Simultaneous stimulation of the myocardial surface and Purkinje network excitable gaps improved defibrillation success from 55% to 100% in a computational model of ventricular fibrillation.
Does simultaneous stimulation of the Purkinje network and myocardial surface excitable gap improve low-energy ventricular defibrillation success in a computational human biventricular model?
Defibrillation strategies targeting only the myocardium may fail due to accessory pathways in the Purkinje network, suggesting painless defibrillation should also target the Purkinje network.
Absolute Event Rate: 100% vs 55%
BACKGROUND: During ventricular fibrillation (VF), targeting the excitable gap (EG) of reentry throughout the myocardium with low-energy surface stimulation shows promise for painless defibrillation. However, the Purkinje network may provide alternative pathways for reentry to evade termination. This study investigates the role of the Purkinje network in painless defibrillation. METHODS: In a computational human biventricular model featuring a Purkinje network, VF was initiated with 4 Hz epicardial pacing. Defibrillation was attempted by stimulating myocardial surface EG with a low-energy 2 ms duration pulse at 2x stimulus capture, which was administered at coupling intervals incremented by 0.25 s between 0.25 and 5 s after VF initiation. Defibrillation was accomplished if reentry ceased ≤ 1 s after the defibrillation pulse. The protocol was repeated with the Purkinje network and myocardial surface EG stimulated simultaneously, and again after uncoupling the Purkinje network from the myocardium. RESULTS: VF with the Purkinje network coupled and uncoupled had comparable dominant frequency in the left (3.81 ± 0.44 versus 3.77 ± 0.53 Hz) and right (3.80 ± 0.37 versus 3.76 ± 0.48 Hz) ventricles. When uncoupling the Purkinje network, myocardial surface EG stimulation terminated VF for all defibrillation pulses. When coupled, myocardial EG surface stimulation terminated VF for only 55% of the defibrillation pulses, but improved to 100% when stimulated simultaneously with Purkinje network EG. Defibrillation failures were attributed to EG evading stimulation in the Purkinje network. CONCLUSIONS: Defibrillation that exclusively targets myocardium can fail due to accessory pathways in the Purkinje network that allow for reentrant activity to evade termination and maintain VF. Painless defibrillation strategies should be adapted to include the Purkinje network.
Bayer et al. (Tue,) conducted a other in Ventricular fibrillation. Simultaneous stimulation of myocardial surface and Purkinje network excitable gaps vs. Myocardial surface excitable gap stimulation alone was evaluated on Defibrillation success (reentry ceased ≤ 1 s after the defibrillation pulse). Simultaneous stimulation of the myocardial surface and Purkinje network excitable gaps improved defibrillation success from 55% to 100% in a computational model of ventricular fibrillation.
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