AF-Triggered Bundle Branch Re-Entrant Ventricular Tachycardia Prevented by Atrial Fibrillation Ablation

Abstract

Background

Bundle branch re-entrant ventricular tachycardia (BBR-VT) is a macroreentrant tachycardia involving the right and left bundle branches,¹ with the right bundle branch typically targeted for ablation.

Case Summary

A 68-year-old man with prior myocardial infarction presented with recurrent ventricular tachycardia (VT). Electrophysiological study suggested BBR-VT. VT was inducible only by atrial pacing and occurred clinically exclusively during atrial fibrillation (AF). Therefore, AF ablation alone was performed, resulting in complete suppression of VT.

Discussion

Previous reports have described BBR-VT induced by atrial pacing² or AF.³ When BBR-VT is triggered exclusively by AF, AF ablation may be an effective therapeutic strategy.

Take-Home Messages

In patients with BBR-VT that is triggered exclusively by atrial fibrillation or atrial pacing, elimination of the triggering atrial arrhythmia may suppress VT without the need for bundle branch ablation. Even when AF ablation is effective, implantable cardioverter-defibrillator implantation and careful long-term follow-up remain essential because recurrence of atrial tachyarrhythmias may precipitate VT recurrence.

Visual Summary

Bundle branch re-entrant ventricular tachycardia (BBR-VT) is a macroreentrant tachycardia involving the right and left bundle branches as essential components of the reentrant circuit and accounts for 6% of inducible sustained ventricular tachycardia (VT).¹ In most reported cases, VT can be induced by ventricular stimulation, and catheter ablation of the right bundle branch (RBB) is considered the standard treatment. Although several cases of BBR-VT induced by atrial pacing² or atrial fibrillation (AF)³ have been reported, to our knowledge, this is the first report of BBR-VT induced exclusively by AF or atrial pacing in which AF ablation alone was effective in suppressing the arrhythmia.

History of Presentation

A 68-year-old man with a history of myocardial infarction and triple-vessel coronary artery disease was transferred to our hospital because of recurrent wide QRS complex tachycardia and severe heart failure with a left ventricular ejection fraction of 20%. Emergency percutaneous coronary intervention was performed, but frequent episodes of tachycardia consistently initiated by AF occurred incessantly (Figure 1A), and catheter ablation was performed.

Figure 1.

Monitor Electrocardiogram at the Onset of Wide QRS Complex Tachycardia and 12-Lead Electrocardiograms During Sinus Rhythm and Tachycardia

(A): Continuous electrocardiographic monitoring in the intensive care unit demonstrated the initiation of atrial fibrillation (AF), followed by incessant Wide QRS Complex tachycardia. (B and C): 12-lead electrocardiograms recorded during sinus rhythm (B) and during tachycardia (C). SR = sinus rhythm.

On the 12-lead electrocardiogram during sinus rhythm, the QRS complex did not fulfill the Strauss criteria for strict left bundle branch block (LBBB) and showed an intraventricular conduction delay (IVCD) pattern with a QRS complex duration of 124 ms (Figure 1B). During tachycardia, the electrocardiogram demonstrated an LBBB morphology with a QRS complex duration of 196 ms and a tachycardia cycle length of 228 ms (Figure 1C).

Past Medical History

Ulcerative colitis, hypertension, and dyslipidemia.

Differential Diagnosis

Based on the electrocardiogram findings, the differential diagnoses included VT, supraventricular tachycardia with aberrant conduction, antidromic reciprocating tachycardia, and pre-excited supraventricular tachycardia.

Investigations

During the electrophysiological study, programmed ventricular burst pacing (Figure 2A) and extrastimulus pacing (Figure 2B) from the right ventricle (RV) failed to induce tachycardia. Similar pacing from the left ventricle (LV) also failed. In contrast, programmed atrial burst pacing reproducibly induced the clinical wide QRS complex tachycardia (Figure 2C). Up to S7, RV and LV potentials conducted 1:1 (black arrow), each preceded by the RBB potential (RBP, blue arrow) and left bundle branch (LBB) potential (LBP, red arrow), respectively, with slight QRS complex widening. At S8, RV activation remained similar to the preceding RBP, whereas the LV potential became markedly delayed and the LBP appeared after the LV electrogram, both showing polarity reversal. These findings indicated development of LBBB at S8, resulting in LV activation via the RV (black dotted arrow), followed by retrograde conduction through the LBB and initiation of tachycardia. During tachycardia, ventriculoatrial dissociation and slight cycle length variability were observed, with the RBP–RBP interval determining the RV–RV interval, followed sequentially by the LBP–LBP interval (Figure 2D). Overdrive pacing from the RV apex could not be evaluated because it induced ventricular fibrillation, representing a limitation in establishing the diagnosis of BBR-VT. However, the RBP consistently preceded the ventricular electrogram, and Figure 2D demonstrates that the RBP–RBP interval drove the ventricular cycle length, indicating antegrade conduction over the RBB during tachycardia. In addition, tachycardia was induced simultaneously with the development of unidirectional block in the LBB (Figure 2C), suggesting that the LBB was not merely a bystander but an essential component of the reentrant circuit. Collectively, these electrophysiological findings strongly support the diagnosis of BBR-VT.

