The objective of this article is to present a set of methods for constructing realistic computational models of cardiac structure from high-resolution structural and diffusion tensor magnetic resonance images and to demonstrate the applicability of the models in simulation studies. The structural image is segmented to identify various regions such as normal myocardium, ventricles, and infarct. A finite element mesh is generated from the processed structural data, and fiber orientations are assigned to the elements. The Purkinje system, when visible, is modeled using linear elements that interconnect a set of manually identified points. The methods were applied to construct 2 different models; and 2 simulation studies, which demonstrate the applicability of the models in the analysis of arrhythmia and defibrillation, were performed. The models represent cardiac structure with unprecedented detail for simulation studies.

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.

Key points• Defibrillation is known to be less efficient in infarcted than in healthy hearts.• In a rabbit model of myocardial infarction, altered 3D distribution of virtual electrodes and propagation delay in the peri-infarct zone caused increased vulnerability to electric shocks in infarcted hearts.• The infarct scar alone -without the presence of a peri-infarct zone -did not cause an increase in vulnerability.• The results help us to understand the mechanisms of increased vulnerability and decreased defibrillation efficacy in infarcted hearts.Abstract Defibrillation efficacy is decreased in infarcted hearts, but the mechanisms by which infarcted hearts are more vulnerable to electric shocks than healthy hearts remain poorly understood. The goal of this study was to provide insight into the 3D mechanisms for the increased vulnerability to electric shocks in infarcted hearts. We hypothesized that changes in virtual electrode polarizations (VEPs) and propagation delay through the peri-infarct zone (PZ) were responsible. We developed a microanatomically detailed rabbit ventricular model with chronic myocardial infarction from magnetic resonance imaging and enriched the model with data from optical mapping experiments. We further developed a control model without the infarct. The simulation protocol involved apical pacing followed by biphasic shocks. Simulation results from both models were compared. The upper limit of vulnerability (ULV) was 8 V cm −1 in the infarction model and 4 V cm −1 in the control model. VEPs were less pronounced in the infarction model, providing a larger excitable area for postshock propagation but smaller transmembrane potential gradients to initiate new wavefronts. Initial post-shock transmural activation occurred at a later time in the infarction model, and the PZ served to delay propagation in subsequent beats. The presence of the PZ was found to be responsible for the increased vulnerability.