Core EP Topics

Bundle Branch Reentrant VT

A macroreentrant VT utilizing the His-Purkinje system — associated with structural heart disease and wide-complex tachycardia

Macroreentry His-Purkinje System Structural Heart Disease

Mechanism

Bundle branch reentrant ventricular tachycardia (BBR-VT) is a macroreentrant VT that uses the specialized His-Purkinje conduction system as its circuit. The reentrant loop consists of the right bundle branch (RBB), the left bundle branch (LBB), and the interventricular septum (ventricular myocardium connecting the terminal Purkinje fibers of each bundle). This is fundamentally different from most VTs, which utilize ventricular myocardial scar as the substrate — BBR-VT instead exploits the normal conduction system rendered abnormal by disease.

In typical (type A) BBR-VT, the wavefront conducts antegradely down the right bundle branch, crosses the interventricular septum from right to left, and returns retrogradely up the left bundle branch to the His bundle, then back down the RBB to complete the circuit. Because ventricular activation proceeds from right to left via the RBB, the QRS morphology is LBBB. In reverse (type B) BBR-VT, the circuit is reversed: antegrade conduction down the LBB, transseptal conduction left to right, and retrograde up the RBB, producing an RBBB morphology. Reverse BBR-VT is less common.

Prerequisites for BBR-VT

Diseased His-Purkinje system: slowed conduction in one or both bundle branches is required to sustain reentry (analogous to the slow pathway in AVNRT)
Prolonged HV interval (>55–60 ms) in sinus rhythm is the hallmark baseline finding
Structural heart disease: dilated cardiomyopathy (most common, ~60%), ischemic cardiomyopathy (~25%), valvular heart disease, myotonic dystrophy, Lamin A/C mutations, post-cardiac surgery
BBR-VT accounts for approximately 5–8% of all sustained monomorphic VTs referred for EP study
May coexist with scar-mediated VT in up to 30–60% of patients

The prerequisite for BBR-VT is slowed conduction in the His-Purkinje system. In the normal heart, the bundle branches conduct so rapidly (HV interval 35–55 ms) that a reentrant circuit cannot be sustained — the wavefront would return to the starting point before it has recovered from refractoriness. In patients with His-Purkinje disease (fibrosis, degeneration, or infiltration), conduction is slow enough to allow the circuit to perpetuate. This is why BBR-VT is almost exclusively seen in patients with structural heart disease and baseline conduction abnormalities.

The clinical significance of BBR-VT extends beyond the arrhythmia itself. Its presence is a marker of severely diseased His-Purkinje system and is associated with a high risk of sudden cardiac death from other mechanisms (coexisting scar-mediated VT, progressive conduction disease). This is why ICD implantation is mandatory even after successful ablation.

Clinical Pearl: Always consider BBR-VT in any patient with dilated cardiomyopathy, LBBB at baseline, and wide-complex tachycardia. It is one of the few VTs that is essentially curable with catheter ablation, but the underlying substrate (His-Purkinje disease) confers ongoing risk for other arrhythmias.

ECG Clues

The surface ECG in BBR-VT can be deceptively similar to SVT with LBBB aberrancy, making the diagnosis challenging. The key is to recognize the clinical context and subtle differences.

Typical BBR-VT — Key ECG Features

LBBB morphology (typical BBR-VT, type A)
Wide QRS >140 ms, often >160 ms
Rapid rate: 180–250 bpm — often the fastest VT a patient presents with
QRS morphology may be identical to the patient’s baseline LBBB in sinus rhythm (key differentiating point)
Inferior axis is common (left axis deviation less typical)
Poorly tolerated hemodynamically — frequently presents as syncope, pre-syncope, or cardiac arrest
AV dissociation may be present but is often difficult to identify at rapid rates

A critical diagnostic clue is that the VT QRS morphology may look identical to or very similar to the patient's native QRS in sinus rhythm. This is because BBR-VT activates the ventricles via the same His-Purkinje system that produces the baseline QRS (albeit with altered sequence). In contrast, scar-mediated VT typically produces a QRS morphology that differs substantially from sinus rhythm because it exits from the scar region and activates the ventricles myocardium-to-myocardium.

Baseline ECG Findings

The resting ECG in patients with BBR-VT typically shows evidence of His-Purkinje disease: prolonged PR interval, LBBB or bifascicular block (RBBB + LAHB or LPHB), or nonspecific intraventricular conduction delay (IVCD). These findings should heighten suspicion for BBR-VT when the patient presents with VT.

