Читать книгу Interventional Cardiology - Группа авторов - Страница 27

The neointimal tissue inside the stents is subject to similar atherogenic forces as the native vessels [99, 100]. Neoatherosclerosis is the development of atherosclerosis within this neointima following bare metal stent (BMS) and drug eluting stent (DES). See Figure 1.1. Histologically it is recognized by the presence of clusters of lipid‐laden foamy macrophages within the neointima with or without necrotic core formation [100,101]. Although the exact pathogenesis of this phenomenon is yet to be proven, inflammation and endothelial dysfunction have been shown to play a fundamental role [100–102]. It has been reported in autopsy and in‐vivo imaging studies that neoatherosclerosis occurs at an earlier stage and with higher frequency in DES than BMS [100,103], suggesting that mechanisms of failure after BMS and DES implantation are quite different. Indeed, in general, patients with BMS are likely to develop in‐stent restenosis (ISR) early due to neointima hyperplasia, whereas patients with DES are likely to develop less neointima in the early period, leading to less frequency of target lesion revascularization (TLR) after one year follow‐up compared to BMS. However, patients with DES are likely to develop neoatherosclerosis later, which possibly related to the late catch‐up phenomenon and very late stent thrombosis (VLST) [99,101,104].