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EP 101

A Tale of Two Bundle Branches: Case Reports of a Classic VT

Keywords
May 2016
1535-2226

Introduction

Bundle branches can be reliable in the best of times, but be a culprit for sustained ventricular tachycardia (VT) in the worst of times. Bundle branch reentry was first described in 1974 as a mechanism behind some isolated ventricular beats during ventricular programmed electrical stimulation (PES).1 Although isolated ventricular reentry beats involving the His-Purkinje system (HPS) can be induced in those with structurally normal hearts with normal HPS, sustained VT involving the HPS generally requires baseline disease or delay in the HPS. Bundle branch reentry ventricular tachycardia (BBRVT) is a specific type of VT involving the HPS that is common in patients with structural heart disease. It can also occur rarely in patients with no apparent structural heart disease.2 During VT, the surface ECG closely mimics classic right or left bundle branch block patterns, sometimes leading to misdiagnosis as supraventricular tachycardia with aberrant conduction. In patients with prior valve surgery or non-ischemic cardiomyopathy, up to 30-40% of sustained inducible VT can be classified as BBRVT.3-5 Baseline bundle branch patterns and intraventricular conduction delays are common in these patients. The circuit in classic BBRVT consists of anterograde conduction down the left bundle branch (LBB) and retrograde conduction back up the right bundle branch (RBB), or vice versa.6 In this first case, the VT morphology will show right bundle branch block (RBBB). In the second case, the VT morphology shows left bundle branch block (LBBB) (Figure 1). Radiofrequency ablation of the right bundle has been shown to be effective for BBRVT acutely and in long-term follow-up.7 The following two cases highlight the clinical and electrophysiologic features of this classic VT mechanism.

Case #1

A 56-year-old male with history of aortic stenosis, mechanical aortic valve replacement for severe aortic stenosis, and concurrent single-vessel coronary artery bypass graft surgery two years ago was admitted with sustained VT (Figure 2). He was symptomatic with near-syncope, and was defibrillated successfully in the emergency department. An echocardiogram was done, which showed normal left ventricular function with an ejection fraction of 60%. At baseline, he was also noted to have RBBB with QRS duration of 120 ms and intermittent infrequent LBBB with QRS duration of 150 ms. Despite intravenous amiodarone and lidocaine therapy, he continued to have recurrent sustained VT with RBBB as well as episodes of LBBB morphology VT at similar rates. 

During the EP study, quadripolar catheters were introduced into the apex of the right ventricle (RV) and the proximal AV septum. With ventricular PES from the RV apex and isoproterenol infusion, a wide complex tachycardia with cycle length of 250 ms was induced with LBBB morphology. There was VA dissociation consistent with VT. This was identical to the LBBB form of the patient’s clinical VT. With the mapping and ablation catheter detecting a RBB potential, there was evidence of retrograde block distal to the RBB prior to induction of VT (Figure 3). The retrograde limb of the VT is likely up the LBB. During VT, there is a RBB potential preceding ventricular activation suggesting anterograde conduction down the RBB. Variations in cycle length of the RBB potential precede the changes in VT cycle length. These findings are consistent with bundle branch reentry VT with anterograde limb of VT down the RBB and retrograde limb up the LBB. The RBBB morphology VT that he also demonstrated clinically was difficult to induce with PES from the RV apex. It may have been easier to induce with PES from the left ventricle. However, given the readily induced LBBB morphology BBRVT that was also clinically seen, we proceeded with empiric RBB ablation.

The distal tip of the externally irrigated ablation catheter stabilized by a steerable long sheath was positioned in the RV, where a RBB potential was detected. RF energy was applied at 35W. During ablation, the RBBB QRS became wider, transitioning from incomplete RBBB to complete RBBB. There was also intermittent complete AV block, rather than intermittent LBBB, which was noted prior to ablation. These findings suggest completion of the RBB ablation with intermittent background complete LBBB. A dual-chamber ICD was implanted post ablation. No further VT was inducible post ablation.

Case #2

A 71-year-old female with diabetes, emphysema, longstanding persistent atrial fibrillation (AF), non-ischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 22%, and history of biventricular ICD implant for baseline LBBB was admitted with recurrent ICD shocks for VT. During telemetry monitoring, she was noted to have frequent episodes of non-sustained wide complex tachycardia with morphology similar to her baseline LBBB morphology (Figure 4). She had previously been treated with amiodarone for AF, but this was discontinued a year ago due to persistent AF and thyroid toxicity. These bursts of wide complex tachycardia continued despite sotalol therapy. Anti-tachycardia pacing from her ICD was quite effective in termination of episodes. Given her symptoms of lightheadedness correlating with non-sustained episodes and sustained episodes leading to ICD shocks, an invasive EP evaluation was performed.

During the EP study, quadripolar catheters were introduced into the RV apex and the proximal septum recording a His potential. With ventricular burst pacing from the RV apex, sustained VT with cycle length of 270-290 ms was induced with LBBB morphology. A His deflection preceded every QRS complex. Variations in His-His (H-H) cycle length predicted changes in VT cycle length (Figure 5). These findings are consistent with BBRVT, with RBB as the anterograde limb and the LBB as the retrograde limb. The RBB was ablated using an externally irrigated ablation catheter stabilized by a long steerable sheath, as in the previous case. During RBB ablation, baseline LBBB transitioned to RBBB without complete AV block, suggesting that her pre-existing LBBB was incomplete. There was no further inducible VT or clinical VT by ICD interrogation in follow-up.

