Key result
In-silico modeling demonstrated that early appearance of a functional endothelium completely inhibits the development of in-stent restenosis, whereas delayed recovery leads to neointimal growth proportional to stent strut deployment depth.
Why the study?
Does functional re-endothelialization prevent neointimal growth and in-stent restenosis in an in-silico model of stented coronary arteries?
Does functional re-endothelialization prevent neointimal growth and in-stent restenosis in an in-silico model of stented coronary arteries?
This in-silico computational model demonstrates that early recovery of a functional endothelium producing nitric oxide can completely inhibit in-stent restenosis, highlighting the importance of functional re-endothelialization after stenting.
Answers are grounded in this paper and cite their sources.
Early functional re-endothelialization may prevent restenosis; leaves open translation to human stent outcomes.
Treatment of stenosed coronary arteries by balloon angioplasty and stenting results in arterial injury including severe damage to the endothelium at the site of treatment and initiates a complex cascade of inflammatory processes that may lead to the development of in-stent restenosis (ISR). Many clinical and biological factors involved in the progression of restenotic lesions have been studied in detail over the past few years but the mystery behind the pathophysiological mechanisms of this disease is still unresolved. In the present work, the effects of re-endothelialization and nitric oxide release on neointimal growth are investigated in-silico using a two dimensional multi-scale model of ISR. The effect of stent deployment depths on the development of ISR is studied as a function of time after stenting. Two dimensional domains were prepared by deploying bare metal stent struts at three different deployment depths into the tissue. Shear stress distribution on endothelial cells, obtained by blood flow simulations, was translated into nitric oxide production that keeps the smooth muscle cells in quiescent state. The cellular growth trends were plotted as a function of time and the data indicate a positive correlation between the neointimal growths and strut deployment depths in the presence of a functional endothelium, in qualitative agreement with in-vivo data. Additionally, no ISR is observed if a functional endothelium appears much earlier.
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Tahir et al. (2013) studied In-stent restenosis. Early functional re-endothelialization vs. Delayed or absent functional endothelium was evaluated on Neointimal area growth. In-silico modeling demonstrated that early appearance of a functional endothelium completely inhibits the development of in-stent restenosis, whereas delayed recovery leads to neointimal growth proportional to stent strut deployment depth.
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