Differences between left and right ventricular chamber geometry affect cardiac vulnerability to electric shocks

Abstract

Although effects of shock strength and waveform on cardiac vulnerability to electric shocks have been extensively documented, the contribution of ventricular anatomy to shock-induced polarization and postshock propagation and thus, to shock outcome, has never been quantified; this is caused by lack of experimental methodology capable of mapping 3-D electrical activity. The goal of this study was to use optical imaging experiments and 3-D bidomain simulations to investigate the role of structural differences between left and right ventricles in vulnerability to electric shocks in rabbit hearts. The ventricles were paced apically, and uniform-field, truncated-exponential, monophasic shocks of reversed polarity were applied over a range of coupling intervals (CIs) in experiment and model. Experiments and simulations revealed that reversing the direction of externally-applied field (RV- or LV- shocks) alters the shape of the vulnerability area (VA), the 2-D grid encompassing episodes of arrhythmia induction. For RV- shocks, VA was nearly rectangular indicating little dependence of postshock arrhythmogenesis on CI. For LV- shocks, the probability of arrhythmia induction was higher for longer than for shorter CIs. The 3-D simulations demonstrated that these effects stem from the fact that reversal of field direction results in relocation of the main postshock excitable area from LV wall (RV- shocks) to septum (LV- shocks). Furthermore, the effect of septal (but not LV) excitable area in postshock propagation was found to strongly depend on preshock state. Knowledge regarding the location of the main postshock excitable area within the 3-D ventricular volume could be important for improving defibrillation efficacy.

Figure 1

Model (A) and experimental (B) preparation with shock electrodes in the perfusing bath generating a uniform applied electric field. A, Anterior view of the rabbit ventricular model. Preshock epicardial transmembrane potential distribution corresponds to CI-CI_max=−25 ms. B, Langendorff-perfused rabbit heart. The square represents the field of view of the optical mapping system.

Figure 2

Vulnerability areas (VAs) for RV– (left) and LV– (right) shocks in the experiments (A) and in the simulations (B). A, Vertical axes represent probability of arrhythmia induction calculated over the 5 experiments for each combination of coupling interval (CI) and shock strength (SS). For better visualization, color, ranging from yellow through orange to red, is used in depicting the increase in SS. B, The dark area represents the VA. Asterisks represent episodes of shock delivery resulting in reentry induction; these were used to construct the VA. SSs and CIs are calculated as deflections from ULV and CI_max.

Figure 3

Transmembrane potential distributions at shock-end for RV– (left) and LV– (right) shocks for 8 combinations of SSs and CIs in experiments and simulations. A, Optical imaging of the anterior epicardial transmembrane potential distribution from 1 rabbit. B, Simulated anterior epicardial transmembrane potential distributions. CIs are represented as a %APD. For comparison between simulations and experiments, the white square in the simulation panels outlines the location of the optical field of view for the experiments in A. Color scale is saturated to emphasize transmembrane potential values around the border between positive and negative polarization.–

Figure 4

Simulated transmembrane potential distributions at shock-end on the anterior epicardium and in a transmural view of the rabbit ventricles for RV– (A) and LV– (C) shocks within and outside the VA, and graphs of the number of ventricular nodes that are of transmembrane potential above +20 mV (red lines) and below −90 mV (blue lines) at shock-end for RV– (B) and LV– (D) shocks as a function of CI. The number of ventricular nodes is expressed as percentage of all nodes in the ventricular volume. Squares and triangles correspond to stronger and weaker shocks, respectively.

Figure 5

Evolution of simulated postshock activity for RV– shocks (top) and LV– shocks (bottom). The 2 episodes in the top correspond to episodes a and b in Figure 4A, whereas the 3 episodes in the bottom are episodes a, b, and c (in top to bottom order) from Figure 4C. Anterior epicardial and transmural views of transmembrane potential distribution are shown on the left, whereas anterior and posterior views are rendered on the right. White arrows represent direction of propagation. Color scale as in Figure 4.

Figure 6

Optical imaging activation maps on the anterior surface of a rabbit heart for RV– and LV– shocks within the VA. Black arrows indicate direction of propagation. RV– shocks result in a single spiral wave, whereas LV– shocks establish a figure-of-eight reentry on the anterior epicardium.