Effects of Arterial Strain and Stress in the Prediction of Restenosis Risk: Computer Modeling of Stent Trials

Authors

Shijia Zhao, University of Nebraska-LincolnFollow
Linxia Gu, University of Nebraska-LincolnFollow
Stacey R. Froemming, Children’s Hospital & Medical Center, Omaha, NE

Document Type

Article

Date of this Version

2012

Citation

Biomedical Engineering Letters 2 (2012), pp.158-163; doi: 10.1007/s13534-012-0067-6

Comments

Copyright © 2012 The Korean Society of Medical & Biological Engineering and Springer. Used by permission.

Abstract

Purpose — In-stenting restenosis is one of the major complications after stenting. Clinical trials of various stent designs have reported different restenosis rates. However, quantitative correlation between stent features and restenosis statistics is scant. In this work, it is hypothesized that stress concentrations on arterial wall caused artery injury, which initiates restenosis. The goal is to assess the correlation between stent-induced arterial stress and strain and the documented restenosis rates.

Methods — Six commercially available stents, including balloon-expandable stents and self-expanding stents, were virtually implanted into the arteries through finite element method. The resulted peak Von Mises stress, principal stress, principal logarithm strain, as well as percentage of intimal area with abnormal higher stress were monitored.

Results — Positive correlation between arterial stress and strain after stent implantations and the documented restenosis rates from the corresponding clinical trials was found regardless of stent types. No statistical significant difference was observed for various stress or strain parameters serving as indicators of artery injury.

Conclusions — In-stent restenosis are less likely to occur as arterial mechanics are least altered by stent implantations. Optimization of stent designs to minimize the stent-induced arterial stresses and strains can reduce the arterial injury, and thus reduce the occurrence of restenosis. This work improved our understanding of the stent-lesion interactions that regulate arterial mechanics and demonstrated that arterial stress and strain could predict the risk of instent restenosis.