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Review
. 2025 Sep 23;86(12):910-939.
doi: 10.1016/j.jacc.2025.07.031.

Outcomes and Management of Stressor-Associated Atrial Fibrillation: JACC State-of-the-Art Review

Affiliations
Review

Outcomes and Management of Stressor-Associated Atrial Fibrillation: JACC State-of-the-Art Review

Julian S Haimovich et al. J Am Coll Cardiol. .

Abstract

Stressor-associated atrial fibrillation (AF) is defined as new onset AF occurring in the setting of an acute and reversible physiologic stressor (eg, cardiac surgery, acute infection). Although historically viewed as transient and potentially benign, a growing body of evidence demonstrates that stressor-associated AF is prognostically important, with long-term rates of AF recurrence and AF-related adverse events (eg, stroke, heart failure) approaching those of AF occurring without a stressor. Nevertheless, key aspects of stressor-associated AF management (eg, prevention, surveillance, treatment) remain highly variable. In this state-of-the-art review, we provide a clinically oriented synthesis of the epidemiology, mechanisms, outcomes, and management of stressor-associated AF across the breadth of characterized precipitants. Within this context, we outline a pathophysiologic framework in which stressor-associated AF represents a spectrum spanning variable relative contributions of direct stressor effects, stressor-mediated substrate, and underlying predisposition (ie, modifiable and nonmodifiable AF risk factors). Stressor-associated AF episodes occurring in the setting of a strong underlying predisposition to AF (sometimes termed "provoked AF") have a higher risk of recurrence, while episodes occurring in response to a profound physiologic stressor with minimal or no underlying predisposition (sometimes termed "reversible AF") have a lower risk of recurrence. Using postcardiac surgery stressor-associated AF as an exemplar, we summarize recent advances translating greater pathophysiologic understanding (eg, role of local inflammation) into novel clinical interventions capable of reducing stressor-associated AF incidence (eg, posterior pericardiotomy). We summarize available evidence for clinical management of stressor-associated AF and offer a conceptual framework to inform care. Finally, we conclude by outlining key priorities for future research designed to facilitate precision management of stressor-associated AF, including identification of more effective preventive measures, development of models to stratify risk of recurrent AF and AF-related adverse events following a stressor-associated AF episode, and integration of patient-centered outcomes.

Keywords: management; outcomes; pathophysiology; review; triggered atrial fibrillation.

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Conflict of interest statement

Funding Support and Author Disclosures Dr Haimovich was supported by grants from the National Institutes of Health (T32HL007208). Dr Kany was supported by the Walter Benjamin Fellowship from the Deutsche Forschungsgemeinschaft (521832260). Dr Ajufo was supported by the John S. LaDue Memorial Fellowship in Cardiovascular Medicine or Vascular Biology grant. Dr Ellinor was supported by grants from the National Institutes of Health (R01HL092577, R01HL157635, 1R01HL177209), the American Heart Association (961045), the European Union (MAESTRIA 965286), and the Fondation Leducq (24CVD01). Dr Khurshid was supported by grants from the National Institutes of Health (K23HL169839) and the American Heart Association (23CDA1050571). Dr Benjamin was supported in part by grants from National Institutes of Health (R01HL092577; 5U54HL120163, R01HL141434, R01AG066010, 1R01AG066914, 1R01NS121419) and the American Heart Association (18SFRN34110082). Dr Sanders was supported by an Investigator Grants from the National Health and Medical Research Council of Australia. Dr Rienstra was supported by an unrestricted research grant from the Dutch Heart Foundation and was conducted in collaboration with and supported by the Dutch CardioVascular Alliance (01-002-2022-0118 EmbRACE); from ZonMW and the Dutch Heart Foundation (DECISION project 848090001); from the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation (RACE V [CVON 2014-9], RED-CVD [CVON2017-11]); from Top Sector Life Sciences and Health to the Dutch Heart Foundation (PPP Allowance; CVON-AI [2018B017]); and from the European Union’s Horizon 2020 research and innovation program under grant agreement; EHRA-PATHS (945260). Dr McIntyre is supported by a Heart and Stroke Foundation of Canada National New Investigator Award and a Population Health Research Institute Career Award; has received consulting fees from AtriCure; and has received speaking fees from iRhythm. Dr Lubitz has received sponsored research support from Bristol Myers Squibb, Pfizer, Boehringer Ingelheim, Fitbit, Medtronic, Premier, and IBM; is an employee of Novartis; and has served as a consultant for Bristol Myers Squibb, Pfizer, Blackstone Life Sciences, and Invitae. Dr Rienstra has served as a consultant for Bayer (OCEANIC-AF national PI), InCarda Therapeutics (RESTORE-SR national PI); has received funding to his institution from Novartis; and has received speaker fees to his institution from Daiichi-Sankyo. Dr Sanders has served on the medical advisory board for Abbott, Medtronic, Boston Scientific, CathRx, and Pacemate; and the University of Adelaide has received on behalf of Dr Sanders research funds from Boston Scientific, Medtronic, Abbott, and Becton Dickenson. Dr Ellinor has received sponsored research support from Bayer AG, Bristol Myers Squibb, Pfizer, and Novo Nordisk; and has served on advisory boards or as a consultant for Bayer AG. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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