This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Bardy, G. H. Articles by Ideker, R. E. Search for Related Content PubMed PubMed Citation Articles by Bardy, G. H. Articles by Ideker, R. E.

Circulation, Vol 67, 52-59, Copyright © 1983 by American Heart Association

ARTICLES

A mechanism of torsades de pointes in a canine model

GH Bardy, RM Ungerleider, WM Smith and RE Ideker

A dog model of torsades de pointes (TdP) was developed. Twenty 18-30-kg dogs had cardiopulmonary bypass instituted to maintain stable temperature, perfusion pressure and oxygenation. Quinidine, 30 mg/kg, was then administered and burst ventricular pacing was used to induce arrhythmias. The left anterior descending coronary artery was occluded for 15 minutes and repeat pacing studies were performed. Maps of epicardial activation were made from 27 simultaneously recorded electrograms obtained from 1-mm bipolar electrodes secured to the epicardium with a nylon mesh sock. Arrhythmias in five dogs met criteria for the diagnosis of TdP: All had the characteristic undulating QRS morphology typically associated with TdP, all occurred in the setting of QT prolongation and all ended spontaneously. The epicardial maps demonstrated that each change in QRS morphology was associated with a change in the site of epicardial breakthrough. Those QRS complexes during the transition from one morphology to the next were associated with fusion cycles in which both the old and new sites of epicardial breakthrough were present. In essence, two or more competing activation sequences were vying for control of epicardial depolarization. This conclusion was strengthened by our ability to simulate TdP in the surface ECG and in epicardial maps by simultaneously pacing from two widely separated ventricular sites at slightly different, varying rates.

This article has been cited by other articles:

				L. Eckardt, W. Haverkamp, M. Borggrefe, and G. Breithardt Experimental models of torsade de pointes Cardiovasc Res, July 1, 1998; 39(1): 178 - 193. [Abstract] [Full Text] [PDF]

				S. Nattel Experimental evidence for proarrhythmic mechanisms of antiarrhythmic drugs Cardiovasc Res, March 1, 1998; 37(3): 567 - 577. [Abstract] [Full Text] [PDF]

				R. A. Gray, J. Jalife, A. Panfilov, W. T. Baxter, C. Cabo, J. M. Davidenko, and A. M. Pertsov Nonstationary Vortexlike Reentrant Activity as a Mechanism of Polymorphic Ventricular Tachycardia in the Isolated Rabbit Heart Circulation, May 1, 1995; 91(9): 2454 - 2469. [Abstract] [Full Text]

				M. A. Vos, S. C. Verduyn, A. P.M. Gorgels, G. C. Lipcsei, and H. J.J. Wellens Reproducible Induction of Early Afterdepolarizations and Torsade de Pointes Arrhythmias by d-Sotalol and Pacing in Dogs With Chronic Atrioventricular Block Circulation, February 1, 1995; 91(3): 864 - 872. [Abstract] [Full Text]