JIANG Xu-dong, TENG Xiao-yan, SHI Dong-yan, ZHANG Yong-feng. NUMERICAL SIMULATION RESEARCH ON MECHANICAL BEHAVIOR OF INTERVENTION COUPLING SYSTEMS FOR CORONARY STENTS[J]. Engineering Mechanics, 2016, 33(8): 231-237. DOI: 10.6052/j.issn.1000-4750.2014.12.1050
Citation: JIANG Xu-dong, TENG Xiao-yan, SHI Dong-yan, ZHANG Yong-feng. NUMERICAL SIMULATION RESEARCH ON MECHANICAL BEHAVIOR OF INTERVENTION COUPLING SYSTEMS FOR CORONARY STENTS[J]. Engineering Mechanics, 2016, 33(8): 231-237. DOI: 10.6052/j.issn.1000-4750.2014.12.1050

NUMERICAL SIMULATION RESEARCH ON MECHANICAL BEHAVIOR OF INTERVENTION COUPLING SYSTEMS FOR CORONARY STENTS

  • A numerical simulation of the mechanical behavior of an intervention coupling system for coronary stents is performed to investigate the induced vascular restenosis from the stent intervention. A hyperelastic constitutive model of the coronary artery, as well as the atherosclerotic plaque, is derived on the basis of the nonlinear elastic theory developed by Ogden. The interactive model of coronary stents with the stenosed vessel is presented by the nonlinear finite element method. The in-vivo expansion performance of stents is evaluated after intervention procedures including crimping, removing of crimping, balloon expansion, and balloon contraction. Subsequently the mechanical effect factors of the vascular injury and the resulting restenosis are analyzed by the stent intervention. The biomechanical response of the stenosed vessel to the S-stent intervention is compared with that of its counterpart to the N-stent intervention. The numerical results indicate that there is extremely high stress gradient on the vascular wall adjacent to the strut peak for both stents. The resulting stress distribution on the vascular intima and atherosclerotic plaque from the S-stent is similar to that from the N-stent, as a result of their analogous link geometry. However, radial recoil and foreshortening for the N-stent are less prevalent than in the counterpart with the S-stent. Thus N-stent intervention results in higher wall peak stresses and stress gradients on the stenosed vessel, contributing to vascular restenosis resulting from vascular injury. This model provides scientific guidance to stent optimization design and clinical reference to the inhibition of vascular restenosis.
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