Prendergast P J, Lally C, Daly S, Reid A J, Lee T C, Quinn D, Dolan F
Center for Bioengineering, Department of Mechanical Engineering, Trinity College, Dublin 2, Ireland.
J Biomech Eng. 2003 Oct;125(5):692-9. doi: 10.1115/1.1613674.
The effectiveness of a cardiovascular stent depends on many factors, such as its ability to sustain the compression applied by the vessel wall, minimal longitudinal contraction when it is expanded, and its ability to flex when navigating tortuous blood vessels. The long-term reaction of the tissue to the stent is also device dependant; in particular some designs provoke in-stent restenosis (i.e., regrowth of the occlusion around the stent). The mechanism of restenosis is thought to involve injury or damage to the vessel wall due to the high stresses generated around the stent when it expands. Because of this, the deflection of the tissue between the struts of the stent (called prolapse or "draping") has been used as a measure of the potential of a stent to cause restenosis. In this paper, uniaxial and biaxial experiments on human femoral artery and porcine aortic vascular tissue are used to develop a hyperelastic constitive model of vascular tissue suitable for implementation in finite-element analysis. To analyze prolapse, four stent designs (BeStent 2, Medtronic AVE; NIROYAL, Boston Scientific; VELOCITY, Cordis; TETRA, Guidant) were expanded in vitro to determine their repeating-unit dimensions. This geometric data was used to generate a finite element model of the vascular tissue supported within a repeating-unit of the stent. Under a pressure of 450 mm Hg (representing the radial compression of the vessel wall), maximum radial deflection of 0.253 mm, 0.279 mm, 0.348 mm and 0.48 mm were calculated for each of the four stents. Stresses in the vascular wall were highest for the VELOCITY stent. The method is proposed as a way to compare stents relative to their potential for restenosis and as a basis for a biomechanical design of a stent repeating-unit that would minimize restenosis.
心血管支架的有效性取决于许多因素，例如其承受血管壁施加压力的能力、扩张时最小的纵向收缩以及在迂曲血管中导航时的弯曲能力。组织对支架的长期反应也取决于器械；特别是一些设计会引发支架内再狭窄（即支架周围闭塞的再次生长）。再狭窄的机制被认为涉及支架扩张时在其周围产生的高应力对血管壁造成的损伤。因此，支架支柱之间组织的偏转（称为脱垂或“悬垂”）已被用作衡量支架导致再狭窄可能性的指标。在本文中，对人体股动脉和猪主动脉血管组织进行了单轴和双轴实验，以建立适用于有限元分析的血管组织超弹性本构模型。为了分析脱垂情况，在体外扩张了四种支架设计（BeStent 2，美敦力AVE；NIROYAL，波士顿科学；VELOCITY，科迪斯；TETRA，捷迈）以确定其重复单元尺寸。该几何数据用于生成支架重复单元内支撑的血管组织的有限元模型。在450毫米汞柱的压力下（代表血管壁的径向压缩），计算出四种支架各自的最大径向偏转分别为0.253毫米、0.279毫米、0.348毫米和0.48毫米。VELOCITY支架的血管壁应力最高。该方法被提议作为一种比较支架导致再狭窄可能性的方式，并作为支架重复单元生物力学设计的基础，该设计将使再狭窄最小化。
