Department of Biomedical Engineering, The City College of New York, CUNY, New York, NY 10031, USA.
Ann Biomed Eng. 2010 Mar;38(3):738-47. doi: 10.1007/s10439-009-9897-5.
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 microm show stresses approximately 1400 kPa, three times higher than human ruptured plaques with a mean cap thickness of 23 microm 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 approximately 50 microm 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.
载脂蛋白 E 基因敲除（ApoE KO）小鼠的主动脉窦病变很少出现纤维帽破裂的迹象，而最近有报道称其头臂动脉（BCA）近端出现了纤维帽破裂。我们使用基于组织学的有限元分析来评估 6 只 42-56 周龄高脂喂养的 ApoE KO 小鼠的主动脉和 BCA 病变的峰值周向应力。该分析不仅能够解释小鼠主动脉病变的更大稳定性，还能够深入了解 BCA 病变作为一种模型，用于研究有和无纤维帽微钙化的人类病变的稳定性。预测的主动脉病变纤维帽的平均峰值应力为 205.8 kPa，明显低于 BCA 帽的最大应力平均值 568.8 kPa。主动脉斑块的应力仅略微取决于帽厚度，而 BCA 病变的帽应力随着帽厚度的减小呈指数增长，类似于人类易损斑块。平均帽厚度为 2 µm 的小鼠 BCA 破裂病变的应力约为 1400 kPa，是帽中无微钙化的人类破裂斑块的 3 倍，而与帽厚度约为 50 µm 的人类薄帽中长径比为 2 的拉长微钙化周围的峰值应力几乎相同。我们预测了小鼠 BCA 的生物力学应力模式，类似于无帽微钙化的人类易损斑块，而主动脉病变的应力趋势类似于人类稳定病变。
