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 <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< 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 amenable 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. (Circulation 1989;79:256-270) M acroreentry within the His-Purkinje system commonly referred to as bundle branch reentry (BBR) is a frequently observed phenomenon in the laboratory.1-3Although scattered cases of sustained BBR tachycardia have been reported, no large series dealing with this phenomenon exists in the literature.4-11 The incidence of BBR as a mechanism of sustained ventricular tachycardia (VT), therefore, continues to be underreported in the literature, and consequently, there is less awareness of sustained BBR tachycardia as a significant clinical arrhythmia.

Ibutilide is a useful and safe treatment alternative for the atrial arrhythmias that occur after cardiac surgery.

The present study describes the clinical and electrophysiological characteristics of sustained bundle branch reentrant ventricular tachycardia treated with electrical ablation of the right bundle branch. Seven patients presented with syncopal episodes, and six of the seven had documented episodes of ventricular tachycardia. All

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The term "linking" has been used specifically to describe the mechanism for perpetuation of functional anterograde bundle branch block: namely, repetitive transseptal retrograde concealed penetration by impulses propagating along the contralateral bundle. We present selected examples that demonstrate that linking-type phenomena actually have a wide spectrum of expression in human macroreentry circuits, particularly those incorporating either the bundle branches and His bundle or the normal pathway and Kent bundle. The examples presented are as follows: (1) Circulation 71, No. 2, 254-265, 1985.

Cardiac electrophysiologic studies (EPS) with programmed electrical stimulation (PES) were performed in 30 patients with recurrent syncope to uncover possible arrhythmic etiology. All patients had undergone thorough medical and neurologic evaluation prior to EPS without finding a definitive cause for syncope. In the majority of patients an arrhythmic etiology for syncope was suspected but could not be documented utilizing the 12-lead surface ECG, extended in-hospital and/or ambulatory monitoring (for greater than or equal to 48 hours) and exercise testing prior to the EPS. The studies provided a clue to the possible underlying rhythm disturbance which could have caused syncope in 16/30 patients. Sustained or nonsustained ventricular tachycardia and/or ventricular fibrillation was induced in 11/30, sinus node dysfunction in 4/30 and intra-His block in the remaining one. Fourteen of the 16 have remained free of symptoms following therapy based on results of EPS during a follow-up period ranging from 6-30 months (mean 16.5 +/- 7.8). In 2/16 syncope recurred (one arrhythmic and one non-arrhythmic) despite pacemaker therapy for sinus node dysfunction detected during EPS. In the remaining 14/30 patients, EPS and PES did not induce arrhythmia which could account for patient symptomatology and therefore no specific therapy could be recommended. Eleven of these 14 patients experienced a recurrence of symptoms within a 6-25 month period (mean 16.2 +/- 6.8). Of the 16 patients with inducible arrhythmias considered clinically significant, 15 had associated structural heart disease. On the other hand, of the 14 patients without clinically significant arrhythmias, structural heart disease could be detected in only three. It is concluded that cardiac arrhythmias constitute a common cause of unexplained syncope, particularly in patients with structural heart disease, and that EPS with PES can uncover the type of arrhythmic disturbance in a significant number of cases.

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SUMMARY Animal studies have suggested that spontaneous or programmed ventricular beats that occur simultaneously with atrial activation may facilitate atrioventricular (AV) nodal conduction during subsequent atrial impulses. However, this possibility has not been systematically studied in the human heart. In the present study the AV nodal conduction during a programmed atrial premature beat (S2) was analyzed.The S2 was delivered after a series of atrial drive beats (SjSj) of constant duration; this was termed stimulation method I. The results were compared with stimulation method II, which was similar to method I except that a single ventricular beat (Vs) was introduced simultaneously with the last Sl. The longest and shortest possible paced atrial cycle lengths (CLs) were scanned during both methods. Twenty-six patients were studied: 14 with a normal PR and normal intraventricular conduction (NIVC), four with first-degree AV nodal block and NIVC, three with a complete left bundle branch block (LBBB) pattern, three with a complete right bundle branch block (RBBB) pattern, and two with an incomplete RBBB pattern.At the same SlS2 intervals, the AV nodal conduction times (S2112 intervals) were consistently shorter with method II than with method I except in three patients, two with complete RBBB and one with complete LBBB. The magnitude of S2H2 shortening with method II was more pronounced at the shorter basic CLs and shorter SlS2 intervals. During method I, the effective refractory period (ERP) of the AV node was measured in 13 patients, eight with NIVC and five with preexisting bundle branch block. With method II, the ERP of the AV node shortened in all but three patients (one with complete RBBB, one with incomplete RBBB and one with complete LBBB pattern), in whom this variable did not change. The findings suggest that intranodal collison from antegrade and retrograde impulses facilitates AV nodal conduction and shortens the ERP. The magnitude of this change is greater at shorter atrial CLs and is probably related to deeper intranodal penetration of a Vs. The shortening in AV nodal conduction and refractoriness is not noted in patients with bundle branch block when retrograde conduction delay or block in the bundle branches coexists with the antegrade counterpart producing delayed or ineffective input of Vs into the AV node.ATRIOVENTRICULAR (AV) nodal conduction and refractoriness in the antegrade direction have been extensively investigated in both animals and man.'-'0 Although several studies have addressed the effects of programmed ventricular premature stimulation on subsequent AV nodal conduction in animals,9' 11 rarely has such a study been carried out systematically in the human heart. This study was designed to examine the effect of simultaneous AV stimulation on the functional properties of the AV node in man. Patients and MethodsTwenty-six patients ( ously introduced through the femoral and antecubital veins and were positioned under fluoroscopic guidance, in the region of the tricuspid valve to permit...