THE ROLE OF FLUID-MECHANICS IN THE LOCALIZATION AND DETECTION OF ATHEROSCLEROSIS
THE ROLE OF FLUID-MECHANICS IN THE LOCALIZATION AND DETECTION OF ATHEROSCLEROSIS
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DOI：
10.1115/1.2895545
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发表时间：
1993-11-01
影响因子：
1.7
通讯作者：
GLAGOV, S
中科院分区：
文献类型：
--
作者：
GIDDENS, DP;ZARINS, CK;GLAGOV, S
流体动力学研究在过去的二十年里为我们对动脉粥样硬化的认识做出了巨大的贡献。通过对动脉狭窄引起的速度紊乱的性质和发生率的研究，使用非侵入性超声方法检测局部动脉粥样硬化斑块的能力得到了显着提高，并且使用超声成像和多普勒血流速度测量相结合诊断颈动脉分叉疾病现在是相当常规的。由于动脉粥样硬化斑块往往局限于分支和动脉弯曲的部位，而且这些部位可能存在复杂的血流模式，因此研究人员推测流体动力学可能在动脉粥样硬化形成中起起始作用。提出了几个流体动力学变量作为启动因素。在20世纪80年代期间进行了调查，其中采用具有生理几何形状和流动条件的流体动力学模型实验来模拟动脉流动，并且其中在人体动脉中进行内膜厚度的形态测量映射。流体动力学变量和内膜厚度之间的相关性表明，动脉粥样硬化斑块往往发生在低和振荡的壁剪切应力的网站，这些观察结果得到了加强，在猴模型动脉粥样硬化的研究。同时，人们认识到，动脉调整其直径，以保持壁剪切应力在一个狭窄的范围内的值约15达因/厘米2，这是基于正常动脉的观察和动物研究的结果，其中流速被操纵和动脉直径的适应性进行了测量。目前，关于流体动力学在动脉粥样硬化形成中的作用的工作假设是内膜增厚是对低壁剪切应力的正常反应，并且这种内膜增厚在某些情况下可以发展成早期动脉粥样硬化斑块，例如血液中过量的低密度脂蛋白浓度。
Fluid dynamics research over the past twenty years has contributed immensely to our knowledge of atherosclerosis. The ability to detect localized atherosclerotic plaques using noninvasive ultrasonic methods was advanced significantly by investigations into the nature and occurrence of velocity disturbances created by arterial stenoses, and diagnosis of carotid bifurcation disease using a combination of ultrasonic imaging and Doppler measurement of blood velocity is now quite routine. Since atherosclerotic plaques tend to be localized at sites of branching and artery curvature and since these locations would be expected to harbor complex flow patterns, investigators postulated that fluid dynamics might play an initiating role in atherogenesis. Several fluid dynamic variables were proposed as initiating factors. Investigations were undertaken during the 1980s in which fluid dynamic model experiments with physiologic geometries and flow conditions were employed to simulate arterial flows and in which morphometric mapping of intimal thickness was performed in human arteries. Correlations between fluid dynamic variables and intimal thickness revealed that atherosclerotic plaques tended to occur at sites of low and oscillating wall shear stress, and these observations were reinforced by studies in a monkey model of atherosclerosis. Concomitantly, it was realized that arteries adapt their diameters so as to maintain wall shear stress in a narrow range of values around 15 dynes/cm2, findings which were based both on observations of normal arteries and on animal studies in which flow rates were manipulated and arterial diameter adaptation was measured. Currently, a working hypothesis for the role of fluid dynamics in atherogenesis is that intimal thickening is a normal response to low wall shear stress, and this intimal thickening can develop into an early atherosclerotic plaque under certain circumstances such as excessive low density lipoprotein concentrations in blood.