Cardiovascular diseases are the most important disease that can cause approximately one-third of deaths worldwide. It consists of ischemic heart disease, peripheral arterial disease, heart failure and stroke. The major form of cardiovascular diseases in the general population is coronary heart disease, which remains a significant proplem over the past several years. The treatment of coronary artery disease has been developed by the use of percutaneous coronary intervention, which becomes the focus of many researches in the cardiology field. However, the novel complication associated with this medical procedure is inflammatory reaction after coronary interventionthat might be interfering with patient outcome. Balloon angioplasty was the first landmark in treatment of coronary artery disease and was performed by Andreas Grüntzig in 1977. However, this technique had two major drawbacks: thrombosis and acute occlusion occurred in patients immediately after the procedure, and development of neointimal proliferation with restenosis occurred in patients within the first six months. Further efforts encouraged the introduction of bare metal stent which performed by Sigwart et al. following balloon angioplasty. In 1987 the bare metal stent was the first food and drug administration approved stent in the USA. Also this new technology had major problems: stent thrombosis and in-stent restenosis. However, during 1he 1990s follow-up studies sought to elucidate the molecular mechanisms underlying the vascular response to percutaneous coronary intervention and stenting. The introduction of the first generation of drug-eluting stent aimed at reducing neointimal hyperplasia has been explored. Second-generation drug eluting stent showed superiority to first-generation drug eluting stent by lower rates of stent thrombosis. To overcome the hypersensitivity reaction to the durable polymer, non-polymeric third-generation drug eluting stent with biodegradable polymers also developed. In parallel, fourth-generation drug eluting stent constructed with fully bioresorbable scaffolds designed to provide vessel support and deliver the antiproliferative drug to prevent neointimal proliferation for a defined period after coronary intervention procedure followed by gradual resorption leaving behind no permanent foreign material. In 2017, the FDA released a warning related to the increased incidence of device thrombosis and it was subsequently removed from the global market. Inflammation plays an important role in the development of atherosclerosis which is the underlying cause for most cardiovascular disease and is a process that starts early in life and progresses slowly and silently for decades. Recent studies has demonstrated that implant of coronary artery stents induces the beginning of a local and systemic inflammatory response and restenosis after percutaneous coronary intervention. An initial acute inflammatory cell response was shown within 0 to 3 days but  acute inflammation subsides is replaced by chronic inflammatory cells within 2 to 4 weeks post intervention. This inflammatory reaction triggered by the stent insertion is maintained by the mechanism of stent expansion with vessel wall rupture, in addition to permanent radial mechanical strain applied to arterial wall and thepresence of an intravascular residual metallic foreign material. Several studies have demonstrated that percutaneous coronary intervention induces the release of multiple inflammatory markers that are associated with a later poor prognosis in patients.


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