The renin-angiotensin system: a therapeutic target in atrial fibrillation.

There is growing evidence to suggest a role for the renin-angiotensin system (RAS) in the pathogenesis of atrial fibrillation (AF). Experimental animal data suggest RAS-dependent mechanisms for the development of a structural and electrophysiologic substrate for AF. This is consistent with clinical data demonstrating the effectiveness of RAS blockade in preventing new-onset or recurrent AF in a variety of patient populations including patients with hypertension and left ventricular hypertrophy, congestive heart failure, and those undergoing electrical cardioversion for AF. This review summarizes experimental and clinical evidence to date relating to the role of RAS in the pathogenesis of AF, and the efficacy of its inhibition in managing this common arrhythmia.