This Article Full Text (PDF) 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Brugada, J. Articles by Allessie, M. A. Search for Related Content PubMed PubMed Citation Articles by Brugada, J. Articles by Allessie, M. A.

Circulation, Vol 83, 1621-1629, Copyright © 1991 by American Heart Association

ARTICLES

On the mechanisms of ventricular tachycardia acceleration during programmed electrical stimulation

J Brugada, P Brugada, L Boersma, L Mont, C Kirchhof, HJ Wellens and MA Allessie
Department of Physiology, University of Limburg, Maastricht, The Netherlands.

BACKGROUND. The pathophysiological mechanisms leading to acceleration of ventricular tachycardia (VT) are still unclear. METHODS AND RESULTS. High-resolution epicardial mapping was used to study the mechanisms of VT acceleration by programmed electrical stimulation (PES) in a model of sustained reentrant VT in Langendorff-perfused rabbit hearts (n = 40). Three different mechanisms responsible for acceleration of VT were identified: 1) induction of double-wave reentry (n = 6), defined as the occurrence of two successive activation waves circulating in the same direction in the same circuit; 2) change to a functionally determined circuit (n = 4), defined as reentry of the impulse around a functional line of block without involvement of a fixed obstacle; and 3) change of the reentrant circuit to reentry within a different, faster anatomic pathway (n = 3). Analysis of 81 episodes of sustained monomorphic VT induced by PES in 74 patients with clinically documented sustained VT in the setting of chronic coronary artery disease showed that in 22 episodes VT was suddenly accelerated by PES (mean cycle length, from 345 +/- 73 to 277 +/- 71 msec, p less than 0.01). CONCLUSIONS. With the observations made in the experimental model, the following tentative classification of the mechanisms of VT acceleration of the 22 episodes was made: 1) induction of double-wave reentry in two, 2) change to a functionally determined circuit in four, and 3) change to reentry within a faster anatomic circuit in 16. Simple criteria suggest that these mechanisms may apply in the clinical situation.

This article has been cited by other articles:

				D. O. Arnar, D. Xing, and J. B. Martins Overdrive pacing of early ischemic ventricular tachycardia: evidence for both reentry and triggered activity Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1124 - H1130. [Abstract] [Full Text] [PDF]

				E. Garcia-Moran, L. Mont, A. Cuesta, M. Matas, and J. Brugada Low recurrence of syncope in patients with inducible sustained ventricular tachyarrhythmias treated with an implantable cardioverter-defibrillator Eur. Heart J., June 1, 2002; 23(11): 901 - 907. [Abstract] [Full Text] [PDF]

				J. Cheng and M. M. Scheinman Acceleration of Typical Atrial Flutter Due to Double-Wave Reentry Induced by Programmed Electrical Stimulation Circulation, April 28, 1998; 97(16): 1589 - 1596. [Abstract] [Full Text] [PDF]

				H. Fei, M. S. Hanna, and L. H. Frame Assessing the Excitable Gap in Reentry by Resetting: Implications for Tachycardia Termination by Premature Stimuli and Antiarrhythmic Drugs Circulation, November 1, 1996; 94(9): 2268 - 2277. [Abstract] [Full Text]

				S. L. Pinski and G. J. Fahy The Proarrhythmic Potential of Implantable Cardioverter-Defibrillators Circulation, September 15, 1995; 92(6): 1651 - 1664. [Abstract] [Full Text]

				J. J. Goldberger, J. R. Smith, Y.-H. Kim, R. S. Damle, and A. H. Kadish Effect of Increased Drive-train Stimulus Intensity on Dispersion of Ventricular Refractoriness Circulation, August 15, 1995; 92(4): 875 - 880. [Abstract] [Full Text]