Spontaneous sustained ventricular tachycardia in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) Trial

Cardiac Electrophysiology Program, University of Pittsburgh Medical Center, Pennsylvania, USA.

OBJECTIVES. We compared the QRS waveforms of the initial and subsequent complexes of spontaneous sustained monomorphic ventricular tachycardia and the rhythm induced at electrophysiologic study to test the theory that premature ventricular complexes "trigger" spontaneous ventricular tachycardia and that a stable substrate exists such that the spontaneous arrhythmia can be reproduced at electrophysiologic study. BACKGROUND. Failure rates have been high in several recent studies in which prevention of ventricular tachyarrhythmias was guided by suppression of premature ventricular complexes or induced ventricular tachycardias. METHODS. Digital waveform analysis was used to distinguish events of ventricular tachycardia initiated by configurationally distinct, possibly triggering, complexes (type 1) from events in which the initial QRS waveforms were identical to subsequent complexes, suggesting no requirement for premature ventricular beats (type 2). RESULTS. Of 1,102 episodes of spontaneous ventricular tachycardia, 73 (6.6%) were type 1; 1,012 were type 2 (91.8%); and 17 (1.5%) were uncertain. Of 59 patients only 14 (24%) had only type 1 episodes (group 1), whereas 37 patients (63%) had predominantly type 2 events (group 2) (p < 0.0001). Sustained ventricular tachycardia was inducible in all group 1 patients, and in most (57%) the induced rhythm was similar to the spontaneous rhythm. Ventricular tachycardia could not be induced in 7 patients from group 2 (19%), and in 18 patients (49%) the induced and spontaneous rhythms were dissimilar. Recurrence of arrhythmia rates differed according to the guidance method in group 2. CONCLUSIONS. Discrepancies between observed and predicted modes of initiation of ventricular tachycardia and between spontaneous and induced rhythms could result in inappropriate guidance and subsequent failure of antiarrhythmic treatment.

This article has been cited by other articles:

				S. H. Hohnloser Ventricular Arrhythmias: Antiadrenergic Therapy for the Patient with Coronary Artery Disease Journal of Cardiovascular Pharmacology and Therapeutics, October 1, 2005; 10(4_suppl): S23 - S31. [Abstract] [PDF]

				K. P. Anderson Lipid-lowering therapy for prevention of ventricular tachyarrhythmias J. Am. Coll. Cardiol., July 2, 2003; 42(1): 88 - 92. [Full Text] [PDF]

				V. Shusterman, B. Aysin, V. Gottipaty, R. Weiss, S. Brode, D. Schwartzman, K. P. Anderson, and for the ESVEM Investigators Autonomic nervous system activity and the spontaneous initiation of ventricular tachycardia J. Am. Coll. Cardiol., December 1, 1998; 32(7): 1891 - 1899. [Abstract] [Full Text] [PDF]

				R. Goyal, M. Harvey, E. G. Daoud, K. Brinkman, B. P. Knight, M. Bahu, R. Weiss, F. Bogun, K. C. Man, S. A. Strickberger, et al. Effect of Coupling Interval and Pacing Cycle Length on Morphology of Paced Ventricular Complexes: Implications for Pace Mapping Circulation, December 1, 1996; 94(11): 2843 - 2849. [Abstract] [Full Text]