O-017 Effect of biomechanical environment in vessel wall on stent restenosis

IntroductionStenting has become a standard procedure to treat atherosclerotic vessels. However, restenosis is reported in approximately one-third of patients treated with intracranial stenting, and its avoidance is drawing attention. The cause of restenosis includes vessel injury due to pressure from stent expansion and neointimal thickening due to decrease in vessel wall shear stress (WSS). Although the severity of vessel injury is proportional to neointimal thickness and restenosis, they are discussed separately. The object of this research is to examine the stress concentration and wall shear stress by a numerical analysis and reveal their configuration dependent relationship and effect to stent structure.Materials and methodsA commercial open cell coronary stent model was used in this research to make a comparison with other research. Firstly, stent expansion in an intact vessel was simulated by the finite element method and the stress distribution of stented vessel was analyzed. Next, computational fluid dynamics was conducted to examine blood flow and WSS distribution. Furthermore, stent structure was modified to improve stress concentration and WSS. Stress concentration was avoided by connecting adjacent stent struts and making a closed cell model. This model was named model 1. In contrast, low WSS was avoided by reducing the number of stent struts in the longitudinal direction, named model 2. Vessel stress and WSS distribution was examined to look into the effect of stent structure on vessel stress and WSS.Results and discussionVon Mises stress and WSS distribution of stented arterial lumen is shown in Abstract O-017 figure 1. Localized radial stress and low WSS, below 1 Pa, was observed around intersections of stent struts after stent expansion. Since endothelial cells and internal elastic lamina within the vessel is deformed in the same area, vessel injury is implied. Moreover, decrease in WSS and hoop stress was observed throughout the stented vessel lumen. Like WSS, hoop stress promotes neointimal thickening. Therefore, restenosis is assumed due to the interaction of vessel injury and neointimal thickening. Also, the modified model 1 moderated stress concentration but induced low WSS. On the other hand, model 2 improved low WSS in the vessel lumen but stress concentration was observed. It is presumed that stress concentration improves when the contact area of the stent strut increases whereas the area subjected to low WSS increases with the add