Interfacial biology of in-stent restenosis

Abstract

Percutaneous angioplasty is a nonsurgical method able to restore patency in atherosclerotic blood vessels through the expansion of a balloon. The clinical outcome of this technique has been significantly enhanced by the combined deployment of a stent. Although stents are successful in the majority of cases, a large percentage of patients (20-30%) still suffer a second vessel lumen reduction known as in-stent restenosis. In-stent restenosis is recognized to be caused by the mechanical and foreign body challenges elicited by the device. Drug-eluting stents have been recently made available to tackle restenosis, but their short clinical history and high costs may limit their future use. The present review links the most recent biologic findings related to in-stent restenosis to the devices' phyisico-chemical features in an attempt to demonstrate that a new generation of stents may be developed without the need of drug elution.

Substrate-induced phenotypic switches of human smooth muscle cells: anin vitrostudy of in-stent restenosis activation pathways

“…In the case of the implantation of bare metal stents (e.g. stainless steel devices), ISR occurs in 20-30% of cases and its incidence can only be significantly reduced by the use of drug-eluting stents (DESs) [1]. However, the use of these medicated devices has been linked to the occurrence of late thrombosis and patient death by infarction [2,3].…”

“…These are widely recognized to be relevant to ISR owing to their ability to stimulate SMC proliferation [8][9][10]. It has been suggested that the combined surface activation of both inflammatory cells and SMCs play a major role in the thickening of the neointima [1,2,4].…”

Substrate‐induced phenotypical change of monocytes/macrophages into myofibroblast‐like cells: A new insight into the mechanism of in‐stent restenosis

“…1 However, clinical studies have shown that over 20% of the patients still undergo restenosis after stent deployment unless drug-eluting stents are implanted. 1 Recent investigations suggest that instent restenosis (ISR) is a consequence of the tissue damage following balloon and stent expansion.…”

“…1 However, clinical studies have shown that over 20% of the patients still undergo restenosis after stent deployment unless drug-eluting stents are implanted. 1 Recent investigations suggest that instent restenosis (ISR) is a consequence of the tissue damage following balloon and stent expansion. 2 In particular, when stent struts penetrate the atherosclerotic plaque, they activate cells of the monocyte/ macrophage (MM) lineage as well as platelets.…”

Stainless Steel Ions Stimulate Increased Thrombospondin-1-Dependent TGF-Beta Activation by Vascular Smooth Muscle Cells: Implications for In-Stent Restenosis

“…ISR remains a significant clinical problem despite advances in stent design and the use of drug-eluting stents [2]. Metal alloys commonly used for stents are subject to stress/strain fracture related to crevice and pitting corrosion due to both mechanical and environmental factors.…”