Currently available agents for pharmacologic management of
atrial fibrillation (AF) are limited by their suboptimal efficacy and nonnegligible proarrhythmic risk.
Ranolazine (RN) is a novel antianginal agent with increasingly appreciated antiarrhythmic properties that can suppress ventricular and supraventricular arrhythmias including AF. In this review, we describe the electrophysiological properties of RN, focusing on atrial-selective inhibition of a number of
ion channels implicated in the development of AF, particularly the
sodium current. We further summarize evidence from experimental studies that demonstrate a potent AF-suppressing effect of RN, alone or in combination with other
antiarrhythmic drugs. Of clinical relevance, we present growing evidence from preliminary clinical investigations indicating the safety and efficacy of RN for prevention and treatment of AF in various clinical settings including prevention of AF in patients with
acute coronary syndromes, prevention and conversion of postoperative AF after surgical coronary revascularization, sinus rhythm maintenance in
drug-resistant recurrent AF, and facilitating of electrical or pharmacological
cardioversion in
cardioversion-resistant patients. While current experimental and clinical evidence points to RN as a potentially promising agent for suppression of AF, well-designed, large-scale trials will be required before RN can be considered for pharmacological treatment of AF in clinical practice.