Adenosine‐Sensitive Bundle Branch Reentry

Rubenstein, Donald S.; Burke, Martin C.; Kall, John G.; Kinder, Charles; Kopp, Douglas E.; Wilber, David J.

doi:10.1111/j.1540-8167.1997.tb00612.x

Cited by 13 publications

(6 citation statements)

References 26 publications

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“…The effect of adenosine on these tachycardias has not been systematically studied, although adenosine is generally not believed to influence conduction in the His–Purkinje system. Nonetheless, there is at least 1 report of BBR VT induced during isoproterenol infusion that reproducibly terminated with adenosine 4 . Finally, the echocardiographic findings are compatible with all 3 tachycardias.…”

Section: Commentarymentioning

confidence: 70%

“…Nonetheless, there is at least 1 report of BBR VT induced during isoproterenol infusion that reproducibly terminated with adenosine. 4 Finally, the echocardiographic findings are compatible with all 3 tachycardias. While often associated with dilated cardiomyopathy, BBR VT has occasionally been reported in the setting of isolated conduction system disease with no apparent structural heart abnormalities.…”

Section: Commentarymentioning

confidence: 77%

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Tachycardia With Typical Left Bundle Branch Block Morphology and VA Block: What is the Differential Diagnosis?

Zarraga

MacMurdy

Raitt

2010

Journal of Cardiovascular Electrophysiology

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A 63-year-old man developed left bundle branch block (LBBB) several hours after percutaneous coronary intervention of the left anterior descending artery for a non-STsegment elevation myocardial infarction (Figs. 1A and B). Echocardiography revealed a normal left ventricular size, with an ejection fraction of 40%. After developing LBBB, he began experiencing recurrent sustained, but hemodynamically tolerated, wide-complex tachycardia, initiated by either atrial or ventricular premature complexes (Fig. 1C). On one occasion, the tachycardia persisted for over an hour and was terminated with intravenous adenosine. What is the differential diagnosis for this wide-complex tachycardia, and what findings and maneuvers can help differentiate one mechanism from the other in the electrophysiology laboratory? CommentaryThe tachycardia had an LBBB morphology that was identical to that seen during sinus rhythm, suggesting that this was a supraventricular tachycardia (SVT) with aberrancy. At the same time, VA Wenckebach was present (most evident in the inferior leads), indicating that the atria were not required for perpetuation of the tachycardia and suggesting that this was ventricular tachycardia (VT). The differential diagnosis for an SVT that would not require the atria and have a typical LBBB morphology is limited and includes (a) aberrantly conducted AV nodal reentrant tachycardia (AVNRT) with an upper common pathway, (b) aberrantly conducted orthodromic reciprocating tachycardia (ORT) utilizing a concealed nodofascicular or nodoventricular bypass tract, (c) aberrantly conducted nonreentrant junctional tachycardia (JT), (d) aberrantly conducted intra-Hisian reentry, and (e) antidromic reciprocating tachycardia utilizing a nodofascicular bypass tract. On the other hand, if this were VT, the differential diagnosis would include (a) bundle branch reentrant (BBR) VT utilizing the right and left bundle branches for its anterograde and retrograde limbs, respectively, and (b) intramyocardial VT originating or exiting near the exit of the right bundle branch.Interestingly, a few hours prior to the electrophysiologic study, the LBBB resolved completely, and since that time no more spontaneous runs of the wide-complex tachycardia were observed. In the electrophysiologic study, the atrial-His and His-ventricular (HV) intervals were 80 and 55 ms, respectively. There was no evidence of dual AV nodal physiology or AV accessory pathway. A wide-complex tachycardia similar to his spontaneous tachycardia was reproducibly induced with double atrial extrastimuli. It had an average cycle length of 400 ms (range: 350-450 ms) and typical LBBB morphology, and demonstrated both VA Wenckebach and 2:1 VA block. Induction of the tachycardia only occurred when the atrial extrastimuli conducted with LBBB and produced some HV prolongation (Fig. 2). During the tachycardia, there was a His bundle potential preceding every QRS complex, and the HV interval (48-50 ms) was consistently shorter than the HV interval produced by any of the atrially conducted ...

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Section: Commentarymentioning

confidence: 70%

Section: Commentarymentioning

confidence: 77%

Tachycardia With Typical Left Bundle Branch Block Morphology and VA Block: What is the Differential Diagnosis?

