A Method for Incorporating Changes in Extracellular Volume and Myocyte Size Into the Cardiac Bidomain Equations.

This study aims to develop a robust approach for integrating simultaneous changes in extracellular volume (ECV) and myocyte size into the cardiac bidomain equations. We developed a straightforward method for scaling conduction velocity (CV) in cardiac tissue as a function of ECV and myocyte radius (r). Simulations of apical pacing were performed in a computational model of human ventricular epicardium under control conditions $(r=10.6 \ \mu m)$ and in myocyte hypertrophy $(r=15.45\mu m)$ , and for three different ECV levels (21.5, 25 and 30%) that correspond to values reported in healthy and diseased hearts. Increasing ECV shortened total activation time (faster CV) under both control and hypertrophic conditions (control: 200, 189 and 178 ms; myocyte hypertrophy: 162, 154 and 145 ms; values for ECV of 21.5, 25 and 30, respectively). Increasing r to the myocyte hypertrophy state also shortened total activation time on average by 23%. These findings demonstrate that changes in both ECV and cell radius noticeably alter ventricular conduction. Future work will expand the method to include diffuse fibrosis and to match QRS durations in patient-specific hearts with normal and hypertrophic geometries.