Feature	BBR-VT (Typical)	LBBB in Sinus Rhythm	SVT with LBBB Aberrancy
QRS morphology	LBBB, may match baseline	LBBB (baseline)	LBBB (aberrant)
QRS duration	>140 ms, often >160 ms	>120 ms	Varies
Rate	180–250 bpm	60–100 bpm	Depends on SVT type
AV relationship	AV dissociation or 1:1 retrograde	1:1 normal	Depends on SVT type
HV interval (EP study)	H precedes V; HV ≥ sinus HV	Often prolonged	H precedes V; HV ≤ sinus HV
Hemodynamic tolerance	Often poorly tolerated	N/A	Usually tolerated

Clinical Pearl: In a patient with dilated cardiomyopathy and LBBB at baseline who presents with a fast, wide-complex tachycardia with the same LBBB morphology, BBR-VT should be the leading diagnosis. The tachycardia rate in BBR-VT is typically much faster (180–250 bpm) than what is seen with scar-mediated VT (usually 130–200 bpm) in the same population.

EP Study Findings

The EP study is essential for diagnosing BBR-VT, as the surface ECG alone cannot reliably distinguish it from SVT with aberrancy or scar-mediated VT. The pathognomonic finding is the His bundle electrogram preceding each QRS during tachycardia.

Baseline Findings

Sinus Rhythm Findings

Prolonged HV interval (>55–60 ms) — the single most important baseline finding suggesting BBR-VT is possible; some patients have HV >80–100 ms
Prolonged AH interval is also common (diseased AV node often accompanies His-Purkinje disease)
LBBB, RBBB + LAHB, or IVCD at baseline
Infra-Hisian block may be demonstrable with atrial pacing

Diagnostic Criteria During VT

The definitive diagnosis of BBR-VT rests on demonstrating that the His-Purkinje system is an obligatory part of the tachycardia circuit:

The His Bundle — Key Diagnostic Finding

His bundle electrogram precedes each ventricular electrogram during VT
HV interval during VT ≥ HV interval in sinus rhythm — this is critical. In SVT with aberrancy, HV is ≤ sinus HV. In BBR-VT, HV is equal or longer because conduction is retrograde through the LBB, across the His bundle, and antegrade down the RBB
H-H interval predicts V-V interval: changes in H-H precede and predict changes in V-V (the His drives the ventricle, not the other way around)
Changes in RBB potential timing predict V-V changes (in typical BBR-VT)

Entrainment and Pacing Maneuvers

Entrainment pacing during BBR-VT provides critical confirmatory data:

Entrainment Criteria

Entrainment from the RV apex: overdrive pacing from the RV apex with concealed fusion confirms the RV is part of the circuit. Post-pacing interval minus TCL (PPI − TCL) ≤30 ms from the RV apex strongly supports BBR-VT
Entrainment resets both the His bundle and the tachycardia, confirming His-Purkinje involvement
Adenosine or vagal maneuvers: may terminate BBR-VT by blocking retrograde conduction through the His-AV node–LBB limb (though this is inconsistent)

An important distinction: in scar-mediated VT with LBBB morphology, a His bundle deflection may be present but it occurs after the onset of the QRS (passively activated) and does not drive the VV cycle length. In BBR-VT, the His is actively part of the circuit and always precedes the V.

Clinical Pearl: Always record from a His bundle catheter during VT mapping in patients with structural heart disease and LBBB morphology VT. Missing BBR-VT and ablating scar instead will fail to cure the patient’s clinical arrhythmia. Up to 30% of patients with BBR-VT also have coexisting scar-mediated VT, which should be evaluated after RBB ablation eliminates BBR-VT.

Ablation Targets & Strategy

Catheter ablation of BBR-VT is highly effective and conceptually straightforward: interrupt one limb of the reentrant circuit. The standard approach is right bundle branch ablation, which eliminates the antegrade limb of the circuit in typical BBR-VT.

Right Bundle Branch Ablation

The ablation catheter is advanced across the tricuspid valve and positioned on the right ventricular septum where a sharp RBB potential is recorded — typically just distal to the His bundle recording site. The RBB potential is a discrete, high-frequency deflection between the His bundle potential (proximal) and the ventricular electrogram. Radiofrequency energy is delivered at this site to ablate the right bundle branch.

