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Nakazawa et al reported that insufficient endothelialization of stent struts was a cause of ST based on autopsy cases of 1st-generation DES including SES and the paclitaxel-eluting stent, and they also found less endothelialization of stent struts of 1st-generation DES compared with BMS.2 There is also a report that hypersensitivity to the polymer is more noticeable in SES lesions than with other types of stent.3 Furthermore, angiographic evidence of exudation of the contrast agent surrounding the stent (peri-stent contrast staining: PSS) was observed especially after SES deployment and considered as one of the causes of ST.4 Another major concern of SES was impairment of the endothelial function of the coronary arteries. Fuke et al5 showed that abnormal endothelial reaction to intracoronary acetylcholine infusion was significantly greater after implantation of SES compared with BMS and they suggested that SES deployment causes coronary endothelial dysfunction (Figures 1,2) As Beltrame et al have stated that the primary pathophysiology of coronary artery spasm is vascular smooth muscle cell hyper-reactivity,6 SES-induced coronary endothelial C oronary angioplasty was first introduced in 1977 by Andreas Roland Grüntzig and since then various devices for percutaneous coronary intervention (PCI) have been developed over many years. After the procedure of PCI shifted from balloon dilation to stent implantation, stents themselves gradually developed from bare metal (BMS) to drug-eluting (DES). To date, dozens of stents have come onto the market and disappeared, the sirolimus-eluting stent (SES) being one with the most conspicuous and memorable existence. At the time of its initial appearance, because of a very low target lesion revascularization ratio, it was welcomed and utilized by all catheter interventionists as the perfect stent. The SES was characterized by its overwhelming reduction of late loss by sirolimus, which suppresses the proliferation of vascular endothelial cells, and the strong radial force applied by a relatively rigid stent platform. It was a report of stent thrombosis (ST) after SES implantation, which was a fatal complication, that shadowed its majesty. The number of reports gradually increased and finally SES became a synonym of very late ST (VLST). A variety of mechanisms have been proposed as the cause of VLST, such as insufficient endothelialization, stent fracture,1 off-label use and neoatheroscrerosis2 and so on. Article p 469

Impact of Stent Type on the Long-Term Prognosis of Patients With Vasospastic Angina ― Can We Judge a Stent Just by Its Cover? ―