Department of Aerospace and Mechanical Engineering, University of Notre Dame, 143 Multidisciplinary Research Building, Notre Dame, IN 46556-5637, USA.
Biomech Model Mechanobiol. 2012 Sep;11(7):1085-96. doi: 10.1007/s10237-012-0375-x.
The bicuspid aortic valve (BAV) is associated with a high prevalence of calcific aortic valve disease (CAVD). Although abnormal hemodynamics has been proposed as a potential pathogenic contributor, the native BAV hemodynamic stresses remain largely unknown. Fluid-structure interaction models were designed to quantify the regional BAV leaflet wall-shear stress over the course of CAVD. Systolic flow and leaflet dynamics were computed in two-dimensional tricuspid aortic valve (TAV) and type-1 BAV geometries with different degree of asymmetry (10 and 16% eccentricity) using an arbitrary Lagrangian–Eulerian approach. Valvular performance and regional leaflet wallshear stress were quantified in terms of valve effective orifice area (EOA), oscillatory shear index (OSI) and temporal shear magnitude (TSM). The dependence of those characteristics on the degree of leaflet calcification was also investigated. The models predicted an average reduction of 49% in BAV peak-systolic EOA relative to the TAV. Regardless of the anatomy, the leaflet wall-shear stress was side-specific and characterized by high magnitude and pulsatility on the ventricularis and low magnitude and oscillations on the fibrosa. While the TAV and non-coronary BAV leaflets shared similar shear stress characteristics, the base of the fused BAV leaflet fibrosa exhibited strong abnormalities, which were modulated by the degree of calcification (6-fold, 10-fold and 16-fold TSM increase in the normal, mildly and severely calcified BAV, respectively, relative to the normal TAV). This study reveals the existence of major differences in wall-shear stress pulsatility and magnitude on TAV and BAV leaflets. Given the ability of abnormal fluid shear stress to trigger valvular inflammation, the results support the existence of a mechano-etiology of CAVD in the BAV.
二叶式主动脉瓣（BAV）与钙化性主动脉瓣疾病（CAVD）的高患病率相关。尽管异常的血流动力学已被提出是潜在的致病因素，但原生 BAV 的血流动力学应激仍知之甚少。采用流固耦合模型来量化 CAVD 过程中 BAV 瓣叶壁面切应力的区域性。使用任意拉格朗日-欧拉方法，计算二维三尖瓣主动脉瓣（TAV）和 1 型 BAV 几何结构的二维 TAV 和 1 型 BAV 的收缩期流动和瓣叶动力学，其中不对称度分别为 10%和 16%。采用阀有效开口面积（EOA）、振荡剪切指数（OSI）和时变剪切幅度（TSM）来量化瓣膜性能和瓣叶壁面切应力的区域性。还研究了这些特征与瓣叶钙化程度的关系。模型预测 BAV 峰值收缩期 EOA 平均比 TAV 减少 49%。无论解剖结构如何，瓣叶壁面切应力都是瓣叶侧特异性的，心室侧瓣叶壁面切应力幅度大且脉动性强，纤维侧瓣叶壁面切应力幅度小且振荡性强。虽然 TAV 和非冠状动脉 BAV 瓣叶具有相似的剪切应力特征，但融合 BAV 瓣叶纤维侧的底部表现出强烈的异常，这些异常受钙化程度的调节（与正常 TAV 相比，正常、轻度和重度钙化的 BAV 的 TSM 分别增加 6 倍、10 倍和 16 倍）。本研究揭示了 TAV 和 BAV 瓣叶壁面切应力脉动性和幅度存在显著差异。鉴于异常的流体切应力能够引发瓣膜炎症，研究结果支持 BAV 中 CAVD 的存在机械病因。
