Terminating ventricular tachyarrhythmias using far-field low-voltage stimuli: Mechanisms and delivery protocols

Abstract

Background Low-voltage termination of VT and atrial fibrillation has shown promising results, however the mechanisms and full range of applications remain unexplored. Objective This study aimed to elucidate the mechanisms for low-voltage cardioversion and defibrillation, and to develop an optimal low-voltage defibrillation protocol. Methods We developed a detailed MRI-based computational model of the rabbit right ventricular wall. We applied multiple low-voltage far-field stimuli of various strengths (≤1 V/cm) and stimulation rates in VT and VF. Results Out of the five stimulation rates tested, stimuli applied at 16 or 88% of VT cycle length (CL) were most effective in cardioverting VT, the mechanism being consecutive excitable gap decreases. Stimuli given at 88% of VF CL defibrillated successfully, whereas a faster stimulation rate (16%) often failed because the fast stimuli did not capture enough tissue. In this model, defibrillation threshold (DFT) energy for multiple low-voltage stimuli at 88% VF CL was 0.58% of the DFT energy for a single strong biphasic shock. Based on the simulation results, a novel two-stage defibrillation protocol was proposed. The first stage converted VF into VT by applying low-voltage stimuli at times of maximal excitable gap, capturing large tissue volume and synchronizing depolarization; the second stage terminated VT. The energy required for successful defibrillation using this protocol was 57.42% of the energy for low-voltage defibrillation when stimulating at 88% CL. Conclusion A novel two-stage low-voltage defibrillation protocol using the excitable gap extent to time multiple stimuli defibrillated VF with the least energy by first converting VF into VT, then terminating VT.

Control of electrical turbulence by periodic excitation of cardiac tissue

“…Such a choice of pacing frequency allows for an efficient scanning of the phase of the vortex in order to find the vulnerable window for vortex termination 27,28 . A simulation study in a realistic three-dimensional cardiac geometry demonstrated for selected examples that LEAP works for a pacing period of 88% of the VF cycle length, but often fails for much faster pacing with a period of 16% of the VF cycle length 29 .…”

A Cell-Based Framework for Numerical Modeling of Electrical Conduction in Cardiac Tissue

“…At that time, an accurate representation of cardiac tissue in terms of the representation of individual cells was inconceivable for reasons of both storage and computing time. This has changed dramatically; in recent computational studies, 29 million computational nodes were used to represent cardiac tissue [27,47]. The computational mesh size in these simulations was about 59 µm, which should be compared with 100 µm, the typical length of a cardiac cell.…”

“…The numerical accuracy of the discretizations considered was assessed using a single-cell problem (24)(25)(26)(27)(28)(29)(30) and the method of manufactured solutions. As seen in Tables 2-4, all the discretizations provide converging numerical solutions.…”

“…The classical models (monodomain, bidomain) have been successfully used to study the propagation of the electrochemical wave in cardiac tissue (e.g., [14][15][16]), the initiation of excitation waves (e.g., [17][18][19][20][21]), the development of cardiac arrhythmias (e.g., [14,17,18]), the effect of defibrillation (e.g., [22][23][24][25][26][27][28]), and the effect of various drugs (e.g., [29][30][31][32]). …”

Cardiac Arrhythmias: Mechanistic Knowledge and Innovation from Computer Models

“…The recent simulation study by Rantner at al. [97] aimed to elucidate these mechanisms and to develop an optimal low-voltage defibrillation protocol. Based on the simulation results using a complex high-resolution MRI-based ventricular wall model, a novel two-stage low-voltage defibrillation protocol was proposed that did not involve the delivery of the stimuli at a constant cycle length.…”