Bundle Branch Reentrant Tachycardia
Introduction
Bundle branch reentrant tachycardia (BBRT) (“bundle to bundle” tachycardia) is a macroreentrant ventricular tachycardia (VT) that utilizes both right bundle (RB) and left bundle (LB) branches as integral components of the reentry circuit.1 Classically, BBRT occurs in patients with severe His-Purkinje disease with a clinical triad of 1) prolonged HV interval, 2) left bundle branch block (LBBB) (or IVCD), and 3) dilated cardiomyopathy. However, it can also occur in patients with isolated (fixed or functional) His-Purkinje system disease without cardiomyopathy (e.g., myotonic dystrophy, prior aortic valve replacement).2,3,4,5 BBRT presents as syncope or cardiac arrest in 75% of patients.6
The purpose of this chapter is to:
Define the circuit and electrophysiologic features of BBRT.
Discuss mapping and ablation of the RB and LB branches.
Discuss the circuit and electrophysiologic features of interfascicular reentrant tachycardia (IFRT).
CIRCUIT
During typical BBRT, the antegrade and retrograde limbs of the circuit are the RB and LB branches, respectively, resulting in counterclockwise activation of the bundle branches (Fig. 21-1). Onset of ventricular activation occurs at the terminal branches of the RB resulting in typical LBBB QRS complexes that can appear identical to baseline LBBB (Fig. 21-2). After activating the RB, the depolarizing wavefront crosses the lower interventricular septum to retrogradely activate the LB. Following activation of the LB, the wavefront crosses the upper interventricular septum to again depolarize the RB. Sustained tachycardia requires that conduction times over each bundle exceed the refractory period of its counterpart. During atypical BBRT, the circuit is reversed and the bundle branches are activated in clockwise fashion.
ELECTROPHYSIOLOGIC FEATURES
The characteristic electrophysiologic features of typical BBRT are 1) typical LBBB QRS complexes, 2) His bundle potentials preceding QRS complexes, 3) HV(BBRT) ≥ HV(NSR), and 4) H-RB-LB activation sequence (Figs. 21-3, 21-4, 21-5 and 21-6).6 Onset of ventricular activation from the RB produces QRS complexes showing typical LBBB. His bundle potentials precede each QRS complex. Although the HV interval is a pseudo-interval (simultaneous activation of the His bundle retrogradely and RB-V antegradely), anisotropic conduction across the His-Purkinje system produces HV intervals that exceed or equal those during sinus rhythm.7 Close proximity between the upper turnaround site and the His bundle results in oscillations of the HH interval preceding and predicting oscillations in the tachycardia cycle length (TCL).8,9 However, the His bundle itself is not truly an integral part of the circuit and can rarely be dissociated from BBRT.10 In contrast to BBRT, septal VT with retrograde activation of the His bundle demonstrates shorter HV intervals during tachycardia compared to sinus rhythm (HV[VT] < HV[NSR]). Counterclockwise activation of the bundle branches produces H-RB-LB activation sequence. Atypical (reverse) BBRT manifests right bundle branch block (RBBB) QRS complexes and H-LB-RB activation sequences.
During sinus rhythm, QRS complexes often show typical LBBB resulting from antegrade His-LB conduction delay rather than failure. A rare finding is the occurrence of a second His bundle potential after conducted LBBB QRS complexes due to late retrograde activation of the LB and His bundle that can mimic a dual antegrade His bundle response (see Fig. 1-40).3,11
ZONES OF TRANSITION
INITIATION
Induction of typical BBRT by right ventricular (RV) extrastimulation requires that an impulse fall into the tachycardia window (defined as the difference in retrograde refractory periods between the RB and LB branches). A critically timed impulse 1) fails to conduct over the RB (unidirectional block) and 2) crosses the septum to retrogradely activate the LB and His
bundle resulting in a “VH jump” (slow conduction) (Figs. 21-7 and 21-8).12 Sufficient VH delay allows the RB to recover excitability, conduct antegradely, and initiate tachycardia. The length of the VH jump is inversely related to the subsequent HV interval (VH/HV reciprocity). While induction of single BBR complexes by programmed ventricular extrastimulation is a common finding in normal individuals, development of sustained BBRT only occurs in patients with diseased His-Purkinje tissue. Induction of BBRT can be facilitated by procainamide (which further slows His-Purkinje conduction) or short-longshort sequences (pause protocol—which widens the tachycardia window by increasing the dispersion of refractoriness between the bundle branches) (Fig. 21-9).13,14 Induction of BBRT can be abolished by simultaneous RV and left ventricular (LV) stimulation, which prevents transeptal conduction and the “VH jump.” BBRT can also be induced from the atrium by pacing-induced functional block in the His-Purkinje system (e.g., abrupt HV prolongation with development of phase 3 LBBB).4
bundle resulting in a “VH jump” (slow conduction) (Figs. 21-7 and 21-8).12 Sufficient VH delay allows the RB to recover excitability, conduct antegradely, and initiate tachycardia. The length of the VH jump is inversely related to the subsequent HV interval (VH/HV reciprocity). While induction of single BBR complexes by programmed ventricular extrastimulation is a common finding in normal individuals, development of sustained BBRT only occurs in patients with diseased His-Purkinje tissue. Induction of BBRT can be facilitated by procainamide (which further slows His-Purkinje conduction) or short-longshort sequences (pause protocol—which widens the tachycardia window by increasing the dispersion of refractoriness between the bundle branches) (Fig. 21-9).13,14 Induction of BBRT can be abolished by simultaneous RV and left ventricular (LV) stimulation, which prevents transeptal conduction and the “VH jump.” BBRT can also be induced from the atrium by pacing-induced functional block in the His-Purkinje system (e.g., abrupt HV prolongation with development of phase 3 LBBB).4
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