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The principle pathogenesis of atherosclerosis is inflammation caused by infiltration of foamy macrophages through impaired endothelium into the vessel wall. Metallic coronary stents are deployed into the atherosclerotic lesions in order to preserve wide coronary lumen and dissolve myocardial ischemia. Transformation of proliferating neointima derived from medial smooth muscle cells into the atheromatous lesion is now called neoatherosclerosis which can lead to stent restenosis or thrombosis at the late phase. In the DES (drug-eluting stent) era, the second-generation DESs have launched and they have new technologies, such as biocompatible (or biodegradable) polymer to inhibit the inflammatory response for reducing endothelial damage compared to the first-generation DES. Although the second-generation DESs of everolimus-, zotarolimus-, and biolimus-eluting stents actually reduce the incidence of very late stent thrombosis according to large-scale clinical trials, neoatherosclerosis plays an important role of late (or very late) DES failure. However, there are few reports showing neoatherosclerosis in the second-generation DESs.

Very Late In-stent Restenosis due to Neoatherosclerosis in the Second-generation Everolimus-eluting Stent