维持张力稳态的组织生长模型及其在高血压和支架动脉中的应用

Pengfei Dong, K. Nunes, Linxia Gu
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引用次数: 0

摘要

在这项工作中,建立了一个维持稳态机械环境的理论生长模型,以捕捉动脉的生长行为及其与机械环境的关联。采用乘法分解方法将变形矩阵分解为弹性项和生长项。一种与内稳态应激相关的生长因子被用来调节动脉形态的进行性变化。此外,为了避免无限生长,还采用了生长系数。动脉生长模型在商业有限元软件中实现,并在高血压和支架置入的情况下进行测试。结果表明,高血压引起的动脉生长可以减轻动脉异常应激,使动脉应激水平恢复到稳态。支架植入术后动脉生长模式与von Mises应力在动脉内的分布一致。动脉生长均匀化了动脉内的应力分布,除了支架支撑下的区域。动脉的不均匀生长破坏了动脉内最大主应力的排列,延长了支架,缩小了管腔面积,并聚集了组织脱垂。期望本研究建立的生长模型有助于理解和调节组织的慢性反应。适当的动脉生长模型与张力稳态相关,为预测动脉力学环境的改变、识别导致再狭窄的生物力学因素以及设计治疗策略来调节组织适应提供了见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tissue Growth Model for Maintaining Tensional Homeostasis with Applications to Hypertension and Stented Artery
In this work, a theoretical growth model for maintaining a homeostatic mechanical environment was developed to capture the growth behavior of the artery and its association with its mechanical environment. The multiplicative decomposition approach was adopted to decompose the deformation matrix into an elastic term and a growth term. A growth factor in relation to homeostatic stress was used to regulate the progressive changes in the arterial morphology. In addition, a growth coefficient was adopted to avoid unlimited growth. Arterial growth model was implemented in a commercial finite element software and tested in the cases of hypertension and stenting. Results have demonstrated that the arterial growth induced by hypertension can mitigate abnormal arterial stresses and restore the stress level in the artery back to its homeostasis. Following stenting, the arterial growth pattern was consistent with the distribution of the von Mises stresses in the artery. The arterial growth homogenized the stress distribution in the artery, except for the regions under the stent struts. The heterogeneous growth of the artery disrupted the alignment of the maximum principal stresses in the artery, elongated the stent, reduced lumen area, and aggregated the tissue prolapse. It is expected that the growth model developed in this work could help to understand and regulate the chronic response of the tissue. Appropriate modeling of arterial growth in connection with tensional homeostasis provided insights for predicting alterations to the arterial mechanical environment, identifying biomechanical factors leading to restenosis, and design therapeutic strategies to regulate the tissue adaptations.
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