Mechanistic evaluation of long-term in-stent restenosis based on models of tissue damage and growth

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ORIGINAL PAPER

Mechanistic evaluation of long‑term in‑stent restenosis based on models of tissue damage and growth Ran He1 · Liguo Zhao1   · Vadim V. Silberschmidt1 · Yang Liu1 Received: 12 August 2019 / Accepted: 17 December 2019 © The Author(s) 2020

Abstract Development and application of advanced mechanical models of soft tissues and their growth represent one of the main directions in modern mechanics of solids. Such models are increasingly used to deal with complex biomedical problems. Prediction of in-stent restenosis for patients treated with coronary stents remains a highly challenging task. Using a finite element method, this paper presents a mechanistic approach to evaluate the development of in-stent restenosis in an artery following stent implantation. Hyperelastic models with damage, verified with experimental results, are used to describe the level of tissue damage in arterial layers and plaque caused by such intervention. A tissue-growth model, associated with vessel damage, is adopted to describe the growth behaviour of a media layer after stent implantation. Narrowing of lumen diameter with time is used to quantify the development of in-stent restenosis in the vessel after stenting. It is demonstrated that stent designs and materials strongly affect the stenting-induced damage in the media layer and the subsequent development of in-stent restenosis. The larger the artery expansion achieved during balloon inflation, the higher the damage introduced to the media layer, leading to an increased level of in-stent restenosis. In addition, the development of in-stent restenosis is directly correlated with the artery expansion during the stent deployment. The correlation is further used to predict the effect of a complex clinical procedure, such as stent overlapping, on the level of in-stent restenosis developed after percutaneous coronary intervention. Keywords  Finite element · In-stent restenosis · Stent deployment · Arterial damage · Tissue-growth model

1 Introduction Atherosclerosis is a progressive vascular disease, resulting in the narrowing of lumen, compared to its healthy condition, due to the build-up of plaque inside an artery wall (Libby 2002). The plaque development is caused by migration and proliferation of native cells and local accumulation of bloodborne species, which include lipid, fibro-fatty composites and calcium salts (Singh et al. 2002). Percutaneous coronary intervention (PCI) is a minimally invasive surgical procedure to treat atherosclerotic arteries. The development of PCI started with angioplasty, for which a small balloon, inserted to the diseased part of an artery, is used to open the blocked artery through inflation. However, an acute vessel recoil * Liguo Zhao [email protected] 1



Wolfson School of Mechanical, Electrical, and Manufacturing Engineering, Loughborough University, Epinal Way, Loughborough LE11 3TU, UK

often occurs after angioplasty. To eliminate the problem, stents, either balloon- or self-expandable, were developed and introduced to PCI, aiming to sup