Abstract
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.
Highlights
An estimated 18 million lives are lost each year as a consequence of cardiovascular diseases (CVD), making it the primary cause of death worldwide [1]
The causes and molecular mechanisms associated with restenosis and thrombosis have been discussed
We have highlighted the currently available and most widely used stents on the market, which do mitigate many of the complications following percutaneous coronary intervention (PCI), except for those associated with pre-existing conditions that contribute to endothelial dysfunction such as diabetes mellitus
Summary
An estimated 18 million lives are lost each year as a consequence of cardiovascular diseases (CVD), making it the primary cause of death worldwide [1]. CAD is characterised by the deposition of lipids, such as cholesterol, into the arterial wall This process is known as atherosclerosis and can lead to partial or total occlusion of the vessel, causing cardiac ischemia and potentially leading to a myocardial infarction [2–4]. Despite the current reduced restenosis rates, patients with comorbidities such as diabetes mellitus (DM) remain at a significantly elevated risk of ISR or ST, potentially enhanced by the pathological state within the arteries [9,10]. In designing more effective stents, it is important to consider the underlying pathology that drives restenosis and thrombosis with a clear focus on the mechanisms involved This will facilitate the development of novel stent coatings and biomaterials that target these key drivers of ISR and ST. We highlight the progress that has been made to date, yet offer new alternative approaches that circumvent some of the key issues that limit the use of current DES
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