Bundle branch reentrant ventricular tachycardia

Pathophysiology

Bundle branch reentrant (BBR) ventricular tachycardia (VT) is a reentrant VT with a well-defined macroreentry circuit, incorporating the right bundle branch (RB) and left bundle branch (LB) as obligatory limbs of the circuit, connected proximally by the His bundle (HB) and distally by the ventricular septal myocardium ( Fig. 30.1 ). The QRS during BBR VT can display either left bundle branch block (LBBB) or right bundle branch block (RBBB) when anterograde ventricular activation occurs over the RB or LB, respectively. The vast majority of BBR VTs exhibit LBBB configuration (“counterclockwise” BBR), whereby the reentrant wavefront propagates anterogradely down the RB, crosses the septum, and then travels retrogradely up the LB. In clockwise BBR, the reentrant wavefront propagates in the opposite direction, and ventricular activation occurs via anterograde conduction over the LB, resulting in an RBBB configuration.

Single BBR beats can be induced in up to 50% of patients with normal intraventricular conduction undergoing electrophysiological (EP) study. The QRS during BBR typically exhibits an LBBB pattern, although an RBBB pattern (clockwise BBR) can rarely be induced by right ventricular (RV) pacing; the latter condition requires that the effective refractory period of the LB be longer than that of the RB, or that retrograde conduction over the RB be resumed after an initial bilateral block in the His-Purkinje system (HPS) (i.e., gap phenomenon). Left ventricular (LV) pacing does not seem to increase the yield of induction of BBR with RBBB morphology.

In patients with normal intraventricular conduction, BBR is a self-limiting phenomenon. The rapid conduction and long refractory period of the HPS prevent sustained BBR in normal hearts. Spontaneous termination of BBR most commonly occurs in the retrograde limb between the ventricular muscle and the HB. Sometimes, anterograde block can also occur, making refractoriness in the RB-Purkinje system the limiting factor. Continuation of BBR as a tachycardia is critically dependent on the interplay between conduction velocity and recovery of the tissue ahead of the reentrant wavefront. Two changes from normal physiology must occur for BBR to become sustained: (1) an anatomically longer reentrant pathway caused by a dilated heart, providing sufficiently longer conduction time around the HPS; and (2) slow conduction in the HPS caused by HPS disease. These two factors are responsible for sufficient prolongation of conduction time to permit expiration of the refractory period of the HPS ahead of the propagating reentrant wavefront.

Rarely, self-terminating BBR can occur with a narrow QRS during ventricular extrastimulation (VES) in the setting of normal intraventricular conduction. After retrograde conduction via the left anterior fascicle (LAF) or left posterior fascicle (LPF), anterograde propagation occurs over the RB and the remaining LB fascicle, resulting in a narrow QRS with either LAF or LPF block.

Epidemiology

Sustained BBR VT usually occurs in patients with structural heart disease, especially dilated cardiomyopathy. In fact, idiopathic dilated cardiomyopathy is the anatomical substrate for BBR VT in 45% of cases, and BBR VT accounts for up to 13% to 41% of all inducible sustained VTs in this patient population. BBR VT can also be associated with cardiomyopathy secondary to valvular or ischemic heart disease and has been reported with Ebstein anomaly, hypertrophic cardiomyopathy, LV noncompaction, Brugada syndrome, muscular dystrophy, and isolated conduction system disease in the absence of structural heart disease. ^, Notably, in a recent report, 22% of the patients with BBR VT had a normal His-ventricular (HV) interval, and significant prolongation of the HV interval only developed during tachycardia, suggesting that either a functional or fixed conduction block in the HPS could be sufficient to maintain a BBR mechanism.

In patients with spontaneous sustained monomorphic VT, the incidence of inducible BBR VT ranges from 4.5% to 6% in patients with ischemic heart disease to 16.7% to 41% in patients with nonischemic cardiomyopathy. BBR VT accounts for up to 6% of all forms of induced sustained monomorphic VT. Importantly, additional myocardial VTs occur in about 25% of patients presenting with BBR VT. Of note, BBR VT is more frequently observed in patients with VT clusters (up to 12.5%) than in patients with less frequent episodes of VT. Because the incidence of BBR VT is not trivial, and since this arrhythmia is imminently curable, it is important for the electrophysiologist to consider it as a possible cause of VT.

Clinical presentation

Sustained BBR VT is typically unstable secondary to very rapid ventricular rates (often 200 to 300 beats/min) and poor underlying ventricular function. As a consequence, approximately 75% of patients present with syncope or cardiac arrest.

Initial evaluation

BBR VT should be suspected in the presence of QRS morphology during VT similar to that during normal sinus rhythm (NSR), especially in a patient with dilated cardiomyopathy. Echocardiographic examination and coronary arteriography are required in most patients to evaluate for structural heart disease.

Principles of management

Pharmacological antiarrhythmic therapy is usually ineffective for BBR VT. On the other hand, RF catheter ablation of a bundle branch (typically the RB) is very successful in eliminating BBR VT and, hence, is currently regarded as first-line therapy.

As noted, associated myocardial VT occurs in approximately 25% of patients post ablation of BBR VT, and these patients continue to be at a high risk of sudden cardiac death. Therefore, ICD therapy is indicated for secondary prevention, and additional antiarrhythmic therapy is required for some patients. ICD implantation will also provide backup pacing, which is frequently required postablation secondary to the development of atrioventricular (AV) block or an excessively prolonged HV interval. Implantation of a dual-chamber or biventricular ICD should be considered in these patients.

Because BBR VT has a limited response to antiarrhythmic drugs and can be an important cause of repetitive ICD therapies, catheter ablation of the arrhythmia should always be considered an important adjunct to the device therapy.

EP testing should be considered in patients with repetitive episodes of VT and dilated cardiomyopathy, history of cardiac valve repair or replacement, or QRS morphology during VT similar to sinus rhythm QRS. If sustained BBR VT is inducible during programmed stimulation, catheter ablation is recommended.

Electrocardiographic features

Baseline ECG

The baseline rhythm is usually NSR or atrial fibrillation. Almost all patients with BBR VT demonstrate intraventricular conduction abnormalities. The most common ECG abnormality is nonspecific intraventricular conduction disturbance (IVCD) with an LBBB pattern and PR interval prolongation ( Fig. 30.2 ). Complete RBBB is rare but does not preclude BBR as the mechanism of VT. Although total interruption of conduction in one of the bundle branches would theoretically prevent the occurrence of BBR, an ECG pattern of complete bundle branch block may not be an accurate marker of complete conduction block; a similar QRS configuration can be caused by conduction delay, rather than block, in the bundle branch. In addition, anterograde block can be present with retrograde conduction. Occasionally, complete AV block may be observed.

Electrophysiological testing