{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T17:28:05Z","timestamp":1783358885232,"version":"3.54.6"},"reference-count":178,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T00:00:00Z","timestamp":1779062400000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The lifetime risk of stroke among non\u2010anticoagulated patients with atrial fibrillation (AF) approximates 1 in 3. Oral anticoagulation (OAC) reduces stroke and systemic embolism by at least two thirds and mortality by one fourth.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The present narrative review summarizes current evidence and practical recommendations on OAC in AF and highlights recent advances and remaining gaps in knowledge.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The threshold for net clinical benefit of OAC is met when stroke risk exceeds 1%\u20132% per year, typically corresponding to \u2265\u20091 traditional stroke risk factor (CHA\n                      <jats:sub>2<\/jats:sub>\n                      DS\n                      <jats:sub>2<\/jats:sub>\n                      \u2010VA \u2265\u20091), with increasing risk per additional risk factor. OAC also appears beneficial in device\u2010detected (subclinical) AF, possibly at higher CHA\n                      <jats:sub>2<\/jats:sub>\n                      DS\n                      <jats:sub>2<\/jats:sub>\n                      \u2010VA scores. Direct oral anticoagulants (DOACs) reduce intracranial haemorrhage compared to vitamin K antagonists (VKAs), and meta\u2010analyses of randomized trials showed further reduction in stroke and mortality with DOACs, including in the elderly and chronic kidney disease. VKAs are preferred in patients with mechanical heart valves, mitral stenosis, antiphospholipid syndrome and Child\u2010Turcotte\u2010Pugh C cirrhosis. Modifiable bleeding risk factors should be assessed periodically and mitigated. These include anti\u2010inflammatory drugs, antiplatelet therapy, drug interactions, excessive alcohol consumption, uncontrolled hypertension, diabetes, risk factors for gastrointestinal bleeding, major organ dysfunction and frailty. There are very few contraindications to OAC and most are relative or temporary conditions. Follow\u2010up involves reassessing adherence, thrombotic and bleeding risk, co\u2010medication and dosing. Integrated patient\u2010centred AF management additionally involves risk factor management, symptom control and dynamic reassessment. Lifelong OAC is currently recommended, but recent data suggested that discontinuing OAC after successful catheter ablation of AF and\/or left atrial appendage closure could be safe. OAC in specific settings is discussed, including cardioversion, catheter ablation, surgery, post\u2010operative AF, elderly patients, pregnancy and bleeding.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>OAC is the cornerstone of thromboembolism prevention in AF, but knowledge gaps remain, including on risk stratification, device\u2010detected AF, trigger\u2010induced AF, cardioversion, OAC resumption after major bleeding, and potential safety of OAC discontinuation after successful catheter ablation or left atrial appendage occlusion.<\/jats:p>\n                  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