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

Akhtar, Masood; Damato, Anthony N.; Batsford, William P.; Ruskin, Jeremy N.; Ogunkelu, J. Bimbola; Vargas, Guillermo

doi:10.1161/01.cir.50.6.1150

Cited by 210 publications

(35 citation statements)

References 30 publications

(1 reference statement)

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“…However, in all instances, the retrograde His bundle deflection (H2) emerged from the local V2 electrogram as the S1S2 interval was shortened, and there were measurable and progressive retrograde delays in the His-Purkinje system (S2H2). In three patients, an S3 (patients 5, 11, and 15), and in only one patient (patient 1 (Table 4). As indicated above, another QRS morphology with a typical right bundle branch block appearance was also observed in three patients.…”

Section: Tachycardia Initiationmentioning

confidence: 99%

Sustained bundle branch reentry as a mechanism of clinical tachycardia.

et al. 1989

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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.

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Section: Tachycardia Initiationmentioning

confidence: 99%

Sustained bundle branch reentry as a mechanism of clinical tachycardia.

et al. 1989

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“…It too represents bundle branch reentry, but with an activation sequence opposite to that of the classic laboratory-induced type. [17][18][19] In other figure 3). Both the accessory pathway (AP) and normal pathway are depicted.…”

Section: Resultsmentioning

confidence: 91%

Linking: a dynamic electrophysiologic phenomenon in macroreentry circuits.

Lehmann¹,

Denker²,

Mahmud³

et al. 1985

Circulation

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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.

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“…Macroreentry HPS (12,13). 10 of the 14 cases (3-9, 11, 13, and 14, Table I) demonstrated occurrence of macroreentry HPS in the form of V3 following retrograde H2 activation.…”

Section: Methodsmentioning

confidence: 92%

“…Despite the above reasoning, questions can be raised as to whether the V2 might still have blocked in the AV node rather than HPS, and whether the H2 deflection was either not identifiable for some reason or was obscured by the local V2 electrogram. These questions can be dismissed for the following reasons: (a) Once the retrograde H2 deflection emerges, the V2H2 intervals generally lengthen (rather than shorten) at shorter V1V2 (9,12,14,15). (b) The occurrence of gap phenomenon in most cases suggests retrograde H2 was recordable whenever the His bundle was depolarized.…”

Section: Discussionmentioning

confidence: 99%

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

Akhtar¹,

Shenasa²,

Schmidt³

1981

J. Clin. Invest.

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A B S T R A C T The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V2 method) were analyzed in 14 consecutive patients with Wolff-Parkinson-White Syndrome in whom the PSVT was inducible during retrograde refractory period studies. 9 patients had left-sided and the remaining 5 of 14 had right-sided ventriculo-atrial (VA) accessory pathway (AP). At the basic cycle lengths (V,V1) ranging from 550 to 900 ms (mean, 657.1+139.5), closely coupled V2 (mean V,V2, 357.3+59.2 ms, range 320-500) produced retrograde His bundle (H2) activation via the bundle branches and retrograde atrial (A2) activation via the AP. As the V1V2 were further shortened, the V2 showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A2 impulse conducted anterograde over the atrioventricular node-HPS to initiate a PSVT or an atrial echo response in all nine cases. In none of the patients was a PSVT induced by V2 when the latter produced retrograde H2 activation via the bundle branches. In 10 of 14 cases, however, the retrograde H2 was followed by a V3, due to macroreentry in the HPS. The V3 in turn blocked retrogradely in the HPS while producing A3 via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V2 and/or V3 in the HPS resulted in PSVT initiation in 13 of 14 cases, whereas in the remaining 1 case the exact mechanism was not clear. In none ofthe patients in this series was the PSVT initiated with a retrograde block of

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

Cited by 210 publications

References 30 publications

Sustained bundle branch reentry as a mechanism of clinical tachycardia.

Sustained bundle branch reentry as a mechanism of clinical tachycardia.

Linking: a dynamic electrophysiologic phenomenon in macroreentry circuits.

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

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