Figure 2.

VT Induction by Ventricular and Atrial Pacing

(A and B) Programmed ventricular burst pacing and extrastimulus pacing from the right ventricle (RV) failed to induce ventricular tachycardia (VT). (C) Intracardiac electrograms demonstrating VT induction with programmed atrial burst pacing. (D) Intracardiac electrograms during VT showing slight cycle length variation. CS = coronary sinus; d = distal; LBP = left bundle branch potential; LV = left ventricle; LVP = left ventricular potential; p = proximal; RBP = right bundle branch potential; RV = right ventricle; RVP = right ventricular potential; S = stimulation; V1-V6 = precordial leads V₁ through V₆; other abbreviations as in Figure 1.

Intracardiac electrograms recorded during atrial burst pacing, with simultaneous recordings from the His bundle and basal LBP, are shown in Figure 3A. During sinus rhythm, the atrio-His and His-ventricular intervals were 60 and 62 ms, respectively, suggesting conduction delay distal to the His bundle. Compared with sinus rhythm, the His-ventricular and His-RV intervals remained unchanged during atrial burst pacing, whereas the LBP-LV interval was prolonged. In addition, the LV potential showed marked splitting, with part of the signal becoming a delayed potential. The paced QRS complex morphology demonstrated accentuated LBBB and closely resembled that of the clinical wide QRS complex tachycardia (Figure 3B). Although tachycardia could not be induced with this catheter setup for His bundle and basal LBP recordings, these findings further supported induction of tachycardia through a unidirectional block in the LBB.

Figure 3.

Changes in His-RV and Left Bundle Branch–LV Intervals and QRS Morphology During Atrial Burst Pacing

(A and B): Intracardiac electrograms recorded during atrial burst pacing with simultaneous recordings from the His bundle and basal left bundle branch potential (LBP) (A), and the corresponding paced QRS complex morphology (B). DP = delayed potential; H = His bundle potential; other abbreviations as in Figure 2.

Management

Because the clinical episodes of VT were consistently preceded by AF, and VT was induced only by atrial pacing during the electrophysiological study, AF was considered the primary therapeutic target. Pulmonary vein isolation was performed, and because trigger premature atrial contractions originating from the left atrial posterior wall were identified, left atrial posterior wall isolation was added (Figure 4A). Following the procedure, both AF and VT were completely suppressed.

Figure 4.

AF Ablation and VT Induction During ICD Implantation

(A) Voltage map of the left atrium following atrial fibrillation ablation. (B) During transvenous implantable cardioverter-defibrillator implantation, atrial burst pacing at 180beats/min resulted in second-degree atrioventricular block (Mobitz type I, Wenckebach), and ventricular tachycardia was not inducible. RA = right atrium; other abbreviations as in previous Figures.

Outcome and Follow-Up

After optimization of guideline-directed medical therapy for heart failure, a transvenous implantable cardioverter-defibrillator (ICD) was implanted 15 days after the ablation. At that time, VT inducibility was reassessed. As during the initial electrophysiological study, VT was not inducible with ventricular stimulation. During atrial burst pacing, second-degree atrioventricular block (Mobitz type I, Wenckebach) occurred at 180 beats/min, likely because of beta-blocker therapy, and VT was no longer inducible (Figure 4B).

During the 2-year follow-up after discharge, no atrial or ventricular tachyarrhythmias were detected, and the ventricular pacing burden remained below 1%.

Discussion

Two possible mechanisms for induction of BBR-VT with an LBBB morphology can be considered.

The first mechanism is induction by ventricular pacing (Figure 5A). When retrograde conduction over the RBB is blocked, retrograde activation proceeds via the LBB. If the RBB subsequently recovers from refractoriness, antegrade conduction through the RBB becomes possible, thereby initiating the tachycardia.

Figure 5.

