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ARTICLE |

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

Andrew E. Epstein, MD; Alfred P. Hallstrom, PhD; William J. Rogers, MD; Philip R. Liebson, MD; A. Allen Seals, MD; Jeffery L. Anderson, MD; Jerome D. Cohen, MD; Robert J. Capone, MD; D. George Wyse, MD, PhD
JAMA. 1993;270(20):2451-2455. doi:10.1001/jama.1993.03510200057032.
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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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