Fibrosis effect on left atrial hemodynamics using multi-physics, multi-scale simulations

Atrial fibrillation (AF) is the most frequent arrhythmia, with a prevalence of 0.5% of the world population. During AF, irregular electric impulses cause unsynchronized myocardial motion leading to blood stasis in the left atrial (LA) appendage (LAA), increasing thrombosis and stroke risk. Fibrosis is clinically associated with stroke but the underlying mechanisms are not understood. Fibrotic remodeling modifies myocardial structure impairing LA electrical propagation, myocardium mechanics, and function. To dissect these effects, we perform multi-physics, multi-scale simulations coupling electrophysiology, biomechanics, and hemodynamics. We simulate the LA contraction against a constant ventricular pressure using 4 different models with modified mechanical properties in the fibrotic tissue: no fibrosis effect, 5X increased tissue passive stiffness (iPS), 2X reduced cardiomyocyte peak tension (rPT), and combined effect (iPS+rPT). The results from 4 patient-specific LA anatomies with different fibrotic burdens suggest fibrosis reduces LA kinetic energy (KE) globally, especially in the iPS+rPT model. KE decreases linearly with emptying fraction (LA function impairment measure) in the LA body and in a patient-specific fashion in the LAA.