Atrial structural remodeling as an antiarrhythmic target.
Atrial fibrillation (AF) is the most common clinically encountered arrhythmia. Conventional pharmacological antiarrhythmic approaches suffer from poor efficacy and risk of serious complications, particularly proarrhythmia. More recently, the notion of "upstream" therapy, targeting the processes involved in the development of the substrate that supports AF, has increasingly become the focus of attention. Many clinical conditions associated with AF are characterized by prominent atrial fibrosis, and pharmacological strategies targeted at the fibrotic substrate itself may aid in the management of AF. Experimental and clinical data suggest that there exists an interplay among angiotensin II-related signaling, inflammation, and oxidative stress in the pathogenesis of AF-promoting structural remodeling, and these processes have become of particular therapeutic interest. This review will highlight pharmacologic approaches that have shown promise for attenuating structural remodeling to achieve antiarrhythmic efficacy in AF.
Burstein
Brett
B
Research Center and Department of Medicine, Montreal Heart Institute and Université de Montréal, Montréal, Canada.
Nattel
Stanley
S
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D016275:Atrial Function / Q000187:drug effects; D005355:Fibrosis; D006325:Heart Atria / Q000187:drug effects / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
D000889:Anti-Arrhythmia Agents