Extended bidomain modeling of defibrillation: quantifying virtual electrode strengths in fibrotic myocardium
Defibrillation is a well-established therapy for atrial and ventricular arrhythmia. Here, we shed light on defibrillation in the fibrotic heart. Using the extended bidomain model of electrical conduction in cardiac tissue, we assessed the influence of fibrosis on the strength of virtual electrodes caused by extracellular electrical current. We created one-dimensional models of rabbit ventricular tissue with a central patch of fibrosis. The fibrosis was incorporated by altering volume fractions for extracellular, myocyte and fibroblast domains. In our prior work, we calculated these volume fractions from microscopic images at the infarct border zone of rabbit hearts. An average and a large degree of fibrosis were modeled. We simulated defibrillation by application of an extracellular current for a short duration (5 ms). We explored the effects of myocyte-fibroblast coupling, intra-fibroblast conductivity and patch length on the strength of the virtual electrodes present at the borders of the normal and fibrotic tissue. We discriminated between effects on myocyte and fibroblast membranes at both borders of the patch. Similarly, we studied defibrillation in two-dimensional models of fibrotic tissue. Square and disk-like patches of fibrotic tissue were embedded in control tissue. We quantified the influence of the geometry and fibrosis composition on virtual electrode strength.