Alfred E. Buxton, MD
Moricizine, a relatively new antiarrhythmic agent in the United States, was developed primarily because of its potent ability to suppress premature ventricular complexes (1). It shares these effects with other type IC antiarrhythmic agents such as encainide and flecainide. In this issue of Annals, two studies of the effects of moricizine in patients with sustained ventricular tachyarrhythmias are reported (2, 3). All but 1 of the 47 patients studied had sustained monomorphic ventricular tachycardia induced by electrophysiologic testing in the absence of antiarrhythmic drugs. Suppression of the inducible sustained ventricular tachycardia in response to moricizine was achieved in only three
Buxton AE. Antiarrhythmic Drugs: Good for Premature Ventricular Complexes but Bad for Patients?. Ann Intern Med. 1992;116:420–422. doi: 10.7326/0003-4819-116-5-420
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Published: Ann Intern Med. 1992;116(5):420-422.
Cardiology, Rhythm Disorders and Devices.
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