冠脉血管支架介入耦合系统力学行为数值模拟研究

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

针对冠脉支架植入术后引起的血管内再狭窄问题,开展了冠脉支架介入耦合系统力学行为的数值模拟研究。基于Ogden非线性弹性理论,构建了冠脉血管和动脉粥样硬化斑块的超弹性本构模型。通过非线性有限元法,建立了冠脉支架与狭窄血管的耦合作用模型,研究了冠脉支架在经历压握收缩、压握卸载、球囊扩张与球囊收缩等介入过程后的体内扩张性能,分析了冠脉支架的介入对狭窄血管损伤及再狭窄的力学影响因素。对比分析了S型支架和N型支架介入后狭窄冠脉血管的生物力学响应,数值计算结果表明:狭窄冠脉血管在支架支撑体波峰处存在较高的应力梯度,而且由于2种支架联接筋结构的类似性,血管内膜与斑块的应力分布规律一致。但是,N型支架的径向回弹率与轴向短缩率均小于S型支架,导致了更高的狭窄血管壁面峰值应力和应力梯度,更易于引起冠脉血管损伤造成血管内再狭窄。综上,该文提出的冠脉支架介入耦合系统力学模型,对于优化支架结构、抑制冠脉血管再狭窄问题,提供了重要的理论依据和临床参考。

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 stressgradient on the vascular wall adjacent to the strut peak for both stentts. 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-stentt 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.