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.
Highlights
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)
Escuer et al (2019) developed another damage-related volumetric growth model, in terms of densities/concentrations of important species such as growth factors, matrix metalloproteinases, extracellular matrix and contractile and synthetic smooth muscle cells (SMCs). This model was used to simulate the development of in-stent restenosis (ISR), and the results suggested that the arterial wall response was driven by the damage area, proliferation of SMCs and the collagen turnover
A tissue-growth model, linking the stent-induced tissue damage and the ISR, was introduced and employed together with the finite element (FE) approach to simulate the development of ISR after Percutaneous coronary intervention (PCI)
Summary
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 development of stents began with bare-metal stents (BMSs) and progressed to drug-eluting stents (DESs) and bioresorbable vascular scaffolds (BVSs). BMSs, made of pure metals (no coating), were found to associate with a high occurrence of neointimal hyperplasia—enlargement of internal arterial layer—after implantation, leading to a re-narrowing of the treated artery, i.e., in-stent restenosis (ISR). To reduce the rate of ISR, polymer coatings, loaded with drugs that could inhibit neointimal growth, were introduced to cover the metal struts, leading to the revolutionary development of DESs. Recently, BVSs, made of biodegradable polymers or metals, were developed for complete bioresorption after the implantation, with the hope of further reducing ISR as well as late stent thrombosis caused by the permanent presence of metallic stents
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