Abstract
We studied the epicardial activation sequence during torsade de pointes in canine hearts with quinidine-induced long QT interval. Following a toxic dose of quinidine sulfate (30 mg/kg), polymorphic ventricular tachycardia was induced by extrastimuli. In nine dogs, 22 episodes of nonsustained polymorphic ventricular tachycardia and six episodes of monomorphic ventricular tachycardia were induced. Of 22 episodes of nonsustained polymorphic ventricular tachycardia, 12 episodes showed typical torsion of the spikes of the QRS complex around the isoelectric line (torsade de pointes). Isochronal maps were made from 38 simultaneously recorded bipolar electrograms and showed that each change in QRS morphology was associated with a change in the earliest epicardial activation site and/or a change of epicardial activation sequence. During episodes of torsade de pointes, the earliest epicardial activation site migrated gradually from one site to another site. The transitional QRS complexes had their earliest epicardial activation sites between the new and old site of the earliest epicardial activation. The changes in the earliest epicardial activation site during polymorphic ventricular tachycardia without torsade de pointes pattern was not as great as that noted during torsade de pointes. This study suggests that in a noninfarcted canine model torsade de pointes is produced by alteration in the earliest site of activation rather than by competition from two or more competing foci.
Published Version
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