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Electrophysiologic Response to Moricizine in Patients with Sustained Ventricular Arrhythmias

Anne C. Powell, MB, BS, PhD; Michael R. Gold, MD, PhD; Ross Brooks, MD, MSc; Hasan Garan, MD; Jeremy N. Ruskin, MD; and Brian A. McGovern, MD
[+] Article and Author Information

Grant Support: Dr. Powell is a recipient of a Merck International Fellowship in Clinical Pharmacology.

Requests for Reprints: Brian A. McGovern, MD, Cardiac Arrhythmia Service, Massachusetts General Hospital, 32 Fruit Street, Boston, MA 02114.

Current Author Addresses: Dr. Powell: 32 Bowen Crescent, North Carlton, Victoria 3054, Australia.

Dr. Gold: University of Maryland Hospital, 22 South Greene Street, Baltimore, MD 21201.

Drs. Brooks, Garan, Ruskin, and McGovern: Cardiac Unit, Massachusetts General Hospital, 32 Fruit Street, Boston, MA 02114.


© 1992 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1992;116(5):382-387. doi:10.7326/0003-4819-116-5-382
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Objective: To assess the short-term efficacy and safety of moricizine in patients receiving electrophysiologically guided therapy for sustained ventricular arrhythmias refractory to treatment with class IA antiarrhythmic agents.

Design: Uncontrolled clinical trial.

Setting: Referral-based teaching medical center.

Patients: Twenty-one patients (18 of whom had coronary artery disease) with a mean left ventricular ejection fraction of 32% ± 11% who presented with sustained ventricular tachycardia (13 patients), syncope (4 patients), or cardiac arrest (4 patients).

Interventions: Moricizine, 743 ± 85 mg daily.

Measurements: Electrophysiologic testing in the drug-free state and after administration of moricizine unless sustained arrhythmias occurred.

Main Results: Sustained ventricular tachycardia was inducible in the absence of antiarrhythmic drugs in 20 patients and was not suppressed by moricizine in any patient. Four patients had six episodes of spontaneous ventricular tachycardia while receiving moricizine. A probable proarrhythmic response occurred in four patients. — Conclusion: In patients with compromised left ventricular tricular function caused by coronary artery disease in whom class IA antiarrhythmics were ineffective, moricizine was ineffective in suppressing sustained ventricular arrhythmias and resulted in proarrhythmic effects in some patients.

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