Citation: Marcello Disertori, Silvia Quintarelli
Atrial fibrillation (AF) arises as a result of a complex interaction of triggers, perpetuators and the substrate. The recurrence of AF may be partially related to a biologic phenomenon known as remodeling, in which the electrical, mechanical, and structural properties of the atrial tissue and cardiac cells are progressively altered,creating a more favorable substrate. Atrial remodeling is in part a consequence of arrhythmia itself. Therefore,to prevent and to treat AF, much attention has been directed to upstream therapies to alter the arrhythmia substrate and to reduce atrial remodeling. The renin-angiotensin-aldosterone system (RAAS) plays a keyrole in these strategies. In this review we analyze the experimental and clinical evidence regarding the efficacy of RAAS inhibitors in AF treatment. In the primary prevention of AF, meta-analyses have shown that risk of new-onset AF in patients with congestive heart failure and left ventricular dysfunction is reduced by RAAS inhibitors, whereas in hypertensive and post–myocardial infarction patients, the results are less evident. In the secondary prevention of AF, some large, prospective, randomized, placebo-controlled studieswith angiotensin II-receptor blockers returned negative results. Unfortunately, the approach of using RAASinhibitors as antiarrhythmic drugs to prevent both new-onset and recurrent AF is in decline because negativetrial results are accumulating, with the exception of the results in patients with congestive heart failure.
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