Ranolazine was developed as an antianginal agent and was approved by the Food and Drug Administration in 2006 for use in chronic stable angina pectoris. Experimental and clinical studies have shown that it also has antiarrhythmic properties based on the frequency-dependent blockade of peak sodium channel current (peak INa) and rapidly activating delayed rectifier potassium current (IKr) in the atria and blockade of late phase of the inward sodium current (late INa) in the ventricles. Recent clinical studies have revealed the efficacy of ranolazine in prevention of atrial fibrillation in patients with acute coronary syndromes, prevention as well as conversion of postoperative atrial fibrillation after cardiac surgery, conversion of recent-onset atrial fibrillation and maintenance of sinus rhythm in recurrent atrial fibrillation. Ranolazine has also been shown to reduce ventricular tachycardia and drug-refractory implantable cardioverter defibrillator shocks. The antiarrhythmic effect of ranolazine is preserved in the setting of chronic heart failure and clinical studies have demonstrated its safety in patients with heart failure. This review discusses the available preclinical and clinical data on the antiarrhythmic effects of this novel antianginal agent.
Keywords: Atrial fibrillation; Late sodium current; Peak sodium current; Ranolazine; Ventricular tachycardia.
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