Bundle branch reentrant ventricular tachycardia in a patient with complete heart block and no ventricular escape

Bundle branch reentrant ventricular tachycardia (BBRVT) is a form of macroreentry using the cardiac conduction system to produce a ventricular tachycardia (VT) circuit. The most common form of bundle branch reentry involves antegrade conduction over the right bundle branch and retrograde conduction over the left bundle branch. This typically results in a left bundle branch block (LBBB) pattern electrocardiogram with rates in the 200 beats/min range, often resulting in syncope or sudden cardiac arrest. Radiofrequency catheter ablation of the right bundle branch has been recommended as first-line therapy, given the high potential for curative success and the relative infectiveness of antiarrhythmic therapy in this condition.^, In the largest cohort of patients having undergone catheter ablation for BBRVT, over 8 years of follow-up no recurrences of BBRVT were reported.

Establishing the diagnosis of BBRVT during an electrophysiologic study typically relies on (1) identifying a His (H) or right bundle branch potential (RB) preceding ventricular activation, (2) an H-V interval during tachycardia that is usually longer than that in sinus rhythm, (3) changes in the H-H interval or RB-RB interval preceding changes in the V-V interval during tachycardia, and ventricular entrainment from the RV apex.^, Thus, it can be challenging to confirm a diagnosis in patients with baseline complete atrioventricular (AV) block who do not have an intrinsic sinus H-V interval. Here, we report a case of successful diagnosis and catheter ablation of BBRVT in a patient with previous AV node ablation without ventricular escape.

A 78 year old male patient with a history of nonischemic cardiomyopathy with ejection fraction <20%, biventricular pacemaker defibrillator, prior episodes of VT on chronic amiodarone, permanent atrial fibrillation with AV nodal ablation performed 4 months prior to admission at an outside hospital presented with syncope. He reported several other episodes of syncope in the days leading up to his presentation. An interrogation of his device showed 5 episodes of monomorphic VT typically initiated with a premature ventricular contraction and with a cycle length in the 290–310 ms range (Figure 1A). The first 4 episodes were successfully treated with antitachycardia pacing (ATP). The fifth episode required defibrillation after an unsuccessful attempt at ATP. Review of his event history showed he was having 3–4 episodes of VT per month treated with ATP. Further review of the failed ATP therapy showed a postpacing interval of 410 ms with tachycardia cycle length of 300 ms and difference of 110 ms, indicating relatively close proximity of the defibrillator lead to the tachycardia circuit (Figure 1B). He was referred to the electrophysiology service for catheter ablation of VT given recurrent VT despite amiodarone therapy. Cardiac magnetic resonance imaging demonstrated diffuse subendocardial late gadolinium enhancement in a non-coronary artery disease pattern.

An electrophysiology study was performed using a Decanav decapolar catheter along the right ventricular (RV) basal to mid septum, PentaRay NAV multielectrode mapping catheter for voltage mapping, and a ThermoCool SmartTouch SF Bi-Directional Catheter for ablation (all Biosense Webster, Irving, CA). A fluoroless ablation workflow was used with intracardiac echocardiography and CartoSound 3D electroanatomic mapping (Biosense Webster). The patient was found to be completely dependent on ventricular pacing with no intrinsic ventricular conduction. The device was reprogrammed to left ventricular pacing only to allow for uniform ventricular activation. Programmed stimulation from the RV apex at 600/280/320 ms led to induction of VT with cycle length of 294 ms. The VT had an LBBB pattern with superior axis and late transition at V₆, seeming more suggestive of an RV free wall exit (Figure 1C). The patient did not tolerate VT and so was cardioverted back to a paced rhythm. Given the LBBB VT morphology and underlying nonischemic cardiomyopathy, BBRVT was in the differential diagnosis. The RV decapolar catheter was retracted to the anatomic region of RB. The RV was then mapped, with evidence of minimal basal septal scar on voltage mapping. During mapping, the patient again went into VT requiring cardioversion. There was evidence of mid-diastolic potentials on the RV decapolar catheter, likely consistent with an RB potential given the discrete, short-duration electrogram not consistent with myocardial conduction (Figure 2A). There was no change in electrogram morphology/fractionation, with different pacing wavefronts also favoring a true RB potential. Given the underlying AV block, a conducted RB potential could not be obtained for comparison. However, during RV pacing a similar potential could be seen without any associated atrial signal, further suggestive of an RB potential (Figure 3). This was owing to either retrograde conduction into the RB with pacing or via trans-septal conduction going retrograde within the left bundle and ultimately antegrade conduction into the RB, leading to the potential recorded. With ventricular stimulation, the potential could be discretely discerned with progressive delay before block. During VT, changes in the RB-RB interval were noted to precede changes in the V-V interval, implicating participation of the right bundle branch in the tachycardia circuit (Figure 2B). Entrainment from the RV apex could not be performed owing to the immediate hemodynamic instability. The RB potential was targeted for ablation at 40 W (Figure 3). Postablation, VT was no longer inducible down to RV effective refractory period with double extrastimuli. The patient tolerated the remainder of the study and was subsequently discharged home in stable condition. At 6 months follow-up postablation, the patient remained free of any device therapies or clinical VT recurrence.

BBRVT remains a significant and likely under-recognized etiology of VT in patients with and without structural heart disease. Recent cohort data found that among patients with structural disease who had undergone ablation and had non-scar/Purkinje-VT, BBRVT was attributed in 28 out of 37 cases. Ablation is recommended as first-line therapy in these patients, with a demonstrated high success rate of freedom from recurrence.^, The current paradigm of diagnosing BBRVT relies on the demonstration of an H-V interval that is often longer during tachycardia than in sinus rhythm. This, however, represents a challenge in patients with underlying AV block in whom sinus H-V measurements and intrinsic RB potential identification are no longer feasible. In this case, we demonstrate a successful ablation of BBRVT in such a patient. The diagnosis of BBRVT was achieved by demonstrating a discrete RB potential with variations in the RB-RB interval preceding any changes in the V-V interval. Targeted ablation of the RB potential led to noninducibility of VT and no clinical recurrence at 6 months of follow-up.

This case demonstrates that successful diagnosis and ablation of BBRVT is achievable in patients with underlying AV block and the diagnosis of BBRVT may not necessitate an intrinsic RB potential or HV interval.

BBRVT remains an important cause of clinical VT, with ablation providing curative therapy. Underlying AV block poses a diagnostic challenge; however, a diagnosis and successful ablation may still be achieved via successful identification of a bundle potential with demonstrated RB-RB interval variations preceding V-V interval changes.