Ranolazine, a newly introduced, FDA-approved antianginal agent, has more recently
been shown to have additional beneficial antiarrhythmic actions attributed to its inhibitory effect on
both peak and late sodium current. The first clinical evidence of ranolazine’s antiarrhythmic
efficacy has been provided by the MERLIN-TIMI 36 trial, which showed that ranolazine may
suppress both supraventricular and ventricular arrhythmias in patients with non-ST-segment elevation
acute coronary syndrome. An interesting observation of available studies is that ranolazine seems to
be more effective in pathological conditions, such as heart failure, ischemia, tachyarrhythmias or long
QT3 syndrome, and has little effect on normal myocytes. Importantly, the drug may have an
antiarrhythmic effect without causing proarrhythmia. The mechanisms involved in the antiarrhythmic action of ranolazine,
experimental and clinical data for its antiarrhythmic efficacy in suppressing atrial fibrillation and ventricular tachyarrhythmias,
are herein reviewed. Current data from small randomized trials indicate that further larger randomized controlled trials are
needed that will examine the antiarrhythmic effects of ranolazine and its potential use in patients with arrhythmias.
Keywords: Antiarrhythmic agents, atrial fibrillation, late sodium current, myocardial ischemia, proarrhythmia, ranolazine,
ventricular fibrillation, ventricular tachycardia.
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