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The Mechanisms of Restenosis and Relevance to Next Generation Stent Design

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journal contribution
posted on 2022-05-17, 05:10 authored by J Clare, J Ganly, CA Bursill, H Sumer, P Kingshott, Judy de HaanJudy de Haan
Stents are lifesaving mechanical devices that re‐establish essential blood flow to the coronary circulation after significant vessel occlusion due to coronary vessel disease or thrombolytic blockade. Improvements in stent surface engineering over the last 20 years have seen significant reductions in complications arising due to restenosis and thrombosis. However, under certain conditions such as diabetes mellitus (DM), the incidence of stent‐mediated complications remains 2–4‐ fold higher than seen in non‐diabetic patients. The stents with the largest market share are designed to target the mechanisms behind neointimal hyperplasia (NIH) through anti‐proliferative drugs that prevent the formation of a neointima by halting the cell cycle of vascular smooth muscle cells (VSMCs). Thrombosis is treated through dual anti‐platelet therapy (DAPT), which is the continual use of aspirin and a P2Y12 inhibitor for 6–12 months. While the most common stents currently in use are reasonably effective at treating these complications, there is still significant room for improvement. Recently, inflammation and redox stress have been identified as major contributing factors that increase the risk of stent‐related complications following percutaneous coronary intervention (PCI). The aim of this review is to examine the mechanisms behind inflammation and redox stress through the lens of PCI and its complications and to establish whether tailored targeting of these key mechanistic pathways offers improved outcomes for patients, particularly those where stent placement remains vulnerable to complications. In summary, our review highlights the most recent and promising research being undertaken in understanding the mechanisms of redox biology and inflammation in the context of stent design. We emphasize the benefits of a targeted mechanistic approach to decrease all‐cause mortality, even in patients with diabetes.


J.C. is supported by a Swinburne-Baker Scholarship, J.G. is supported by an Australian Government Research Training Program Scholarship, C.A.B. is supported by the Heart Foundation Lin Huddleston Fellowship and the Centre of Excellence for Nanoscale BioPhotonics, through the Australian Research Council (ARC, CE140100003), and H.S., P.K. and J.B.d.H. acknowledge the Percy Baxter Charitable Trust's generous funding via a Perpetual IMPACT grant. J.B.d.H. also acknowledges support from a Baker Fellowship.


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© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// 4.0/)