Impact of transmural heterogeneities on arterial adaptation
Impact of transmural heterogeneities on arterial adaptation
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DOI：
10.1007/s10237-009-0177-y
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发表时间：
2010-06-01
影响因子：
3.5
通讯作者：
Itskov, M.
中科院分区：
文献类型：
--
作者：
Schmid, H.;Watton, P. N.;Itskov, M.
最近的实验和计算研究表明，穿过动脉壁的跨壁非均质材料特性对于理解成分降解分子的异质性表达至关重要。鉴于这些分子的表达被认为与局部应力的大小密切相关，模拟跨壁应力分布对于理解疾病期间的动脉适应至关重要。这项研究的目的是开发一种动脉生长和重塑框架，可以将跨壁不均匀成分分布和残余应力合并到三维有限元模型中。作为一个说明性的例子，我们模拟了梭形动脉瘤的发展，并研究了弹性体和胶原体的异质性在演化过程中对应力分布的影响。观察到生长和重塑的适应过程表现出跨壁变化。生理成分分布不均时，中膜向内膜出现应力峰值，外膜出现应力平台。这些特征主要可以归因于弹性成分的潜在异质性。在动脉适应过程中，胶原蛋白的应变被调节为保持在其恒定水平；因此，胶原蛋白的部分应力对总应力的影响小于弹性蛋白。然而，在显著的弹性蛋白降解之后，胶原在跨壁应力分布中起主导作用，并且向外膜方向出现明显的应力峰值。我们的结论是，为了提高我们对动脉适应性和动脉疾病病因学的理解，有必要在组织病理学检查中量化跨壁成分分布，了解并模拟演变中的跨壁应力分布的作用。
Recent experimental and computational studies have shown that transmurally heterogeneous material properties through the arterial wall are critical to understanding the heterogeneous expressions of constituent degrading molecules. Given that expression of such molecules is thought to be intimately linked to local magnitudes of stress, modelling the transmural stress distribution is critical to understanding arterial adaption during disease. The aim of this study was to develop an arterial growth and remodelling framework that can incorporate both transmurally heterogeneous constituent distributions and residual stresses, into a 3-D finite element model. As an illustrative example, we model the development of a fusiform aneurysm and investigate the effects of elastinous and collagenous heterogeneities on the stress distribution during evolution. It is observed that the adaptive processes of growth and remodelling exhibit transmural variations. For physiological heterogeneous constituent distributions, a stress peak appears in the media towards the intima, and a stress plateau occurs towards the adventitia. These features can be primarily attributed to the underlying heterogeneity of elastinous constituents. During arterial adaption, the collagen strain is regulated to remain in its homoeostatic level; consequently, the partial stress of collagen has less influence on the total stress than the elastin. However, following significant elastin degradation, collagen plays the dominant role for the transmural stress profile and a marked stress peak occurs towards the adventitia. We conclude that to improve our understanding of the arterial adaption and the aetiology of arterial disease, there is a need to: quantify transmural constituent distributions during histopathological examinations, understand and model the role of the evolving transmural stress distribution.