存在低细胞和钙化斑块时自膨胀支架与动脉壁的相互作用。

IF 3 3区 医学 Q2 BIOPHYSICS
Zubeir Allum Saib, Farid Abed, Mergen H Ghayesh, Marco Amabili
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引用次数: 0

摘要

由镍钛诺合金制造的自扩张支架通常与传统的球囊扩张支架一起用于为狭窄的动脉提供支架。然而,阻碍支架疗效的一个重要限制因素是再狭窄,再狭窄是由新内膜增生引发的,并导致介入后管腔尺寸增大的损失。在这项研究中,开发了一个非线性有限元模型,用于模拟支架卷曲和扩张,以及在存在斑块的情况下支架与周围血管的相互作用。主要目的是确定存在低细胞斑块和钙化斑块的动脉壁与扩张支架之间的接触压力和力。结果表明了斑块钙化的弊端,斑块钙化会在界面处引发急剧的接触压力和径向力激增,血管内的冯米塞斯应力也会显著上升,从而可能导致血管破裂和再狭窄。然后建立了一条回归线,将低细胞斑块和钙化斑块联系起来。调整后的决定系数表明,钙化斑块和低细胞斑块模型的接触压力之间具有良好的相关性。关于动脉壁特性的方向性,各向同性动脉和各向异性动脉之间的接触压力和力观测结果没有显著差异。此外,摩擦系数的变化也不会对界面接触压力产生重大影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Interaction of a self-expandable stent with the arterial wall in the presence of hypocellular and calcified plaques.

Self-expandable stents manufactured from nitinol alloys are commonly utilized alongside traditional balloon-expandable stents to provide scaffolding to stenosed arteries. However, a significant limitation hampering stent efficacy is restenosis, triggered by neointimal hyperplasia and resulting in the loss of gain in lumen size, post-intervention. In this study, a nonlinear finite element model was developed to simulate stent crimping and expansion and its interaction with the surrounding vessel in the presence of a plaque. The main aim was to determine contact pressures and forces induced at the interface between an artery wall with hypocellular and calcified plaques and an expanded stent. The results demonstrated the drawbacks of plaque calcification, which triggered a sharp contact pressure and radial force surge at the interface as well as a significant rise in von Mises stress within the vessel, potentially leading to rupture and restenosis. A regression line was then established to relate hypocellular and calcified plaques. The adjusted coefficient of determination indicated a good correlation between contact pressures for calcified and hypocellular plaque models. Regarding the directionality of wall properties, contact pressure and force observations were not significantly different between isotropic and anisotropic arteries. Moreover, variations in friction coefficients did not substantially affect the interfacial contact pressures.

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来源期刊
Biomechanics and Modeling in Mechanobiology
Biomechanics and Modeling in Mechanobiology 工程技术-工程:生物医学
CiteScore
7.10
自引率
8.60%
发文量
119
审稿时长
6 months
期刊介绍: Mechanics regulates biological processes at the molecular, cellular, tissue, organ, and organism levels. A goal of this journal is to promote basic and applied research that integrates the expanding knowledge-bases in the allied fields of biomechanics and mechanobiology. Approaches may be experimental, theoretical, or computational; they may address phenomena at the nano, micro, or macrolevels. Of particular interest are investigations that (1) quantify the mechanical environment in which cells and matrix function in health, disease, or injury, (2) identify and quantify mechanosensitive responses and their mechanisms, (3) detail inter-relations between mechanics and biological processes such as growth, remodeling, adaptation, and repair, and (4) report discoveries that advance therapeutic and diagnostic procedures. Especially encouraged are analytical and computational models based on solid mechanics, fluid mechanics, or thermomechanics, and their interactions; also encouraged are reports of new experimental methods that expand measurement capabilities and new mathematical methods that facilitate analysis.
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