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Abstract 15940: Wall Shear Stress and Vorticity in Atrial Fibrillation, Pulmonary Hypertension, and Normal Atrial Anatomy Models

医学 心脏病学 心房颤动 内科学 涡度 舒张期 血流 剪应力 肺动脉高压 血压 机械 涡流 物理
作者
David Rutkowski,Alexey V. Glukhov,Alejandro Roldán‐Alzate
出处
期刊:Circulation [Ovid Technologies (Wolters Kluwer)]
卷期号:142 (Suppl_3)
标识
DOI:10.1161/circ.142.suppl_3.15940
摘要

Introduction: Atrial fibrillation (AF) is a common cardiac rhythm disorder that is often comorbid with pulmonary hypertension (PH) and other conditions associated with abnormal atrial pressure and/or volume overload. In the setting of atrial dilation, mechanoelectric feedback has been linked to the development of ectopic beats that trigger paroxysmal AF mainly originating from pulmonary veins (PVs). However, the precise mechanisms remain poorly understood. Here, we aimed to characterize atrial wall shear stress (WSS) and vorticity in the left atrium of AF, healthy, and at-risk for AF (PH) patient models to develop predictors of AF risk. Methods: Magnetic resonance imaging and computed tomography data (10 AF, 10 PH, and 10 healthy volunteers) were obtained retrospectively. The left atria were manually segmented from each data set. Four-dimensional flow MRI was performed on one patient to derive PV flow data. The 30 atrial geometries and PV flow conditions were used to run numerical blood flow simulations, and atrial WSS and blood flow vorticity were analyzed. Results: As seen in Figure 1, wall shear stress was highest near the PV roots and on the posterior atrial wall, the most common sources of AF triggers. Average WSS and vorticity were significantly lower in PH patients than in both the healthy (p=0.003(WSS), p=0.011(vorticity)) and AF (p=0.046(WSS), p=0.069(vorticity)) groups. Both WSS (r=-0.66) and vorticity (r=-0.68) were moderately correlated to atrial volume in the PH group. Atrial volume was significantly larger in PH (p<0.001) and AF (p<0.001) groups than in the healthy group. Conclusions: The larger atrial volumes of PH and AF patients lead to altered flow profiles and less frequently flow jet impingement on the atrial wall models, leading to abnormal vorticity and WSS profiles. These long term flow abnormalities may influence the development and/or localization of electrical abnormalities and AF; although further study is needed to confirm this hypothesis.

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