Schematic Representation of BBR-VT Induction

(A and B) Schematic representation of bundle branch reentrant ventricular tachycardia induction during ventricular pacing (A) and atrial pacing (B). A = atrium; LAF = left anterior fascicle; LBB = left bundle branch; LPF = left posterior fascicle; RBB = right bundle branch; V = ventricle; other abbreviations as in Figure 2.

The second mechanism is induction by atrial pacing (Figure 5B). When antegrade conduction over the LBB is blocked, ventricular activation proceeds via the RBB. If the LBB subsequently recovers from refractoriness, retrograde conduction through the LBB becomes possible, thereby initiating the tachycardia.

In the present case, VT could not be induced by either RV or LV stimulation and was induced only by AF or atrial pacing via the second mechanism. The inability to induce VT by ventricular pacing suggests that retrograde block in the RBB was unlikely to occur, whereas the intracardiac recordings demonstrated that antegrade block in the LBB readily developed during rapid atrial activation. These findings indicate that conduction impairment was more advanced in the LBB than in the RBB.

This electrophysiological profile influenced the treatment strategy. Although RBB ablation is generally effective in preventing recurrence of BBR-VT, it was considered to carry a risk of worsening atrioventricular conduction in this case because conduction impairment appeared to be more advanced in the LBB. Given the LV ejection fraction of 20%, temporary ventricular pacing dependence resulting from RBB ablation could have worsened heart failure; therefore, if needed, it was considered safer to perform the procedure after ICD implantation. In addition, preservation of the RBB may be advantageous in reducing RV pacing burden after ICD implantation. It may also be beneficial in the event that cardiac resynchronization therapy becomes necessary in the future, as it would allow fusion between LV pacing and intrinsic atrioventricular conduction. Although LBB ablation could be considered in patients with advanced LBB conduction disease, the procedure was deferred in this case because creating complete LBBB in a patient with severe heart failure was considered likely to worsen heart failure by increasing LV dyssynchrony.

Given that AF consistently preceded the clinical VT and that VT was inducible only by atrial stimulation, AF itself was considered both a trigger and a potentially modifiable substrate. AF ablation successfully suppressed both AF and VT, and neither arrhythmia recurred during 2 years of follow-up. This outcome suggests that, in selected patients with BBR-VT triggered exclusively by atrial tachyarrhythmias, treatment of the atrial arrhythmia alone may be a reasonable initial strategy.

Nevertheless, recurrence of AF or other atrial tachyarrhythmias may re-establish the conditions necessary for VT induction. Therefore, even when catheter ablation of the triggering atrial tachyarrhythmia appears to be successful, ICD implantation and careful long-term follow-up remain essential. If findings suggestive of VT recurrence emerge during follow-up, bundle branch ablation should be reconsidered. As in the present case, if beta-blocker therapy prolongs atrioventricular nodal refractoriness and VT is confirmed to be no longer inducible by atrial pacing at the time of ICD implantation, this may provide additional support for a strategy of careful follow-up without RBB ablation.

Conclusions

We report a rare case of BBR-VT that was induced exclusively by AF or atrial pacing and was successfully controlled with AF ablation alone, without bundle branch ablation. In selected patients in whom BBR-VT is consistently triggered by atrial tachyarrhythmias, elimination of the triggering atrial arrhythmia may represent an effective initial treatment strategy. Nevertheless, because recurrence of atrial tachyarrhythmias may precipitate VT recurrence, implantable cardioverter-defibrillator implantation and careful long-term follow-up remain essential.

Visual Summary.

AF and Atrial Pacing–Induced BBR-VT via Unidirectional Left Bundle Branch Block and Its Suppression by AF Ablation

A = atrium; AF = atrial fibrillation; CS = coronary sinus; H = His bundle; LAF = left anterior fascicle; LAPWI = left atrial posterior wall isolation; LBB = left bundle branch; LBBB = left bundle branch block; LBP = left bundle branch potential; LPF = left posterior fascicle; LV = left ventricle; LVP = left ventricular potential; PVI = pulmonary vein isolation; RBB = right bundle branch; RBP = right bundle branch potential; RV = right ventricle; RVP = right ventricular potential; S = stimulation; SR = sinus rhythm; V = ventricle; V_I-V₆ = precordial leads V1 through V6.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Take-Home Messages

• •In patients with bundle branch reentrant ventricular tachycardia (VT) that is triggered exclusively by atrial fibrillation or atrial pacing, elimination of the triggering atrial arrhythmia may suppress VT without the need for bundle branch ablation.
• •Even when atrial fibrillation ablation is effective, implantable cardioverter-defibrillator implantation and careful long-term follow-up remain essential because recurrence of atrial tachyarrhythmias may precipitate VT recurrence.