Author + information
- Received September 2, 2019
- Revision received November 25, 2019
- Accepted December 20, 2019
- Published online March 16, 2020.
- Jithin K. Sajeev, MBChBa,b,
- Jonathan M. Kalman, MBBS, PhDc,d,
- Helen Dewey, MBBS, PhDa,e,
- Jennifer C. Cooke, MBBSa,b and
- Andrew W. Teh, MBBS, PhDa,b,d,f,∗ ()
- aMonash University, Melbourne, Victoria, Australia
- bDepartment of Cardiology, Eastern Health, Melbourne, Victoria, Australia
- cDepartment of Cardiology, Royal Melbourne Hospital, Melbourne, Victoria, Australia
- dUniversity of Melbourne, Melbourne, Victoria, Australia
- eDepartment of Neuorosciences, Eastern Health, Melbourne, Victoria, Australia
- fDepartment of Cardiology, Austin Health, Melbourne, Victoria, Australia
- ↵∗Address for correspondence:
Dr. Andrew W. Teh, Department of Cardiology, Box Hill Hospital, Level 2, Building B, 8 Arnold Street, Box Hill, Victoria 3128, Australia.
• AF is associated with LA thrombogenesis and cardioembolic stroke.
• Adverse atrial remodeling may lead to cardioembolic stroke even in the absence of AF.
• Novel markers of abnormal atrial substrate are associated with ischemic stroke.
• Robust nonfibrillatory markers of thrombogenesis may allow for early identification of at-risk patients.
Atrial fibrillation (AF) is well-recognized in the pathophysiology of left atrial thrombogenesis and resultant cardioembolic stroke. Subclinical AF is believed to account for a significant proportion of embolic stroke. However, recent randomized control trials failed to demonstrate a significant benefit for oral anticoagulation, in an unselected population with embolic stroke of undetermined source. This has reinvigorated the focus on finding robust markers to identify patients at risk of cardioembolic stroke. Several nonfibrillatory atrial electrical markers, along with structural and biochemical abnormalities, have been associated with ischemic stroke, independently of AF. An increasingly complex relationship exists among vascular risk factors, atrial remodeling, and thrombogenesis. Identifying robust markers of an underlying atrial myopathy may allow for early identification of patients at risk for cardioembolic stroke. This review outlines the inconsistencies in the evidence for AF as the prerequisite for left atrial thrombogenesis and embolic stroke. It will highlight the current evidence and controversies for adverse atrial remodeling, independent from rhythm, as a plausible mechanism for left atrial thrombogenesis and ischemic stroke.
Dr. Kalman has received research fellowships from Medtronic Inc., Biosense Webster, and Abbott. Dr. Teh has received speaking honoraria from Medtronic Inc. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Katja Zeppenfeld, MD, served as Guest Editor for this paper.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received September 2, 2019.
- Revision received November 25, 2019.
- Accepted December 20, 2019.
- 2020 American College of Cardiology Foundation
This article requires a subscription or purchase to view the full text. If you are a subscriber or member, click Login or the Subscribe link (top menu above) to access this article.