Wallace H. Coulter School of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA 30332-0535, USA.
Biomech Model Mechanobiol. 2012 Jan;11(1-2):231-44. doi: 10.1007/s10237-011-0306-2. Epub 2011 Apr 5.
Aortic valve (AV) calcification is a highly prevalent disease with serious impact on mortality and morbidity. The exact causes and mechanisms of AV calcification are unclear, although previous studies suggest that mechanical forces play a role. It has been clinically demonstrated that calcification preferentially occurs on the aortic surface of the AV. This is hypothesized to be due to differences in the mechanical environments on the two sides of the valve. It is thus necessary to characterize fluid shear forces acting on both sides of the leaflet to test this hypothesis. The current study is one of two studies characterizing dynamic shear stress on both sides of the AV leaflets. In the current study, shear stresses on the ventricular surface of the AV leaflets were measured experimentally on two prosthetic AV models with transparent leaflets in an in vitro pulsatile flow loop using two-component Laser Doppler Velocimetry (LDV). Experimental measurements were utilized to validate a theoretical model of AV ventricular surface shear stress based on the Womersley profile in a straight tube, with corrections for the opening angle of the valve leaflets. This theoretical model was applied to in vivo data based on MRI-derived volumetric flow rates and valve dimension obtained from the literature. Experimental results showed that ventricular surface shear stress was dominated by the streamwise component. The systolic shear stress waveform resembled a half-sinusoid during systole and peaks at 64-71 dyn/cm(2), and reversed in direction at the end of systole for 15-25 ms, and reached a significant negative magnitude of 40-51 dyn/cm(2). Shear stresses from the theoretical model applied to in vivo data showed that shear stresses peaked at 77-92 dyn/cm(2) and reversed in direction for substantial period of time (108-110 ms) during late systole with peak negative shear stress of 35-38 dyn/cm(2).
主动脉瓣(AV)钙化是一种发病率很高的疾病,对死亡率和发病率有严重影响。尽管先前的研究表明机械力起作用,但 AV 钙化的确切原因和机制尚不清楚。临床上已经证实,钙化优先发生在 AV 的主动脉面。这被假设是由于瓣膜两侧的机械环境不同。因此,有必要对小叶两侧的流体剪切力进行特征描述,以检验这一假设。本研究是对 AV 小叶两侧动态剪切力进行特征描述的两项研究之一。在本研究中,使用二维激光多普勒速度仪(LDV)在体外脉动流回路中对具有透明小叶的两个假体 AV 模型的 AV 小叶心室面进行了实验测量。实验测量用于验证基于直管中沃默斯利轮廓的 AV 心室面剪切应力理论模型,该模型对阀瓣开度进行了修正。该理论模型应用于基于 MRI 获得的容积流量和从文献中获得的瓣膜尺寸的体内数据。实验结果表明,心室面剪切应力主要由流向分量决定。收缩期剪切应力波形在收缩期类似于半正弦,峰值为 64-71 dyn/cm²,在收缩期末反转方向,持续 15-25 ms,并达到显著的负幅度 40-51 dyn/cm²。应用于体内数据的理论模型的剪切应力表明,在收缩晚期,剪切应力峰值为 77-92 dyn/cm²,在收缩末期持续相当长的时间(108-110 ms)反转方向,峰值负剪切应力为 35-38 dyn/cm²。