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(Circulation. 1995;91:245-247.)
© 1995 American Heart Association, Inc.

Articles

The Cardiac Arrhythmia Suppression Trial

Casting Suppression in a Different Light

Craig M. Pratt, MD; Lemuel A. Moyé, MD, PhD

From the Section of Cardiology, Department of Internal Medicine, Baylor College of Medicine and the School of Public Health, University of Texas Health Science Center, Houston.

Correspondence to Craig M. Pratt, MD, Professor of Medicine, Baylor College of Medicine, 6535 Fannin, MS F1001, Houston, TX 77030.

Key Words: trials • Editorials • arrhythmia

	Introduction

 
The Cardiac Arrhythmia Suppression Trial (CAST) was instituted in 1986 by the National Heart, Lung, and Blood Institute (NHLBI) after the completion of a 502-patient pilot study (CAPS).^{1 2 3} The initial results of CAST I was published in 1989 and the CAST II results published in 1992.^{2 3} In both trials, antiarrhythmic drugs effectively suppressed asymptomatic ventricular arrhythmias but increased arrhythmic death. Because the suppression hypothesis was refuted, the common practice of using antiarrhythmic drugs to suppress asymptomatic arrhythmias in patients after acute myocardial infarction has been curtailed. In CAST I, encainide and flecainide-treated patients had a 3.6-fold excessive risk of arrhythmic death compared with placebo-treated patients. The CAST results have been extrapolated to include other antiarrhythmic drugs, resulting in a concern of lethal proarrhythmia when using all antiarrhythmic drugs. Consequently, there have been substantial changes in the labeling of antiarrhythmic drugs and significant changes in the regulatory guidelines from the Food and Drug Administration.⁴ There has also been a dramatic restructuring of antiarrhythmic drug development by the pharmaceutical industry.

At least a decade before the initiation of CAST, it was recognized that myocardial infarction patients with frequent and complex ventricular premature depolarizations (VPDs) detected on ambulatory ECG monitoring had an increased risk of subsequent arrhythmic death as compared with patients without these arrhythmias.^{5 6 7 8} Like most noninvasive markers of increased risk, VPDs lack specificity (3% to 6% arrhythmic death rate in 1 year), meaning that most post–myocardial infarction patients with asymptomatic VPDs survive.⁹ Thus, for each 100 patients exposed to empiric antiarrhythmic . . . [Full Text of this Article]

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