• Abhishek Maan, Moussa Mansour, Elad Anter, Vickas V Patel, Alan Cheng, Marwan M Refaat, Jeremy N Ruskin, and E Kevin Heist.
• From the *Division of Electrophysiology, Massachusetts General Hospital, Boston, MA; †Harvard Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Boston, MA; ‡Department of Physiology, Cardiovascular Research Center, Section of Clinical Cardiac Electrophysiology, Temple University School of Medicine, Philadelphia, PA; §Division of Electrophysiology, Johns Hopkins University, Baltimore, MD.
• Crit Pathw Cardiol. 2015 Jun 1; 14 (2): 81-5.

AbstractObstructive sleep apnea (OSA) is increasingly recognized as an important risk factor for arrhythmogenesis. Epidemiological and clinical studies have suggested a strong association between OSA and atrial fibrillation (AF). With the increasing global epidemic of obesity, the incidence of OSA is also expected to rise. Various mechanisms mediated through adverse electrical and structural changes have been proposed to explain the increased risk of AF in patients with OSA. Multiple studies have also observed a greater risk of AF recurrence after cardioversion and catheter ablation (CA) in the patients with untreated OSA. The epidemiological and pathophysiological associations between OSA and AF have significant implications on the treatment outcomes of rhythm-control strategies for AF. Adequate screening and optimal management of OSA are of key importance to help improve the clinical outcomes following cardioversion and CA. In this review, we sought to describe the role of various mechanisms by which OSA mediates the pathogenesis of AF and contributes to adverse outcomes following CA.

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