Drug-eluting stents (DES) have significantly reduced in-stent restenosis and target lesion revascularisation after percutaneous coronary intervention (PCI) as compared with bare metal stents (BMS). In spite of these benefits, concern over increased stent thrombosis (ST) still exists. Although the incidences of ST are low, ST is an immediate life-threatening complication and may occur consistently up to at least five years after implantation of first-generation DES, sirolimus-eluting stents (SES) and paclitaxel-eluting stents (PES). Several pathophysiological factors could be associated with ST, such as delayed re-endothelialisation, incomplete stent strut coverage, prolonged inflammation, hypersensitivity reactions, late acquired malapposition, strut fractures, and neoatherosclerosis. In particular, delayed re-endothelialisation and incomplete stent strut coverage have been considered as significant factors with regard to ST in human autopsy studies. The use of durable polymer coating, the thickness of the stent struts, and the dose of the antiproliferative drug and its release kinetics in first-generation DES have been implicated as important contributory factors in these issues.
Meanwhile, second-generation DES, including everolimus-eluting stents (EES), have been developed with different drugs, more biocompatible polymers, improved drug release kinetics and thinner stent struts. Indeed, EES showed better outcomes including a lower risk of ST compared with first-generation DES in realworld patients. This favourable clinical performance might be associated with better vascular response to EES. However, there have been few investigations on endothelial function and arterial healing in EES.