Increased artery wall stress post-stenting leads to greater intimal thickening.
Increased artery wall stress post-stenting leads to greater intimal thickening.
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DOI：
10.1038/labinvest.2011.57
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发表时间：
2011-06
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影响因子：
--
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中科院分区：
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自20世纪80年代末第一例人类手术以来，血管支架植入已被公认为治疗动脉粥样硬化的标准形式。尽管这些医疗器械取得了巨大的成功，但它们也不是没有问题，因为过度的新生内膜增生会导致新的阻塞(再狭窄)的形成。临床资料表明，支架设计是导致再狭窄发生的关键因素。此外，计算研究表明，生物力学环境强烈依赖于支架的几何构型，因此可能与再狭窄的发生有关。我们假设，支架在动脉壁上引起更高的应力会导致更具侵袭性的病理生物学反应，这是由新生内膜增生量决定的。本研究的目的是检验固体生物力学在再狭窄发生中的作用。采用计算建模技术和活体分析相结合的方法，研究了两种支架设计对动脉壁施加更大或更小应力的病理生物学反应。将支架设计植入猪模型(猪)中约28天，并利用新的综合病理学技术(定量显微计算机断层扫描、组织形态计量学)来量化病理生物学反应。与此同时，计算方法被用来量化两个支架对动脉施加的机械负荷。结果显示，动脉壁上的应力值与病理生物学反应之间有很强的相关性，承受较高应力的支架支架上的新生内膜厚度显著增加(高应力支架为0.197±0.020 mm，低应力支架为0.071±0.016 mm)。因此，我们得出结论，这种病理生物学差异是坚实的生物力学环境的直接结果，证实了施加更高壁应力的支架将引发更具侵袭性的病理生物学反应的假设。
Since the first human procedure in the late 1980s, vascular stent implantation has been accepted as a standard form of treatment of atherosclerosis. Despite their tremendous success, these medical devices are not without their problems, as excessive neointimal hyperplasia can result in the formation of a new blockage (restenosis). Clinical data suggest that stent design is a key factor in the development of restenosis. Additionally, computational studies indicate that the biomechanical environment is strongly dependent on the geometrical configuration of the stent, and therefore possibly involved in the development of restenosis. We hypothesize that stents that induce higher stresses on the artery wall lead to a more aggressive pathobiologic response, as determined by the amount of neointimal hyperplasia. The aim of this investigation was to examine the role of solid biomechanics in the development of restenosis. A combination of computational modeling techniques and in vivo analysis were employed to investigate the pathobiologic response to two stent designs that impose greater or lesser levels of stress on the artery wall. Stent designs were implanted in a porcine model (pigs) for approximately 28 days and novel integrative pathology techniques (quantitative micro-computed tomography, histomorphometry) were utilized to quantify the pathobiologic response. Concomitantly, computational methods were used to quantify the mechanical loads that the two stents place on the artery. Results reveal a strong correlation between the computed stress values induced on the artery wall and the pathobiologic response; the stent that subjected the artery to the higher stresses had significantly more neointimal thickening at stent struts (high stress stent: 0.197 ± 0.020 mm vs. low-stress stent: 0.071 ± 0.016 mm). Therefore, we conclude that the pathobiologic differences are a direct result of the solid biomechanical environment, confirming the hypothesis that stents that impose higher wall stresses will provoke a more aggressive pathobiological response.
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DOI：
10.1016/s0735-1097(97)00450-6
发表时间：
1998-01-01
影响因子：
24
作者：
Kornowski, R;Hong, MK;Leon, MB
通讯作者：
Leon, MB
影响因子：
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Rogers, C
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作者：
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Chaikof, EL
影响因子：
2.6
作者：
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通讯作者：
Beregi, Jean-Paul