MULTI-FIDELITY, MULTI-PHYSICS MODELS OF FIBROSIS-INDUCED LEFT ATRIAL THROMBOSIS

Ischemic strokes cause mortality and long-term disability in patients with left atrial (LA) fibrosis but the underlying mechanisms are poorly understood. Fibrotic remodeling modifies myocardial structure impairing LA electrical propagation, myocardium mechanics, and slowing down atrial blood flow. Fibrotic patches also release inflammatory cytokines and tissue injury factors that can activate the coagulation cascade. We perform multi-physics simulations, coupling electrophysiology, biomechanics, hemodynamics, and the coagulation cascade. We introduce two innovations to reduce the cost of the multi-physics simulations to ~minutes per cardiac cycle. We introduce a multi-fidelity approach leveraging the low diffusivity of coagulation species and implement the solvers to run in GPUs. Fibrotic regions are modeled by locally modifying the myocardial mechanical properties and releasing pro-coagulatory tissue factor in the neighboring endocardium. Each effect is considered both independently and in conjunction with other effects in a systematic simulation campaign. Our resuls shed light onto the complex nexus between fibrosis and stroke. Furthermore, their reduced computational cost is poised to create paradigm changes in clinical diagnosis support.