Elucidating the effect of fibrosis on left atrial flow using multi-physics, multi-scale simulations

Atrial fibrillation (AFib) affects millions of people worldwide and increases the risk of stroke 5-fold, causing higher mortality and more disabilities than strokes in the normal population. During AFib, atria beat irregularly, creating stagnant flow regions where clots can form, typically in the left atrial (LA) appendage. However, the mechanisms by which fibrotic atria are more prone to thrombosis are yet not understood. Atrial motion impairment is caused by fibrosis through electrical, structural, and contractile effects. We use a multi-physics, multi-scale framework that couples electrophysiology, biomechanics, and hemodynamics to investigate the effect of fibrosis in atrial flow and ultimately in thrombosis. We model a LA contraction against a constant pressure in 4 patient-specific anatomies with different fibrotic burdens. In the fibrotic regions, we increase 5-fold the tissue passive stiffness (iPS) and reduce by half the peak tension (rPT) generated by cardiomyocytes. We found that the combined effect of iPS and rPT leads to smaller kinetic energy (KE) inside the left atrium in all cases due to a reduced LA wall motion. The independent effect of iPS and rPT also decreases KE, but their impact on the total contribution varies among patients.