cardiology, H.U.B.-Hôpital
No new data were generated or analysed in support of this research. Erasme, Université Libre de Bruxelles, Brussels, Belgium; Valeria
Caso, Stroke Unit, Santa della Misericordia Hospital, Perugia, Italy;
Harry J.G.M. Crijns, Cardiology Maastricht University Medical
16. Author information Centre, Maastricht, Netherlands, Cardiology Cardiovascular Research
Author/Task Force Member Affiliations: Michiel Rienstra, Institute Maastricht, Maastricht University, Maastricht, Netherlands;
Department of Cardiology, University of Groningen, University Tom J. R. De Potter, Department of Cardiology, OLV Hospital,
70 ESC Guidelines

Aalst, Belgium; Jeremy Dwight (United Kingdom), ESC Patient (France), Bruna Gigante (Sweden), Michael Glikson (Israel), Ziad
Forum, Sophia Antipolis, France; Luigina Guasti, Department of Hijazi (Sweden), Gerhard Hindricks (Germany), Daniela Husser
Medicine and Surgery, University of Insubria, Varese, Italy, Division of (Germany), Borja Ibanez (Spain), Stefan James (Sweden), Stefan Kaab
Geriatrics and Clinical Gerontology, ASST-Settelaghi, Varese, Italy; (Germany), Paulus Kirchhof (Germany), Lars Køber (Denmark),
Thorsten Hanke, Clinic For Cardiac Surgery, Asklepios Klinikum, Konstantinos C. Koskinas (Switzerland), Thomas Kumler (Denmark),
Harburg, Hamburg, Germany; Tiny Jaarsma, Department of Gregory Y.H. Lip (United Kingdom), John Mandrola (United States of
Cardiology, Linkoping University, Linkoping, Sweden, Julius Center America), Nikolaus Marx (Germany), John William Mcevoy (Ireland),
for Health Sciences and Primary Care, University Medical Center Borislava Mihaylova (United Kingdom), Richard Mindham (United

