Abstract

Introduction: Atrial fibrillation (AF) patients are at high risk of stroke, with the left atrial appendage (LAA) found to be the most common site of clot formation. Left atrial (LA) fibrosis is also associated with higher stroke risk. However, the mechanisms for increased stroke risk in patients with atrial fibrotic remodeling are poorly understood. We sought to explore these specific mechanisms using fluid dynamics analysis. Hypothesis: The presence of LA fibrosis leads to aberrant hemodynamics in the atria, contributing to increased stroke risk in AF patients. Methods: We retrospectively collected LGE-MRI images of 3 AF patients and reconstructed their 3D LA endocardial surfaces. Fibrotic regions were identified as those with intensity 3 standard deviations greater than the mean LA blood-pool intensity. Personalized computational fluid dynamic simulations were performed, and hemodynamics at the LA wall were quantified by wall shear stress (WSS, friction of blood) and oscillatory shear index (OSI, temporal directional change of WSS). For each case, WSS and OSI were compared between fibrotic and normal regions. Results: WSS was significantly lower in the fibrotic region as compared to normal region for all 3 cases. Additionally, OSI was higher in the fibrotic region as compared to normal region for all 3 cases. However, this different was statistically significant for cases 1 and 3; case 2 was not statistically significantly different. Low WSS and high OSI in the vicinity of the fibrotic wall suggest that local blood-flow was slow and oscillating, enabling pro-thrombotic conditions for circulating blood. Conclusion: LA fibrosis correlates with regions of aberrant hemodynamics, which renders it susceptible to blood thrombosis. AF patients with high LA fibrosis burden will have more pro-thrombotic regions, in addition to low flow in the LAA, providing more sites for a potential clot formation. These conditions might get exacerbated during an AF event and cause stroke.

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