Vulnerable plaque inside stent.

I T H A S B E E N P R O P O S E D T H A T N O N H E A L I N G E N D O T H E L I U M after percutaeous coronary intervention may allow for insudation of lipids superficial to the stent strut level, specially when the underlying plaque carried a large necrotic core. This may result in formation of a ipid-rich neointima, and the lipid core so created is referred to as nouveau atherosclerosis; the eointimal lipid accumulation is physically not connected to the original (pre-interventional) lipid core 1). The likelihood of development of nouveau atherosclerosis is substantially enhanced in the presence f drug-eluting stents, which further delay the endothelial healing. Furthermore, new atherosclerosis ccurs much earlier in drug-eluting stent–based percutaneous coronary intervention compared to are-metal stent–based interventions. Since endothelial lining is not mature over these atherosclerotic ipid cores, evolving fibrous caps remain predominantly attenuated (1,2). Thin fibrous caps are usceptible to rupture and may contribute to possible late stent thrombosis. Although tacitly believed, n actual plaque rupture has not been documented in such a setting.