title: Sustained bundle branch reentry as a mechanism of clinical tachycardia.
abstract: The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.
authors.affiliation: Electrophysiology Laboratory University of Wisconsin, Sinai Samaritan Medical Center, Milwaukee 53201.
authors.forename: J
authors.initials: J
authors.lastname: Caceres
authors.forename: M
authors.initials: M
authors.lastname: Jazayeri
authors.forename: J
authors.initials: J
authors.lastname: McKinnie
authors.forename: B
authors.initials: B
authors.lastname: Avitall
authors.forename: S T
authors.initials: ST
authors.lastname: Denker
authors.forename: P
authors.initials: P
authors.lastname: Tchou
authors.forename: M
authors.initials: M
authors.lastname: Akhtar
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001696:Biomechanical Phenomena; D002036:Bundle of His / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D005500:Follow-Up Studies; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011690:Purkinje Fibers / Q000503:physiopathology*; D013617:Tachycardia, Supraventricular / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D000889:Anti-Arrhythmia Agents