The genesis of cardiac arrhythmia can be grouped into 3 common mechanisms: abnormal automaticity, triggered activity, and re-entry. Alteration of automaticity, triggered activity, conduction, and/or refractoriness of myocardial tissue by drugs will perturb and often prevent the occurrence of arrhythmias. Ranolazine is a novel agent approved in the United States for antianginal therapy. The potential of ranolazine as an antiarrhythmic drug stems from observation of its ability to modify multiple ionic currents in cardiac cells responsible for generation of the action potential. In contrast to currently available antiarrhythmic drugs, ranolazine is well tolerated and has few side effects. Small clinical trials suggest that ranolazine may have a role in the treatment of patients with non–STelevation acute coronary syndrome, atrial fibrillation, long QT syndromes, and sinus node dysfunction.