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Utrecht, Utrecht, Netherlands; Maddalena Lettino, Department Kingdom), Denisa Muraru (Italy), Lis Neubeck (United Kingdom), Jens
for Cardiac, Thoracic and Vascular Diseases, Fondazione IRCCS San Cosedis Nielsen (Denmark), Jonas Oldgren (Sweden), Maurizio
Gerardo dei Tintori, Monza, Italy; Maja-Lisa Løchen, Deparment Paciaroni (Italy), Agnes A. Pasquet (Belgium), Eva Prescott
of Clincal Medicine UiT, The Arctic University of Norway, Tromsø, (Denmark), Filip Rega (Belgium), Francisco Javier Rossello (Spain),
Norway, Department of Cardiology, University Hospital of North Marcin Rucinski (Poland), Sacha P. Salzberg (Switzerland), Sam
Norway, Tromsø, Norway; R. Thomas Lumbers, Institute of Schulman (Canada), Philipp Sommer (Germany), Jesper Hastrup
Health Informatics, University College London, London, United Svendsen (Denmark), Jurrien M. ten Berg (Netherlands), Hugo Ten
Kingdom, Saint Bartholomew’s Hospital, Barts Health NHS Trust, Cate (Netherlands), Ilonca Vaartjes (Netherlands), Christiaan Jm.
London, United Kingdom, University College Hospital, University Vrints (Belgium), Adam Witkowski (Poland), and Katja Zeppenfeld
College London Hospitals NHS Trust, London, United Kingdom; (Netherlands).
Bart Maesen, Department of Cardiothoracic Surgery, Maastricht ESC National Cardiac Societies actively involved in the review
University Medical Centre+, Maastricht, Netherlands, Cardiovascular process of the 2024 ESC Guidelines for the management of atrial
Research Institute Maastricht, Maastricht University, Maastricht, fibrillation:
Netherlands; Inge Mølgaard (Denmark), ESC Patient Forum, Albania: Albanian Society of Cardiology, Leonard Simoni; Algeria:
Sophia Antipolis, France; Giuseppe M.C. Rosano, Department of Algerian Society of Cardiology, Brahim Kichou; Armenia: Armenian
Human Sciences and Promotion of Quality of Life, Chair of Cardiologists Association, Hamayak S. Sisakian; Austria: Austrian
Pharmacology, San Raffaele University of Rome, Rome, Italy, Society of Cardiology, Daniel Scherr; Belgium: Belgian Society of
Cardiology, San Raffaele Cassino Hospital, Cassino, Italy, Cardiology, Frank Cools; Bosnia and Herzegovina: Association of
Cardiovascular Academic Group, St George’s University Medical Cardiologists of Bosnia and Herzegovina, Elnur Smajić; Bulgaria:
School, London, United Kingdom; Prashanthan Sanders, Centre Bulgarian Society of Cardiology, Tchavdar Shalganov; Croatia:
for Heart Rhythm Disorders, University of Adelaide, Adelaide, Croatian Cardiac Society, Sime Manola; Cyprus: Cyprus Society
Australia, Department of Cardiology, Royal Adelaide Hospital, of Cardiology, Panayiotis Avraamides; Czechia: Czech Society of
Adelaide, Australia; Renate B. Schnabel, Cardiology University Cardiology, Milos Taborsky; Denmark: Danish Society of
Heart & Vascular Center Hamburg, University Medical Center Cardiology, Axel Brandes; Egypt: Egyptian Society of Cardiology,
Hamburg-Eppendorf, Hamburg, Germany, German Center for Ahmed M. El-Damaty; Estonia: Estonian Society of Cardiology, Priit
Cardiovascular Research (DZHK) Partner site Hamburg/Kiel/Lübeck, Kampus; Finland: Finnish Cardiac Society, Pekka Raatikainen;
Germany; Piotr Suwalski, Department of Cardiac Surgery and France: French Society of Cardiology, Rodrigue Garcia; Georgia:
Transplantology, National Medical Institute of the Ministry of Interior Georgian Society of Cardiology, Kakhaber Etsadashvili; Germany:
and Administration, Centre of Postgraduate Medical Education, German Cardiac Society, Lars Eckardt; Greece: Hellenic Society of
Warsaw, Poland; Emma Svennberg, Department of Medicine, Cardiology, Eleftherios Kallergis; Hungary: Hungarian Society of
Karolinska University Hospital Huddinge, Karolinska Institutet, Cardiology, László Gellér; Iceland: Icelandic Society of Cardiology,
Stockholm, Sweden, Department of Cardiology, Karolinska University Kristján Guðmundsson; Ireland: Irish Cardiac Society, Jonathan
Hospital, Stockholm, Sweden; Juan Tamargo, Pharmacology and Lyne; Israel: Israel Heart Society, Ibrahim Marai; Italy: Italian
Toxicology School of Medicine, Universidad Complutense, Madrid, Federation of Cardiology, Furio Colivicchi; Kazakhstan: Association
Spain; Otilia Tica, Department of Cardiology, Emergency County of Cardiologists of Kazakhstan, Ayan Suleimenovich Abdrakhmanov;
Clinical Hospital of Bihor, Oradea, Romania, Institute of Kosovo (Republic of): Kosovo Society of Cardiology, Ibadete
Cardiovascular Sciences, University of Birmingham, Birmingham, Bytyci; Kyrgyzstan: Kyrgyz Society of Cardiology, Alina
United Kingdom; Vassil Traykov, Department of Invasive Kerimkulova; Latvia: Latvian Society of Cardiology, Kaspars Kupics;
Electrophysiology, Acibadem City Clinic Tokuda University Hospital, Lebanon: Lebanese Society of Cardiology, Marwan Refaat; Libya:
Sofia, Bulgaria; and Stylianos Tzeis, Cardiology Department, Mitera Libyan Cardiac Society, Osama Abdulmajed Bheleel; Lithuania:
Hospital, Athens, Greece. Lithuanian Society of Cardiology, Jūratė Barysienė; Luxembourg:
Luxembourg Society of Cardiology, Patrick Leitz; Malta: Maltese
Cardiac Society, Mark A. Sammut; Moldova (Republic of):
17. Appendix Moldavian Society of Cardiology, Aurel Grosu; Montenegro:
ESC Scientific Document Group Montenegro Society of Cardiology, Nikola Pavlovic; Morocco:
Includes Document Reviewers and ESC National Cardiac Societies. Moroccan Society of Cardiology, Abdelhamid Moustaghfir;
Document Reviewers: Nikolaos Dagres (CPG Review Netherlands: Netherlands Society of Cardiology, Sing-Chien Yap;
Co-ordinator) (Germany), Bianca Rocca (CPG Review Co-ordinator) North Macedonia: National Society of Cardiology of North
(Italy), Syed Ahsan (United Kingdom), Pietro Ameri (Italy), Elena Macedonia, Jane Taleski; Norway: Norwegian Society of Cardiology,
Arbelo (Spain), Axel Bauer (Austria), Michael A. Borger (Germany), Trine Fink; Poland: Polish Cardiac Society, Jaroslaw Kazmierczak;
Sergio Buccheri (Sweden), Barbara Casadei (United Kingdom), Ovidiu Portugal: Portuguese Society of Cardiology, Victor M. Sanfins;
Chioncel (Romania), Dobromir Dobrev (Germany), Laurent Fauchier Romania: Romanian Society of Cardiology, Dragos Cozma; San
ESC Guidelines 71

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