Neoatherosclerosis Within the Implanted Stent

Although it is generally recognized that the long-term clinical outcome of bare-metal stents (BMS) is favorable, a late luminal narrowing with restenosis of BMS can occur during the extended follow-up (beyond 5 years), resulting in clinical events such as stent thrombosis and myocardial infarction. Regarding the mechanisms of progressive late luminal renarrowing, a persistent and remarkable foreign body inflammatory reaction to the metal may promote new atherosclerotic changes and consequent plaque vulnerability of the neointimal tissue around the stent struts. However, neointimal atherosclerotic change (neoatherosclerosis) after BMS implantation is rarely reported. Although drug-eluting stents (DES) have dramatically reduced restenosis and target lesion revascularization compared with BMS, long-term safety remains a clinical major concern due to persistent increase in the incidence of very late stent thrombosis (VLST). While stent thrombosis is a multifactorial process, it has shown that tissue coverage over stent struts is an important determinant of late stent thrombosis. Furthermore, the development of neoatherosclerosis inside the DES may be another rare mechanism of late thrombotic events. Neoatherosclerosis in DES (two years after implantation) can occur earlier than in BMS. Because of high resolution up to 10 μm, it has been described that optical coherence tomography (OCT) has the potential to identify the features of unstable plaques such as thin fibrous cap, large lipid core, thrombus, macrophage infiltration, and neovascularization. Furthermore, even in the evaluation of stent, OCT has been reported to be able to demonstrate the stented lesion morphology in detail including tissue protrusion, thrombus formation, incomplete apposition, late acquired malaposition, edge dissection, tissue coverage over struts, and so on. This chapter describes about the assessment of neoatherosclerosis within BMS and DES by OCT.