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Antiarrhythmic Drugs: Good for Premature Ventricular Complexes but Bad for Patients?

Alfred E. Buxton, MD
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Requests for Reprints: Alfred E. Buxton, MD, Cardiovascular Division, Hospital of the University of Pennsylvania, 9 Founders Pavilion, 3400 Spruce Street, Philadelphia, PA 19104.

Hospital of the University of Pennsylvania and the University of Pennsylvania School of Medicine
Philadelphia, PA 19104

Ann Intern Med. 1992;116(5):420-422. doi:10.7326/0003-4819-116-5-420
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This excerpt has been provided in the absence of an abstract.

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


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