Techniques designed to increase initial luminal diameter during stent implantation may ultimately lead to early restenosis by causing substantial vessel wall trauma and promoting neointimal hyperplasia. The purpose of this study was to evaluate the impact of stent oversizing on resultant arterial wall stress concentrations and examine the concept of a "stress threshold" for neointimal hyperplasia development.
MATERIALS AND METHODS
A previously described three-dimensional large-strain hyperelastic numeric model was used to examine the nonlinear isotropic behavior of a 6-mm-diameter artery during stent deployment. An in situ axial prestretch of 10% and a mean arterial pressure of 100 mm Hg (13.3 kPa) were applied before stepwise expansion of a simulated Palmaz-Schatz stent to a diameter 30% greater than that of the native artery. The variation of arterial wall von Mises stresses with percentage diameter inflation was then compared with the known distribution of stent-induced neointimal hyperplasia.
The order in which location-specific peak stresses exceeded a predetermined stress threshold was constant: the stent ends surpassed the threshold first, followed by the stent cross-links, then the stent struts, and finally the bare area between the stent struts. These locations corresponded in order to the most common locations of intimal proliferation after stent deployment. An exponential relationship between peak stress concentration and percent stent inflation was formulated.
Stent-induced intramural stress injury beyond a certain threshold may cause early restenosis by triggering neointimal hyperplasia. Maximum stress concentrations increase exponentially with stent deployment diameter, highlighting the importance of minimal stent overexpansion and novel stent designs that specifically address peak stress reduction.
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