Computational Stress Analysis of Atherosclerotic Plaques in ApoE Knockout Mice
Computational Stress Analysis of Atherosclerotic Plaques in ApoE Knockout Mice
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DOI：
10.1007/s10439-009-9897-5
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发表时间：
2010-03-01
影响因子：
3.8
通讯作者：
Weinbaum, Sheldon
中科院分区：
文献类型：
--
作者：
Vengrenyuk, Yuliya;Kaplan, Theodore J.;Weinbaum, Sheldon
载脂蛋白E基因敲除（ApoE KO）小鼠的主动脉窦病变很少表现出纤维帽破裂的任何迹象，而最近在其头臂动脉（BCA）的近端部分报道了帽破裂。我们使用基于组织学的有限元分析来评估来自6只42-56周龄脂肪喂养的ApoE KO小鼠的主动脉和BCA病变中的峰值周向应力。该分析能够解释小鼠主动脉病变的更大稳定性，并提供新的见解BCA病变作为模型的稳定性，在其纤维帽中有和没有微钙化的人类病变。主动脉病变纤维帽的预测平均峰值应力为205.8 kPa，显著低于BCA帽的最大应力平均值568.8 kPa。主动脉斑块应力仅略微依赖于帽厚度，而BCA病变表现出与人类易损斑块相似的帽厚度减小的峰值帽应力的指数增长。平均帽厚度为2 μ m的鼠BCA破裂损伤显示出千分之一1400 kPa的应力，比平均帽厚度为23 μ m且帽中无微钙化的人破裂斑块高3倍，但与50 μ m厚的人薄帽中纵横比为2的细长微钙化周围的峰值应力几乎相同。我们预测小鼠BCA的生物力学应力模式接近人类易损斑块，帽中无微钙化，而主动脉病变显示出与人类稳定病变相似的应力趋势。
The aortic sinus lesions of apolipoprotein E knockout (ApoE KO) mice seldom show any signs of fibrous cap disruption, whereas cap ruptures have been recently reported in the proximal part of their brachiocephalic arteries (BCA). We use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from six 42-56 week-old fat-fed ApoE KO mice. This analysis is able to both explain the greater stability of aortic lesions in mice and provide new insight into the BCA lesion as a model for the stability of human lesions with and without microcalcifications in their fibrous caps. The predicted average peak stress in fibrous caps of aortic lesions of 205.8 kPa is significantly lower than the average value of maximum stresses of 568.8 kPa in BCA caps. The aortic plaque stresses only slightly depend on the cap thickness, while BCA lesions demonstrate an exponential growth of peak cap stresses with decreasing cap thickness similar to human vulnerable plaques. Murine BCA ruptured lesions with mean cap thickness of 2 mu m show stresses a parts per thousand 1400 kPa, three times higher than human ruptured plaques with a mean cap thickness of 23 mu m without microcalcifications in the cap, but nearly identical to the peak stress around an elongated microcalcification with aspect ratio 2 in a human thin cap a parts per thousand 50 mu m thick. We predict biomechanical stress patterns in mouse BCA close to human vulnerable plaques without microcalcification in the cap, while aortic lesions show stress tendency similar to stable lesions in human.