Consensus Statement CAST and Beyond Implications of the Cardiac Arrhythmia Suppression Trial

F requent and repetitive forms of premature ventricular complexes (PVCs) have been recognized as independent markers of increased risk for sudden cardiac death in patients with a previous myocardial infarction. On this basis, the Cardiac Arrhythmic Suppression Trial (CAST) was initiated to test the hypothesis that suppression of these ventricular arrhythmias would reduce the incidence of sudden cardiac death.1 As critically reviewed by Furberg,2 previous studies with antiarrhythmic drugs in post-myocardial infarction patients were seriously flawed in one or more ways, such that they could not conclusively demonstrate whether suppression of ventricular arrhythmias by the antiarrhythmic drugs studied affected survival. CAST, a placebo-controlled, double-blind, multicenter study, was initiated in June 1987 to evaluate the effect of three antiarrhythmic drugs (encainide, flecainide, and moricizine) in patients who had sustained a myocardial infarction and had asymptomatic or mildly symptomatic ventricular arrhythmias. Approximately 22 months after its initiation, part of the study was prematurely halted, and the remaining part was significantly modified because of excessive mortality in the group of patients randomized to treatment with encainide or flecainide.1 The study is continuing with the third drug, moricizine. CAST is an important study for several reasons. For the first time, convincing data were provided regarding a mode of antiarrhythmic treatment that existed for some 20 years and was widely applied by practicing physicians. The results of CAST may lead to extensive changes in antiarrhythmic therapy, and they merit careful consideration. Also, results from CAST answered the hypotheses posed for flecainide