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Nakamura, N., Torii, S., Tsuchiya, H., Nakano, A., Oikawa, Y., Yajima, J., Nakamura, S., Nakano, M., Masuda, N., Ohta, H., et al. (2020) Formation of Calcified Nodule as a Cause of Early In-Stent Restenosis in Patients Undergoing Dialysis. Journal of the American Heart Association, 9, e016595.
https://doi.org/10.1161/JAHA.120.016595

has been cited by the following article:

• TITLE: Finite Element Simulation of In-Stent Restenosis with Tissue Growth Model

  AUTHORS: Jie Cheng, Lucy T. Zhang

  KEYWORDS: Stents, In-Stent Restenosis, Tissue Growth, Finite Element Simulation, Growth Model

  JOURNAL NAME: Journal of Biomedical Science and Engineering, Vol.14 No.2, February 5, 2021

  ABSTRACT: In this study, a finite element simulation of in-stent restenosis (ISR) is conducted to simulate the deployment and expansion of a stent in an occluded artery with a contact model and a mechanics-based growth model. A tissue growth model based on the multiplicative decomposition of deformation is applied to investigate the growth of the plaque and artery wall upon the stent’s implantation. Due to the high stresses at the contact points between the stent struts and the tissue, further tissue injury or restenosis is observed. The simulation results show that after the stent deployment, the von Mises stress is significantly larger in the plaque compared to the artery wall, especially in the region that is in contact with the stent. However, the growth of the plaque and artery tends to even out the stress concentration over time. The tissue growth is found to be more significant near the inner wall than the outer layer. A 0.77 mm restenosis is predicted, which agrees with published clinical observations. The features of the artery growth are carefully analyzed, and the underlying mechanism is discussed. This study is the first attempt to apply finite element analysis to artery restenosis, which establishes a framework for predicting ISR’s occurrence and severity. The results also provide insights into understanding the underlying mechanism of in-stent restenosis.