王庆虎,杨少雄,许怡隽,龚晓波.颈动脉分叉处血管粥样硬化斑块的体内应力分析[J].医用生物力学,2019,34(3):268-276
颈动脉分叉处血管粥样硬化斑块的体内应力分析
In Vivo Stress Analysis of an Atherosclerotic Plaque at Carotid Bifurcation
投稿时间:2018-04-21  修订日期:2018-06-06
DOI:
中文关键词:  粥样硬化斑块  颈动脉分叉  残余应力  弹性剪切应力  流体壁面切应力  斑块破裂
英文关键词:atherosclerotic plaque  carotid bifurcation  residual stress  elastic shear stress  fluid wall shear stress  plaque rupture
基金项目:国家自然科学基金项目(11372191, 11232010)
作者单位
王庆虎 上海交通大学 船舶海洋与建筑工程学院工程力学系 
杨少雄 上海交通大学 船舶海洋与建筑工程学院工程力学系 
许怡隽 上海交通大学 船舶海洋与建筑工程学院工程力学系 
龚晓波 上海交通大学 船舶海洋与建筑工程学院工程力学系 
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中文摘要:
      目的 探究颈动脉分叉处血管斑块的体内应力分布,为颈动脉分叉处血管斑块破裂行为的研究和诊断治疗方案的设计提供力学机理参考。方法 基于人体颈动脉分叉血管的平均几何参数,建立三维颈动脉分叉血管及其斑块的几何模型,通过“热-结构”耦合重建颈动脉分叉血管及其斑块的残余应力,并计算血压和血流分别作用下颈动脉分叉处血管斑块的体内应力。结果 斑块的肩部同时存在着最大主应力和弹性剪切应力的应力集中。斑块肩部的弹性剪切应力随着狭窄率增大或血压升高均增加。斑块上游区域的流体壁面切应力明显高于斑块下游区域,斑块下游区域的振荡剪切指数则显著大于上游区域。且斑块的弹性剪切应力和流体壁面切应力大小随着狭窄率的变化呈现出不同的变化规律。结论 斑块从内部中心位置到壁面肩部承受着非均匀的应力分布,血管严重狭窄时“内压外拉”的受力状态更容易导致斑块破裂。随着血压的变化,斑块结构应力的周期性变化可能使斑块产生结构疲劳,增加破裂风险。斑块上下游区域流体动力学参数的差异可能是斑块上下游组分、易损程度等性质不同的原因之一。
英文摘要:
      Objective To investigate the in vivo stress distribution of the atherosclerotic plaque at carotid bifurcation, so as to provide references for the mechanical mechanisms of plaque rupture at carotid bifurcation and the design for further medical treatment. Methods The three-dimensional geometric model of carotid bifurcation and plaque were established according to average geometric parameters of human carotid bifurcation. Residual stress of the carotid bifurcation and plague was reestablished with “thermal-structure” coupling method, and in vivo stresses of vessels with the plaque at carotid bifurcation under blood pressure and blood flow were calculated. Results Both the maximum principal stress and elastic shear stress concentrated on the shoulder of the plaque. Elastic shear stress increased with the increase of stenosis ratio and blood pressure. Wall shear stress in the upstream of the plaque was considerably higher than that of the downstream. The distribution of oscillatory shear index(OSI) was quite the opposite. The changing patterns of the elastic shear stress and flow shear stress were quite different with the change of stenosis ratios. Conclusions Tension grew gradually from the centrality to shoulder surface of the plaque. The centrality of the plaque might bear compression when the stenosis was very severe. The periodic variation of the structural stress might cause structural fatigue of the plaque, thus increasing the rupture risk. Distinction of the component and vulnerability of the plaque between upstream and downstream might be caused by differences in hemodynamic parameters of the plaque between upstream and downstream.
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