Author + information
- Received November 22, 1994
- Revision received March 3, 1995
- Accepted March 14, 1995
- Published online August 1, 1995.
- Kelley P. Anderson, MD, FACC1,a,
- Richard Walker, MDb,
- Ted Dustman, MEc,
- Marc Fuller, PhDc and
- Motomi Mori, PhDd
- ↵1Address for correspondence: Dr. Kelley P. Anderson, Cardiac Electrophysiology Program, Presbyterian University Hospital, Room B535, 200 Lothrop Street, Pittsburgh, Pennsylvania 15213-2582.
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 study was supported by grants from Marquette Electronics Corporation, Milwaukee, Wisconsin and from the American Heart Association, Montana Affiliate. It was presented in abstract form at the 66th Scientific Sessions of the American Heart Association, Atlanta, Georgia, November 1993. A complete list of the ESVEM investigators appears in reference 16.
- Received November 22, 1994.
- Revision received March 3, 1995.
- Accepted March 14, 1995.