Hemodynamics and atherosclerosis. Insights and perspectives gained from studies of human arteries.
Hemodynamics and atherosclerosis. Insights and perspectives gained from studies of human arteries.
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DOI：
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发表时间：
1988-10
影响因子：
4.6
通讯作者：
S. Glagov;C. Zarins;D. Giddens;D. Ku
中科院分区：
文献类型：
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作者：
S. Glagov;C. Zarins;D. Giddens;D. Ku
动脉粥样硬化累及主要的弹性动脉和肌肉动脉，但有些血管基本完好，而另一些血管可能明显病变。颈动脉分叉、冠状动脉、肾下腹主动脉和供应下肢的血管是高危血管。斑块在分叉、分支和弯曲处形成的倾向导致了局部机械因素（如壁剪切应力和壁拉应力）增强动脉粥样硬化的推测。最近对高危人类血管的研究和相应的模型提供了定量证据，表明斑块往往发生在流速和剪切应力降低、血流偏离层流、单向模式的地方。这种流动特性往往会增加循环颗粒在敏感区域的停留时间，而在壁面剪切应力较大的区域和层流单向流区域，颗粒被迅速清除。与斑块定位相关的血流模式在收缩期最为突出。因此，长期后果可能因心率升高而大大增强，并可能对冠状动脉产生选择性影响。在几何过渡区域壁面张力的逐点再分布尚未定量地与斑块定位相关。动脉随着斑块的增大而增大，斑块和管壁形态的相关建模倾向于保持足够和规则的管腔横截面。血流动力学力似乎决定了血管直径的变化，从而恢复正常的壁剪切应力水平，而壁厚结构和组成与拉应力密切相关。血流动力学力也可能与斑块产生不稳定的症状有关，特别是与狭窄附近的壁不稳定有关。壁剪切应力、拉应力和动脉壁代谢在动脉粥样硬化的进展和并发症中的相对作用尚不清楚。将血流动力学和张力特性与斑块位置、狭窄和组成联系起来的临床技术的发展，应使病理学家能够对斑块进展和结果的地形和个体差异的基础提供新的见解。
Atherosclerosis affects the major elastic and muscular arteries, but some vessels are largely spared while others may be markedly diseased. The carotid bifurcation, the coronary arteries, the infrarenal abdominal aorta, and the vessels supplying the lower extremities are at highest risk. The propensity for plaque formation at bifurcations, branchings, and curvatures has led to conjectures that local mechanical factors such as wall shear stress and mural tensile stress potentiate atherogenesis. Recent studies of the human vessels at high risk, and of corresponding models, have provided quantitative evidence that plaques tend to occur where flow velocity and shear stress are reduced and flow departs from a laminar, unidirectional pattern. Such flow characteristics tend to increase the residence time of circulating particles in susceptible regions while particles are cleared rapidly from regions of relatively high wall shear stress and laminar unidirectional flow. The flow patterns associated with plaque localization are most prominent during systole. Long-term consequences are therefore likely to be greatly enhanced by elevated heart rate and may exert a selective effect on the coronary arteries. The point-by-point redistribution of wall tension at regions of geometric transition has not been quantitatively related to plaque localization. Enlargement of arteries as plaques increase in size and the associated modeling of plaque and wall configuration tend to preserve an adequate and regular lumen cross section. Hemodynamic forces appear to determine changes in vessel diameter so as to restore normal levels of wall shear stress, while wall thickness architecture, and composition are closely related to tensile stress. Hemodynamic forces may also be implicated in the symptom-producing destabilization of plaques, especially in relation to wall instabilities near stenoses. The relative roles of wall shear stress, tensile stress, and the metabolism of the artery wall in the progression and complication of atherosclerosis remain to be clarified. Development of clinical techniques for relating hemodynamic and tensile properties to plaque location, stenosis, and composition should permit pathologists to provide new insights into the bases for the topographic and individual differences in plaque progression and outcome.