Discussion

These two cases illustrate a common VT mechanism in patients with baseline HPS abnormalities and valvular heart disease or non-ischemic cardiomyopathy. In the first case, although LV function was normal, the patient had a history of valve surgery and baseline incomplete RBBB with intermittent complete LBBB. This case highlights the point that BBRVT can occur in RBBB and LBBB forms within the same patient, with conduction disease in both right and left bundle branches. In the second case, the patient had non-ischemic cardiomyopathy with severe LV dysfunction and baseline LBBB and biventricular pacing. BBRVT observed in this patient was only in the LBBB form. In both cases, RF ablation of the RBB led to resolution of VT. Although BBRVT has been implicated in up to 30-40% of inducible VT in patients with non-ischemic cardiomyopathy or prior history of valvular surgery,2-4 this mechanism may be underappreciated and underreported in recent years due to early implantation of ICDs based on LVEF criteria with no further risk stratification by EP study and ventricular PES.

In both cases, ventricular PES from the RV apex induced a LBBB morphology VT by retrograde block in the RBB with slow retrograde conduction up the LBB, recovery of anterograde RBB excitability, and initiation of reentry circuit (Figure 1). The RBBB morphology form of BBRVT may be more likely to be induced with PES from the left ventricle. The key diagnostic findings in both cases are: (1) His or bundle branch deflection precedes each QRS during VT; and (2) spontaneous variations in H-H or bundle branch to bundle branch (BB-BB) predict changes in VT cycle length. The H-H or BB-BB changes preceding the corresponding ventricular cycle length (V-V) changes suggest that the HPS is driving the reentrant ventricular circuit. In both cases, ablation of the right bundle branch was effective in elimination of inducible and clinical VT.

Curative ablation required careful localization and identification of the RBB. Using a long steerable sheath, we used an externally irrigated ablation catheter, which was advanced across the tricuspid valve until a RBB potential was detected. The long steerable sheath increased the range of the ablation catheter and stabilized the catheter during ablation, allowing for improved catheter contact and more effective RF energy application. In the majority of patients, RBB ablation is effective. However, in patients with incomplete LBBB at baseline and BBRVT, LBB ablation has also been shown to be feasible in elimination of VT.8 However, in all BBRVT cases, it is important to anticipate AV block resulting from RBB ablation due to the pre-existing HPS disease. Device therapy may be necessary post ablation.

Conclusion

In patients with structural heart disease, including non-ischemic cardiomyopathies or valvular disease, and baseline HPS disease, BBRVT may be the most common mechanism leading to VT either with typical RBBB or LBBB morphology. Diagnosis is made during an EP study with induction of VT. His or BB potential precedes each QRS, and spontaneous changes in H-H or BB-BB cycle length predicts VT cycle length changes. BBRVT is frequently resistant to antiarrhythmic agents and recur despite medical therapy. In these cases, ablation of the RBB is often safe and effective. Although many of these patients may have ICDs in place due to cardiomyopathy, successful diagnosis and ablation may reduce ICD therapy. In those without pre-existing ICD/pacemakers, given underlying HPS disease, complete AV block post ablation necessitating device therapy must be anticipated. In the spirit of Charles Dickens, to recognize and successfully treat BBRVT as described in the above ‘tale of two bundle branches’, there is hope to enter the age of wisdom rather than the age of foolishness, or to enter the season of light rather than the season of darkness.

Disclosures: The authors have no conflicts of interest to report regarding the content herein.   

References

  1. Josephson ME. Clinical Cardiac Electrophysiology. Philadelphia: Lippincott Williams & Wilkins, 2002.
  2. Kusa S, Taniguchi H, Hachiya H, et al. Bundle branch reentrant ventricular tachycardia with wide and narrow QRS morphology. Circ Arrhythm Electrophysiol. 2013;6:e87-e91.
  3. Ramprakash B, Rao HB, Kalavakolanu S, Narasimhan C. Catheter ablation of bundle branch reentrant ventricular tachycardia. Heart Rhythm. 2008;5(6):S68-S72.
  4. Caceres J, Jazayeri M, McKinnie J, et al. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation. 1989;79(2):256-269.
  5. Narasimhan C, Jazayeri M, Sra J, et al. Ventricular tachycardia in valvular heart disease. Circulation. 1997;96:4307-4313.
  6. Tchou P, Mehdirad AA. Bundle branch reentry ventricular tachycardia. Pacing Clin Electrophyiol. 1995;18:1427-1437.
  7. Cohen TJ, Chien WW, Lurie KG, et al. Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: results and long-term follow-up. J Am Coll Cardiol. 1991;18(7):1767-1773.
  8. Blanck Z, Deshpande S, Jazayeri MR, et al. Catheter ablation of the left bundle branch for the treatment of sustained bundle branch reentrant ventricular tachycardia. J Cardiovasc Electrophysiol. 1995;6:40-43.

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