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Sustained bundle branch reentry as a mechanism of clinical tachycardia.

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TLDR
The 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.
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.

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Journal ArticleDOI

Role of Mahaim fibers in cardiac arrhythmias in man.

TL;DR: It is postulate that the mechanism of this tachycardia is a macroreentry circuit using the NV fiber for the antegrade limb and the His-Purkinje system with a portion of the atrioventricular node for the retrograde limb.
Journal ArticleDOI

Unusual Properties of Accessory Pathways

TL;DR: Electrophysiologic evaluation in five patients who exhibited manifestations of the pre-excitation syndrome and/or supraventricular tachycardia provided functional evidence that the properties of the accessory fibers may be quite variable, and anomalies in conduction over accessory pathways were demonstrated.
Journal ArticleDOI

Demonstration of Re-entry within the His-Purkinje System in Man

TL;DR: Re-entry within the His-Purkinje system (HPS) was consistently observed in 15/24 consecutive patients in whom retrograde refractory period studies were performed using His bundle electrograms and the ventricular extrastimulus method.
Journal ArticleDOI

Transcatheter electrical ablation of right bundle branch. A method of treating macroreentrant ventricular tachycardia attributed to bundle branch reentry.

TL;DR: Right bundle branch ablation is a safe and promising means of treating ventricular tachycardia because of bundle branch reentry and can obviate the need for antiarrhythmic drug therapy and its frequent undesirable side effects.
Journal ArticleDOI

Atriofascicular connection or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reentrant circuit.

TL;DR: The upper "turn around" of the reentrant circuit involved atrial tissue and the accessory pathway originated directly from the right atrium independent of the atrioventricular node, indicating that late atrial stimuli delivered during tachycardia could preexcite the ventricle via theAccessory pathway despite their inability to enter the atrial node.
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