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Article
November 24, 1993

Mortality Following Ventricular Arrhythmia Suppression by Encainide, Flecainide, and Moricizine After Myocardial InfarctionThe Original Design Concept of the Cardiac Arrhythmia Suppression Trial (CAST)

Author Affiliations

From the Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham (Drs Epstein and Rogers); CAST Coordinating Center, University of Washington, Seattle (Dr Hallstrom); Section of Cardiology, Department of Medicine, Rush-Presbyterian-St Luke's Medical Center, Chicago, III (Dr Liebson); Section of Cardiology, Department of Medicine, University of Florida-Jacksonville (Dr Seals); Cardiology Division, Department of Medicine, LDS Hospital, Salt Lake City, Utah (Dr Anderson); Division of Cardiology, Department of Medicine, St Louis (Mo) University (Dr Cohen); Cardiology Unit, Department of Medicine, University of Rochester (NY) (Dr Capone); Division of Cardiology, Department of Medicine, The University of Calgary (Alberta) (Dr Wyse).

JAMA. 1993;270(20):2451-2455. doi:10.1001/jama.1993.03510200057032
Abstract

Objective.  —To test the hypothesis that in survivors of myocardial infarction, the suppression of ventricular premature depolarizations improves survival free of cardiac arrest and arrhythmic death.

Design.  —International, prospective, multicenter, randomized, placebo-controlled trial.

Setting.  —University and community hospitals.

Patients.  —A total of 3549 patients with myocardial infarction and left ventricular dysfunction.

Intervention.  —Administration of encainide, flecainide, moricizine, or placebo to suppress ventricular premature depolarizations.

Main Outcome Measures.  —Overall survival and survival free of cardiac arrest or arrhythmic death were compared in patients randomized to long-term, active antiarrhythmic drug therapy vs corresponding placebo, using the stratified log rank statistic.

Results.  —At 1 year from the time of randomization to blinded therapy, 95% of placebo-treated patients vs 90% of active drug—treated patients remained alive (P=.0006). Similarly, at 1 year, 96% of placebo-treated patients vs 93% of active drug—treated patients remained free of cardiac arrest or arrhythmic death (P=.003).

Conclusions.  —The suppression of asymptomatic or mildly symptomatic ventricular arrhythmias after myocardial infarction does not improve survival and can increase mortality. Treatment strategies designed solely to suppress these arrhythmias should no longer be followed.(JAMA. 1993;270:2451-2455)

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