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J Am Coll Cardiol, 1993; 22:1718-1722 © 1993 by the American College of Cardiology Foundation |
Electrophysiology Laboratory, University of Wisconsin/Milwaukee Clinical Campus, Sinai Samaritan Medical Center.
OBJECTIVES. The aim of this study was to present bundle branch reentry as the mechanism of sustained ventricular tachycardia in the absence of myocardial or valvular dysfunction. BACKGROUND. Previous reports have documented the relation between structural heart disease and bundle branch reentrant ventricular tachycardia. Myocardial or valvular dysfunction has thus far been recognized as the only anatomic substrate for the development of this tachycardia. METHODS. Three patients with a wide QRS complex tachycardia underwent noninvasive and invasive cardiac evaluation and electrophysiologic studies to identify the substrate and mechanism of tachycardia. Catheter ablation of the right bundle branch using radiofrequency current was performed in each patient. RESULTS. The patients were all men (aged 54, 34 and 72 years) who presented with presyncope, palpitation and cardiac arrest, respectively. Electrocardiography during sinus rhythm revealed nonspecific intraventricular conduction delay in all three patients. Cardiac evaluation revealed no evidence of myocardial or valvular dysfunction in any patient. The baseline HV interval was prolonged in each patient (90, 100 and 75 ms, respectively). Programmed right ventricular stimulation initiated bundle branch reentrant tachycardia with typical left (three patients) and right (one patient) bundle branch block pattern. Catheter ablation of the right bundle branch using radiofrequency current abolished bundle branch reentry in all three patients. After 26-, 13- and 8-month follow-up periods, complete right bundle branch block persisted, and all three patients remained asymptomatic without antiarrhythmic drugs. CONCLUSIONS. Sustained bundle branch reentry can be a clinical arrhythmia in patients with no identifiable myocardial or valvular dysfunction except for isolated conduction abnormalities in the His-Purkinje system. This mechanism of tachycardia should be recognized during electrophysiologic evaluation, given the seriousness of this arrhythmia and the availability of the effective treatment.
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