血流动力学剪切应力导致内膜增厚的成因

Avishek Mukherjee, Navid Mohammad Mirzaei, Pak-Wing Fok
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引用次数: 0

摘要

本文通过使用 FEniCS 计算环境进行有限元模拟,研究了血流动力学剪切应力诱导的动脉内膜生长。在我们的模型中,内膜的生长取决于横截面几何形状和剪切应力。在这项工作中,动脉壁被模拟为三个不同的层次:内膜、介质和外膜,每个层次都具有不同的机械特性。我们假设血管的横截面在轴向没有变化。我们还假设血流是稳定的、非湍流的和单向的。血流会对血管内皮产生剪切应力,刺激血小板衍生生长因子(PDGF)的释放,从而推动血管生长。我们模拟了三种不同动脉横截面几何形状的内膜生长。我们发现,内膜增厚的性质因动脉几何形状而异。对于环形横截面几何形状,内膜在角度方向上的生长是均匀的,内膜生长时内皮保持圆形。对于非环形横截面几何形状,较厚的内膜比较薄的内膜生长得更快,剪切应力和内膜增厚与距离流速最大的血流中心的距离呈负相关。随着时间的推移,曲率的最大值和最小值分别增加和减少,PDGF 浓度增加,管腔变得更加多边形。该模型为血流动力学模拟与动脉粥样硬化数学描述的耦合提供了一个框架,而这两者都曾分别进行过详细的建模。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genesis of intimal thickening due to hemodynamical shear stresses.

This paper investigates intimal growth in arteries, induced by hemodynamical shear stress, through finite element simulation using the FEniCS computational environment. In our model, the growth of the intima depends on cross-section geometry and shear stress. In this work, the arterial wall is modeled as three distinct layers: the intima, the media and the adventitia, each with different mechanical properties. We assume that the cross-section of the vessel does not change in the axial direction. We further assume that the blood flow is steady, non-turbulent and unidirectional. Blood flow induces shear stress on the endothelium and stimulates the release of platelet derived growth factor (PDGF) which drives the growth. We simulate intimal growth for three distinct arterial cross section geometries. We show that the qualitative nature of intimal thickening varies depending on arterial geometry. For cross section geometries that are annular, the growth of the intima is uniform in the angular direction, and the endothelium stays circular as the intima grows. For non-annular cross section geometries, the intima grows more quickly where it is thicker, and shear stress and intimal thickening are negatively correlated with the distance from the flow center, where the flow velocity is maximal. Over time, the maxima and minima of the curvature increase and decrease, respectively, the PDGF concentration increases and the lumen becomes more polygonal. The model provides a framework for coupling hemodynamics simulations to mathematical descriptions of atherosclerosis, both of which have been modeled separately in great detail.

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