Bidomain Predictions of Virtual Electrode-Induced Make and Break Excitations around Blood Vessels

Adam J Connolly,Edward Vigmond,Martin J Bishop

doi:10.3389/fbioe.2017.00018

Abstract

Virtual electrodes formed by field stimulation during defibrillation of cardiac tissue play an important role in eliciting activations. It has been suggested that the coronary vasculature is an important source of virtual electrodes, especially during low-energy defibrillation. This work aims to further the understanding of how virtual electrodes from the coronary vasculature influence defibrillation outcomes. Using the bidomain model, we investigated how field stimulation elicited activations from virtual electrodes around idealized intramural blood vessels. Strength-interval curves, which quantify the stimulus strength required to elicit wavefront propagation from the vessels at different states of tissue refractoriness, were computed for each idealized geometry. Make excitations occurred at late diastolic intervals, originating from regions of depolarization around the vessel. Break excitations occurred at early diastolic intervals, whereby the vessels were able to excite surrounding refractory tissue due to the local restoration of excitability by virtual electrode-induced hyperpolarizations. Overall, strength-interval curves had similar morphologies and underlying excitation mechanisms compared with previous experimental and numerical unipolar stimulation studies of cardiac tissue. Including the presence of the vessel wall increased the field strength required for make excitations but decreased the field strength required for break excitations, and the field strength at which break excitations occurred was generally greater than 5 V/cm. Finally, in a more realistic ventricular slice geometry, the proximity of virtual electrodes around subepicardial vessels was seen to cause break excitations in the form of propagating unstable wavelets to the subepicardial layer. Representing the blood vessel wall microstructure in computational bidomain models of defibrillation is recommended as it significantly alters the electrophysiological response of the vessel to field stimulation. Although vessels may facilitate excitation of relatively refractory tissue via break excitations, the field strength required for this is generally greater than those used in the literature on low-energy defibrillation. However, the high-intensity shocks used in standard defibrillation may elicit break excitation propagation from the coronary vasculature.

Highlights

Introduction and backgroundVirtual electrodes formed by field stimulation during defibrillation of cardiac tissue play an important role in eliciting activations
Prior to investigating the SI curves for the vessel configurations shown in Figure 1, we first show how the virtual electrodes (VEs) patterns change when the low-conductivity vessel wall is included in the bidomain model
The physical reason for these two effects is that: (a) in the case of no vessel wall, boundary VEs from current transiting the extracellular-to-bath-to-extracellular spaces dominate, as current takes the path of least resistance through the vessel cavity, and (b) in the case of a vessel wall, the insulating vessel wall changes the path of least resistance from through the vessel cavity to around the vessel cavity, VEs from dissimilar anisotropy ratios dominate, and boundary VEs are diminished

Summary

Introduction

Introduction and backgroundVirtual electrodes formed by field stimulation during defibrillation of cardiac tissue play an important role in eliciting activations. The strong shocks required to ensure cardioversion render it a sub-optimal therapy, leading to the active pursuit of its refinement or novel lower energy protocols and electrode configurations. Both conventional (strong) and recently suggested low-energy defibrillation (Fenton et al, 2009; Janardhan et al, 2012; Luther et al, 2012; Rantner et al, 2013b) are thought to be driven by virtual electrodes (VEs), formed within tissue distant from the physical electrodes. Refinement of conventional ICD shocks and the advancement of novel low-energy protocols into clinical practice necessitate a greater understanding of the specific mechanisms behind VE formation, around fine-scale intramural anatomical structures

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