MORTALITY FOLLOWING VENTRICULAR ARRHYTHMIA SUPPRESSION BY ENCAINIDE, FLECAINIDE, AND MORICIZINE AFTER MYOCARDIAL-INFARCTION - THE ORIGINAL DESIGN CONCEPT OF THE CARDIAC-ARRHYTHMIA SUPPRESSION TRIAL (CAST)
Ae. Epstein et al., MORTALITY FOLLOWING VENTRICULAR ARRHYTHMIA SUPPRESSION BY ENCAINIDE, FLECAINIDE, AND MORICIZINE AFTER MYOCARDIAL-INFARCTION - THE ORIGINAL DESIGN CONCEPT OF THE CARDIAC-ARRHYTHMIA SUPPRESSION TRIAL (CAST), JAMA, the journal of the American Medical Association, 270(20), 1993, pp. 2451-2455
Objective.-To test the hypothesis that in survivors of myocardial infa
rction, the suppression of ventricular premature depolarizations impro
ves survival free of cardiac arrest and arrhythmic death. Design.-Inte
rnational, prospective, multicenter, randomized, placebo-controlled tr
ial. Setting.-University and community hospitals. Patients.-A total of
3549 patients with myocardial infarction and left ventricular dysfunc
tion. Intervention.-Administration of encainide, flecainide, moricizin
e, 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 t
he stratified log rank statistic. Results.-At 1 year from the time of
randomization to blinded therapy, 95% of placebo-treated patients vs 9
0% of active drug-treated patients remained alive (P=.0006). Similarly
, at 1 year, 96% of placebo-treated patients vs 93% of active drug-tre
ated patients remained free of cardiac arrest or arrhythmic death (P=.
003). Conclusions.-The suppression of asymptomatic or mildly symptomat
ic ventricular arrhythmias after myocardial infarction does not improv
e survival and can increase mortality. Treatment strategies designed s
olely to suppress these arrhythmias should no longer be followed.