Bidirectional ventricular tachycardia: ping pong in the His-Purkinje system

Abstract

Background: Bidirectional ventricular tachycardia (BVT), which is characterized by an alternating beat-to-beat ECG QRS axis, is a rare but intriguing arrhythmia associated with digitalis toxicity, familial catecholaminergic polymorphic ventricular tachycardia (CPVT), and several other conditions that predispose cardiac myocytes to delayed afterdepolarizations (DADs) and triggered activity. Evidence from human and animal studies attributes BVT to alternating ectopic foci originating from the distal His-Purkinje system in the left and/or right ventricle, respectively.

Objective: The purpose of this study was to evaluate a simple "ping pong" model of reciprocating bigeminy to explain BVT.

Methods: We constructed a two-dimensional anatomic model of the rabbit ventricles with a simplified His-Purkinje system, in which different sites in the His-Purkinje system had different heart rate thresholds for DAD-induced bigeminy.

Results: When the heart rate exceeded the threshold for bigeminy at the first site in the His-Purkinje system, ventricular bigeminy developed, causing the heart rate to accelerate and exceed the threshold for bigeminy at the second site. Thus, the triggered beat from the first site induced a triggered beat from the second site. The triggered beat from the second site next reciprocated by inducing a triggered beat from the first site, and so forth. Bigeminy from two sites produced BVT, and that from three or more sites produced polymorphic VT.

Conclusion: This "ping pong" mechanism of reciprocating bigeminy readily produces the characteristic ECG pattern of BVT and its degeneration to polymorphic VT if additional sites develop bigeminy.

Fig. 1

A. Comparison of simulated rabbit ventricular (dashed line) and Purkinje (solid line) APs and Ca_i transients, during pacing at 600 ms. B. Rate dependence of DADs and bigeminy in the Purkinje cell AP models. In the green trace a, the rate threshold for DAD-induced bigeminy was 67 bpm (PCL 900 ms), such that pacing (black arrows) at both 900 and 600 ms induced bigeminy. In purple trace b, the bigeminy rate threshold was 100 bpm (PCL 600 ms), such that pacing at 600 ms, but not 900 ms, induced bigeminy.

Fig. 2

A. The anatomic rabbit ventricles model (green), showing a 2D section (blue) of myocardium with the HPS (red) incorporated. Regions of the HPS susceptible to DAD-induced bigeminy in the RBB (a, green) and LBB (b, purple) are indicated. In some simulations, a third region (yellow) also developed DAD-induced bigeminy. B. Voltage snapshots of normal activation when the His bundle is paced.

Fig. 3. Simulated BVT

A. Voltage snapshots showing the activation sequence at the onset of BVT. Beat #2 is the last paced beat, with normal activation. Beat #3 is the 1^st beat of BVT, due to a DAD-triggered AP arising in the RBB, resulting in a QRS with LBB block pattern. Beat #4 is the 2^nd beat of BVT, due to a DAD-triggered AP arising in the LBB, resulting in a QRS with RBB block pattern. Traces on right show the timing of APs recorded from the His bundle (red), RBB (green), and LBB (purple). B. The computed ECG from the simulation in A, showing BVT. C. ECG recorded in a patient during BVT .

Fig. 4

ECG patterns of BVT corresponding to locations of pairs of foci with reciprocating bigeminy. HIS, His bundle; LBB, left bundle branch; RBB, right bundle branch; LAF, left anterior fascicle; LPF, left posterior fascicle; LBBB, left bundle branch block; RBBB, right bundle branch block; LAD; left axis deviation; RAD, right axis deviation. See text for details.

Fig. 5. Simulated polymorphic VT

A. Voltage snapshots showing the activation sequences corresponding to different QRS morphologies during polymorphic VT caused by 3 foci with reciprocating bigeminy. Red dot in each panel indicates the earliest activation site. B. The computed ECG from the simulation in A, showing polymorphic VT (with beat numbers corresponding to snapshots in A). C. ECG recorded in a patient with CPVT.