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 HighWire Citing Articles via Google Scholar Google Scholar Articles by Costeas, C. Articles by Coromilas, J. Search for Related Content PubMed PubMed Citation Articles by Costeas, C. Articles by Coromilas, J. Pubmed/NCBI databases Medline Plus Health Information Heart Attack

(Circulation. 1997;96:3721-3731.)
© 1997 American Heart Association, Inc.

Articles

Mechanisms Causing Sustained Ventricular Tachycardia With Multiple QRS Morphologies

Results of Mapping Studies in the Infarcted Canine Heart

Constantinos Costeas, MD; Nicholas S. Peters, MD; Bernd Waldecker, MD; Edward J. Ciaccio, PhD; Andrew L. Wit, PhD; ; James Coromilas, MD

From the Departments of Pharmacology and Medicine, College of Physicians and Surgeons, Columbia University, New York, NY.

Correspondence to James Coromilas, MD, Department of Medicine, Columbia University, College of Physicians and Surgeons, 630 W 168 St, New York, NY 10032.

Background Sustained reentrant ventricular tachycardias (VTs) with different QRS morphologies have been observed to occur spontaneously and during programmed stimulation in human hearts. We determined mechanisms that can cause tachycardias with multiple morphologies in a canine model of myocardial infarction by mapping reentrant circuits.

Methods and Results Reentrant VT with multiple QRS morphologies was induced in 11 canine hearts with 4-day-old infarcts. Comparison of activation maps of the reentrant circuits in the epicardial border zone associated with each morphology indicated two basic mechanisms. Less frequently, VTs of different morphologies in the same heart were caused by reentrant circuits in different regions of the infarct. Most commonly, the reentrant circuits associated with different morphologies were in the same region. Three different factors caused different exit routes from circuits in the same region, leading to the multiple morphologies. (1) The reentrant wave front for each morphology rotated around the same line of block but in different directions. (2) Reentrant circuits associated with each morphology were similar, but there were small changes in the extent of the central line of block. (3) Reentrant circuits with completely different sizes and shapes caused different morphologies.

Conclusions In this canine model, tachycardias with multiple morphologies most commonly arise from reentrant circuits in the same region of the infarct, suggesting that most often only one area has electrophysiological properties necessary to sustain reentry.

Key Words: tachycardia • reentry • anisotropy • mapping

This article has been cited by other articles:

				D. J. Milan and C. A. MacRae Animal models for arrhythmias Cardiovasc Res, August 15, 2005; 67(3): 426 - 437. [Abstract] [Full Text] [PDF]

				L. Szumowski, P. Sanders, F. Walczak, M. Hocini, P. Jais, R. Kepski, E. Szufladowicz, P. Urbanek, P. Derejko, R. Bodalski, et al. Mapping and ablation of polymorphic ventricular tachycardia after myocardial infarction J. Am. Coll. Cardiol., October 19, 2004; 44(8): 1700 - 1706. [Abstract] [Full Text] [PDF]

				P. Della Bella, S. Riva, G. Fassini, F. Giraldi, M. Berti, C. Klersy, and N. Trevisi Incidence and significance of pleomorphism in patients with postmyocardial infarction ventricular tachycardia: Acute and long-term outcome of radiofrequency catheter ablation Eur. Heart J., July 1, 2004; 25(13): 1127 - 1138. [Abstract] [Full Text] [PDF]

				K. Soejima, W. G. Stevenson, W. H. Maisel, J. L. Sapp, and L. M. Epstein Electrically Unexcitable Scar Mapping Based on Pacing Threshold for Identification of the Reentry Circuit Isthmus: Feasibility for Guiding Ventricular Tachycardia Ablation Circulation, September 24, 2002; 106(13): 1678 - 1683. [Abstract] [Full Text] [PDF]

				J. Coromilas, C. Costeas, B. Deruyter, S. M. Dillon, N. S. Peters, and A. L. Wit Effects of Pinacidil on Electrophysiological Properties of Epicardial Border Zone of Healing Canine Infarcts: Possible Effects of KATP Channel Activation Circulation, May 14, 2002; 105(19): 2309 - 2317. [Abstract] [Full Text] [PDF]

				D. E. Gutstein, G. E. Morley, H. Tamaddon, D. Vaidya, M. D. Schneider, J. Chen, K. R. Chien, H. Stuhlmann, and G. I. Fishman Conduction Slowing and Sudden Arrhythmic Death in Mice With Cardiac-Restricted Inactivation of Connexin43 Circ. Res., February 16, 2001; 88(3): 333 - 339. [Abstract] [Full Text] [PDF]

				C. Cabo, H. Schmitt, G. Masters, J. Coromilas, A. L. Wit, and M. M. Scheinman Location of Diastolic Potentials in Reentrant Circuits Causing Sustained Ventricular Tachycardia in the Infarcted Canine Heart : Relationship to Predicted Critical Ablation Sites Circulation, December 8, 1998; 98(23): 2598 - 2607. [Abstract] [Full Text] [PDF]