Krams R, Wentzel J J, Oomen J A, Vinke R, Schuurbiers J C, de Feyter P J, Serruys P W, Slager C J
Thoraxcenter, University Hospital Dijkzigt, Rotterdam, The Netherlands.
Arterioscler Thromb Vasc Biol. 1997 Oct;17(10):2061-5. doi: 10.1161/01.atv.17.10.2061.
The predilection sites of atherosclerotic plaques implicate rheologic factors like shear stress underlying the genesis of atherosclerosis. Presently no technique is available that enables one to provide 3D shear stress data in human coronary arteries in vivo. In this study, we describe a novel technique that uses a recently developed 3D reconstruction technique to calculate shear stress on the endothelium with computational fluid dynamics. In addition, we calculated local wall thickness, the principal plane of curvature, and the location of plaque with reference to this plane, relating these results to shear stress in a human right coronary artery in vivo. Wall thickness and shear stress values for the entire vessel for three inflow-velocity values (10 cm/second, 20 cm/second, and 30 cm/second equivalents with the Reynolds numbers 114,229, and 457) were as follows: 0.65 +/- 0.37 mm (n = 1600) and 19.6 +/- 1.7 dyne/cm2; 46.1 +/- 8.1 dyne/cm2 and 80.1 +/- 16.8 dyne/cm2 (n = 1600). Curvature was 25 +/- 9 (m-1), resulting in Dean numbers 20 +/- 8; 46 +/- 16, and 93 +/- 33. Selection of data at the inner curvature of the right coronary artery provided wall thickness values of 0.90 +/- 0.41 mm (n = 100), and shear stress was 17 +/- 17, 38 +/- 44, and 77 +/- 54 dyne/cm2 (n = 100), whereas wall thickness values at the outer curve were 0.37 +/- 0.17 mm (n = 100) and shear stress values were 22 +/- 17, 60 +/- 44, and 107 +/- 79 dyne/cm2 (n = 100). These findings could be reconciled by an inverse relationship between wall thickness and shear stress for each velocity level under study. For the first time for human vessels in vivo, evidence is presented that low shear stress promotes atherosclerosis. As the method is nondestructive, it allows repeated measurements in the same patient and will provide new insights in the progress of atherosclerosis.
动脉粥样硬化斑块的好发部位暗示了诸如剪切应力等流变学因素在动脉粥样硬化发生过程中的作用。目前还没有一种技术能够在人体冠状动脉内提供三维剪切应力数据。在本研究中,我们描述了一种新技术,该技术使用最近开发的三维重建技术,通过计算流体动力学来计算内皮上的剪切应力。此外,我们计算了局部壁厚、主曲率平面以及斑块相对于该平面的位置,并将这些结果与人体右冠状动脉内的剪切应力相关联。三种流入速度值(分别相当于10厘米/秒、20厘米/秒和30厘米/秒,雷诺数分别为114、229和457)下整个血管的壁厚和剪切应力值如下:0.65±0.37毫米(n = 1600)和19.6±1.7达因/平方厘米;46.1±8.1达因/平方厘米和80.1±16.8达因/平方厘米(n = 1600)。曲率为25±9(米-1),对应的迪恩数为20±8;46±16和93±33。选择右冠状动脉内曲率处的数据,得到壁厚值为0.90±0.41毫米(n = 100),剪切应力分别为17±17、38±44和77±54达因/平方厘米(n = 100),而外曲线处的壁厚值为0.37±0.17毫米(n = 100),剪切应力值分别为22±17、60±44和107±79达因/平方厘米(n = 100)。在所研究的每个速度水平下,壁厚与剪切应力之间呈反比关系,这些发现与此相符。首次在人体血管活体中提供了证据,表明低剪切应力会促进动脉粥样硬化。由于该方法是非侵入性的,它允许在同一患者身上进行重复测量,并将为动脉粥样硬化的进展提供新的见解。