This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gettes, L. S. Search for Related Content PubMed PubMed Citation Articles by Gettes, L. S.

(Circulation. 1995;91:1908-1909.)
© 1995 American Heart Association, Inc.

Articles

ESVEM and the Hazards of Clinical Trials

Leonard S. Gettes, MD

From the University of North Carolina at Chapel Hill.

Correspondence to Dr Leonard S. Gettes, University of North Carolina at Chapel Hill, 349 Burnett-Womack Bldg, CB 7075, Chapel Hill, NC 27599-7075.

	Introduction

 
During the past 15 years, our approach to patients with cardiovascular disease has undergone significant and often dramatic changes. These changes have primarily occurred as a result of large-scale multicenter clinical trials involving many patients and extending over several years. One such trial is the ESVEM study,¹ which was initiated in 1985, involved 14 centers, screened more than 2000 patients, and ultimately enrolled 486 patients with life-threatening ventricular arrhythmias. The trial had two major purposes: (1) to determine whether serial electrophysiological testing or serial Holter monitoring provided the better method of predicting the long-term therapeutic efficacy of antiarrhythmic drugs and (2) to determine which of the six antiarrhythmic drugs tested was most effective. In this issue of Circulation, Reiter and coworkers² report on results obtained in a subgroup of 146 patients who were among the 242 patients comprising the electrophysiological arm of the ESVEM trial. In this subgroup of 146, Holter monitoring was also performed. The authors report that the therapeutic efficacy of the various drugs was no greater when predicted by both tests (concordant results) than when predicted by only one of the two tests (discordant results). Although not specifically stated, the hypothesis being tested was that the ability of a drug to suppress the arrhythmia trigger (as reflected by the suppression of the ventricular premature beats recorded by Holter monitoring) and to alter the arrhythmia substrate (as reflected by the inability to induce ventricular tachycardia by electrophysiological testing) should predict better long-term efficacy than the ability to . . . [Full Text of this Article]