Ablation Endpoints

Complete RBBB: development of new right bundle branch block on 12-lead ECG (or worsening of baseline RBBB)
Loss of RBB potential: the discrete RBB potential is no longer recordable at the ablation site
Non-inducibility: BBR-VT is no longer inducible with aggressive programmed stimulation
If baseline conduction was LBBB, post-ablation ECG may show LBBB + RBBB features (bifascicular or trifascicular pattern) or complete heart block

Why RBB and Not LBB?

The RBB is chosen because: (1) it is more accessible (right-sided approach, no need for aortic or transseptal access); (2) ablation of a single compact structure is technically simpler than ablating the fan-shaped LBB; (3) new RBBB after ablation is hemodynamically inconsequential compared to worsening LBBB. For the rare reverse BBR-VT (RBBB morphology), LBB ablation is the target, though this is technically more challenging.

Critical Warning — ICD is Mandatory: ICD implantation is required in virtually all patients with BBR-VT, even after successful ablation. The rationale is threefold: (1) BBR-VT indicates severely diseased His-Purkinje tissue with high risk for sudden death; (2) coexisting scar-mediated VT is present in 30–60% of patients and may not have been evident at the time of the BBR-VT ablation; (3) most patients have significantly reduced LVEF, which independently qualifies them for primary prevention ICD.

Conduction System Considerations

After RBB ablation, the patient may develop a more prolonged HV interval or complete heart block, particularly if the LBB is already diseased (as is common in this population). If complete heart block develops, permanent pacing is required — and with the reduced LVEF typical in these patients, cardiac resynchronization therapy (CRT-D) should be considered rather than standard RV pacing, which could worsen LV function. Even without complete heart block, close monitoring of the PR interval and HV interval is warranted post-ablation.

Special Populations

Myotonic dystrophy: BBR-VT is particularly common; progressive conduction disease means pacing needs often evolve over time
Lamin A/C cardiomyopathy: BBR-VT plus high SCD risk; ICD is Class I regardless of LVEF
Post-aortic valve surgery: surgical trauma to the His-Purkinje system can create the substrate; consider BBR-VT in any post-surgical VT
Non-ischemic DCM: the most common substrate; ablation success >95% for BBR-VT, but long-term survival is determined by the underlying cardiomyopathy

Success and Outcomes

Ablation of BBR-VT has a success rate approaching 100% for eliminating the specific arrhythmia. However, this must be understood in context: these patients have severe underlying heart disease, and the elimination of BBR-VT does not eliminate SCD risk. Long-term follow-up shows that ~30% of patients will have VT recurrence from a different mechanism (scar-mediated VT) within 5 years. All-cause mortality remains significant and is driven by heart failure progression and other arrhythmias rather than recurrent BBR-VT.

Clinical Pearl: After ablating BBR-VT, always perform thorough programmed stimulation to evaluate for inducible scar-mediated VT. If other VTs are inducible, additional ablation targeting the scar substrate should be considered. The EP study should not be considered complete once BBR-VT is eliminated — it is the beginning, not the end, of the evaluation.

Key References

Tchou P, Jazayeri M, Denker S, et al. Transcatheter electrical ablation of right bundle branch: a method of treating macroreentrant ventricular tachycardia attributed to bundle branch reentry. Circulation. 1988;78(2):246–257. DOI: 10.1161/01.CIR.78.2.246
Blanck Z, Dhala A, Deshpande S, et al. Bundle branch reentrant ventricular tachycardia: cumulative experience in 48 patients. J Cardiovasc Electrophysiol. 1993;4(3):253–262. DOI: 10.1111/j.1540-8167.1993.tb01228.x
Nogami A, Sugiyasu A, Kubota S, Kato K. Mapping and ablation of idiopathic ventricular fibrillation from the Purkinje system. Heart Rhythm. 2005;2(1):46–52. DOI: 10.1016/j.hrthm.2004.09.021
Merino JL, Carmona JR, Fernández-Lozano I, et al. Mechanisms of sustained ventricular tachycardia in myotonic dystrophy: implications for catheter ablation. Circulation. 1998;98(6):541–546. DOI: 10.1161/01.CIR.98.6.541
Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. J Am Coll Cardiol. 2018;72(14):e91–e220. DOI: 10.1016/j.jacc.2017.10.054