Zarraga

MacMurdy

Raitt

2010

Journal of Cardiovascular Electrophysiology

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“…In another case study, BBRT with no structural heart disease was reproducibly terminated by intravenous adenosine (35). During an electrophysiology study, BBRT was repeatedly initiated by isoproterenol infusion, suggesting that it originated from triggered activity (35). Schafferhofer-Steltzer et al (37) have also shown how to induce EADs in Purkinje fibers by locally superfusing them with isoproterenol solution.…”

Section: Arrhythmia Induction By Triggered Activitymentioning

confidence: 96%

“…Nicorandil was found to abolish VT arising from afterpolarizations in long-QT syndrome. In another case study, BBRT with no structural heart disease was reproducibly terminated by intravenous adenosine (35). During an electrophysiology study, BBRT was repeatedly initiated by isoproterenol infusion, suggesting that it originated from triggered activity (35).…”

Section: Arrhythmia Induction By Triggered Activitymentioning

confidence: 98%

Arrhythmogenesis by single ectopic beats originating in the Purkinje system

Deo

Boyle

Kim

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Cells in the Purkinje system (PS) are known to be more vulnerable than ventricular myocytes to secondary excitations during the action potential (AP) plateau or repolarization phases, known as early afterdepolarizations (EADs). Since myocytes have a lower intrinsic AP duration than the PS cells to which they are coupled, EADs occurring in distal branches of the PS are more likely to result in propagating ectopic beats. In this study, we use a computer model of the rabbit ventricles and PS to investigate the consequences of EADs occurring at different times and places in the cardiac conduction system. We quantify the role of tissue conductivity and excitability, as well as interaction with sinus excitation, in determining whether an EAD-induced ectopic beat will establish reentrant activity. We demonstrate how a single ectopic beat arising from an EAD in the distal PS can give rise to reentrant arrhythmia; in contrast, EADs in the proximal PS were unable to initiate reentry. Clinical studies have established the PS as a potential substrate for reentry, but the underlying mechanisms of these types of disorder are not well understood, nor are conditions leading to their development clearly defined; this work provides new insights into the role of the PS in such circumstances. Our findings indicate that simulated EADs in the distal PS can induce premature beats, which can lead to the tachycardias involving the conduction system due to interactions with sinus activity or impaired myocardial conduction velocity.

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“…BBRVT is the only one of these clinical entities that usually exhibits no response to adenosine [36] . Although administration of adenosine may occasionally result in VA dissociation during hemodynamically stable VT, it should be noted that BBRVT is usually rapid and hemodynamically unstable, making DC cardioversion the initial option of choice.…”

Section: Diagnostic and Acute Therapeutic Maneuversmentioning

confidence: 99%

Differential diagnosis of tachycardia with a typical left bundle branch block morphology

Neiger¹

2011

WJC

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The evaluation of wide QRS complex tachycardias (WCT) remains a common dilemma for clinicians. Numerous algorithms exist to aid in arriving at the correct diagnosis. Unfortunately, these algorithms are difficult to remember, and overreliance on them may prevent cardiologists from understanding the mechanisms underlying these arrhythmias. One distinct subcategory of WCTs are those that present with a "typical" or "classic" left bundle branch block pattern. These tachycardias may be supraventricular or ventricular in origin and arise from functional or fixed aberrancy, bystander or participating atriofascicular pre-excitation, and bundle branch reentry. This review will describe these arrhythmias, illustrate their mechanisms, and discuss their clinical features and treatment strategies.

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Adenosine‐Sensitive Bundle Branch Reentry

Abstract: Patients with ventricular tachycardia involving a bundle branch reentrant circuit may be sensitive to adenosine. These results suggest that adenosine may not only inhibit catecholamine-mediated triggered activity but also some catecholamine-mediated reentrant ventricular arrhythmias.

Cited by 13 publications

References 26 publications

Tachycardia With Typical Left Bundle Branch Block Morphology and VA Block: What is the Differential Diagnosis?

Tachycardia With Typical Left Bundle Branch Block Morphology and VA Block: What is the Differential Diagnosis?

Arrhythmogenesis by single ectopic beats originating in the Purkinje system

Differential diagnosis of tachycardia with a typical left bundle branch block morphology

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