Abstract
Bundle branch reentrant (BBR) ventricular tachycardia (VT) is a macroreentrant VT with a well-defined reentry circuit, incorporating the right and left bundle branches as obligatory limbs of the circuit, connected proximally by the His bundle and distally by the ventricular septal myocardium. The QRS during BBR VT can display either left bundle branch block or right bundle branch block when anterograde ventricular activation occurs over the right or left bundle, respectively. The vast majority of BBR VTs exhibit left bundle branch block configuration (“counterclockwise” BBR). Interfascicular reentry incorporates the left anterior and posterior fascicles as obligatory limbs of the circuit, connected proximally by the main trunk of the left bundle and distally by the ventricular myocardium. VT secondary to interfascicular reentry is extremely rare.
Sustained BBR VT usually occurs in patients with structural heart disease, especially dilated cardiomyopathy. Sustained BBR VT is typically unstable due to the very rapid ventricular rates and poor underlying ventricular function; most patients present with syncope or cardiac arrest.
Antiarrhythmic drug therapy is usually ineffective for BBR VT. On the other hand, catheter ablation of a bundle branch (typically the right bundle) is very successful in eliminating BBR VT and hence is currently regarded as first-line therapy. Importantly, since myocardial VTs occur in approximately 25% of patients after ablation of BBR VT, these patients continue to be at a high risk of sudden cardiac death. Therefore implantable cardioverter-defibrillator therapy is indicated for secondary prevention, and additional antiarrhythmic therapy is required for some patients.
Keywords
ventricular tachycardia, bundle branch reentry, interfascicular reentry, His-Purkinje system, dilated cardiomyopathy
Outline
Pathophysiology, 897
Epidemiology, 897
Clinical Presentation, 898
Initial Evaluation, 898
Principles of Management, 898
Electrocardiographic Features, 898
Electrophysiological Testing, 898
Baseline Observations During Normal Sinus Rhythm, 898
Induction of Tachycardia, 898
Tachycardia Features, 900
Diagnostic Maneuvers During Tachycardia, 902
Exclusion of Other Arrhythmia Mechanisms, 902
Ablation, 903
Interfascicular Reentrant Ventricular Tachycardia, 905
Pathophysiology
Bundle branch reentrant (BBR) ventricular tachycardia (VT) is a reentrant VT with a well-defined reentry 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. 26.1 ). Fascicular reentry is very uncommon (see below). 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 a RBBB pattern.
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 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-limited 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. 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 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, and even in patients without structural heart disease other than intraventricular conduction abnormalities (and even normal baseline QRS configuration in rare cases).
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 found 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 is imminently curable, it is important for the electrophysiologist to consider it as a possible cause of VT.
Initial Evaluation
BBR VT should be suspected in the presence of typical QRS morphology on the surface electrocardiogram (ECG) during normal sinus rhythm (NSR) and VT (see later), 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 implantable cardioverter-defibrillator (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 post ablation secondary to the development of AV block or an excessively prolonged His bundle–ventricular (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 as 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 Electrocardiogram
The baseline rhythm is usually NSR or AF. Almost all patients with BBR VT demonstrate intraventricular conduction abnormalities. The most common ECG abnormality is nonspecific intraventricular conduction defect (IVCD) with an LBBB pattern and PR interval prolongation ( Fig. 26.2 ). 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 occurrence of BBR, an ECG pattern of complete BBB 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.
Electrocardiogram During Ventricular Tachycardia
Twelve-lead ECG documentation of BBR VT is usually unavailable because the VT is rapid and hemodynamically unstable. The VT rate is usually 200 to 300 beats/min. QRS morphology during VT is a typical BBB pattern and can be identical to that in NSR. BBR VT with an LBBB pattern is the most common VT morphology, and it usually has normal or left axis deviation (see Fig. 26.2 ). In contrast to VT of myocardial origin, BBR with an LBBB pattern characteristically shows a rapid intrinsicoid deflection in the right precordial leads, suggesting that initial ventricular activation occurs through the HPS and not ventricular muscle. BBR VT with an RBBB pattern usually has a leftward axis, but it can have a normal or rightward axis, depending on which fascicle is used for anterograde propagation.
Electrophysiological Testing
Baseline Observations During Normal Sinus Rhythm
Conduction abnormalities in the HPS are almost invariably present and are a critical prerequisite for the development of sustained BBR, regardless of the underlying anatomical substrate ( Fig. 26.3 ). The average HV interval is about 80 milliseconds (range, 60 to 110 milliseconds). Although some patients can have the HV interval in NSR within normal limits, functional HPS impairment in these patients manifests as HV interval prolongation or split HB potentials, commonly becoming evident during atrial programmed stimulation or burst pacing. Nonspecific IVCD with an LBBB pattern and PR interval prolongation are the most common abnormalities.
Induction of Tachycardia
VES from the RV apex is the usual method used to induce BBR with an LBBB pattern. Induction is consistently dependent on the achievement of a critical conduction delay in the HPS (i.e., critical ventricular–His bundle [VH] interval) following the VES.
During RV pacing at a constant PCL and during introduction of VES at relatively long coupling intervals, retrograde conduction to the HB occurs via the RB. At shorter VES coupling intervals, retrograde delay and block occur in the RB when its relative and effective refractory periods are encountered, respectively. When retrograde block occurs in the RB, the impulse propagates across the septum and retrogradely up the LB to the HB, producing a long V 2 -H 2 interval. The LB would still be capable of retrograde conduction because of its shorter refractoriness and because of the delay associated with transseptal propagation. Further shortening of the coupling intervals is associated with increasing delay in LB conduction (i.e., increasing V 2 -H 2 interval). Within a certain range of coupling intervals, increasing retrograde LB delay allows for the recovery of anterograde conduction via the RB, and another ventricular activation ensues, displaying a wide QRS with an LBBB pattern. This beat is called the “BBR beat” or “V 3 phenomenon.”
An inverse relationship exists between retrograde conduction delay in the LB (V 2 -H 2 interval) and the time of anterograde conduction in the RB (H 2 -V 3 interval). This is because the faster the impulse propagates transseptally and up the LB, the more likely it will reach the RB while it is still refractory from the previous retrograde activation (concealment) by the VES, resulting in slower anterograde conduction down the RB.
BBR is more likely to occur when the VES is delivered following pacing drives incorporating long to short CL changes as compared with constant CL drives, because of CL dependency of the HPS refractoriness. An abrupt change in CL (i.e., long to short) can result in a more distal site of retrograde block, and less concealment, along the myocardium-Purkinje-RB axis, which can allow sufficient recovery of excitability in the anterograde limb of the circuit (i.e., the RB-Purkinje-myocardium axis) for reentry to develop. In addition, earlier recovery of excitability along this axis, because of the more distal site of block and less concealment, is associated with a shorter H 2 -V 3 interval in this reentrant beat.
Procainamide (which increases conduction time within the HPS, especially in the diseased HPS), and potentially isoproterenol can facilitate induction of sustained BBR. In some patients, the arrhythmia can be inducible only with atrial pacing.
Tachycardia Features
BBR VT can only be definitively diagnosed using intracardiac recordings ( Box 26.1 ); most particularly, HB recordings are essential. Many electrophysiologists do not use a HB recording catheter during VT diagnostic studies and will thus likely miss diagnosing some cases of BBR. AV dissociation is typically present, during the tachycardia, but 1 : 1 VA conduction can occur. BBR VT is characterized by inscription of the His potential before the QRS complex, with the HV interval during BBR with LBBB pattern generally being similar to or longer than that during baseline rhythm (the HV interval is usually 55 to 160 milliseconds; see Fig. 26.3 ).
