In vascular homeostasis, a functioning endothelial layer inhibits the development of de novo atherosclerosis. After balloon angioplasty and stenting, there is extensive mechanical denudation of the endothelium and subsequently endothelial regeneration. Impaired healing of the endothelium, such that occurs with drug-eluting stents (DES), 1 facilitates lipid deposition within neointima and leads to the development of neoatherosclerosis (NA).
2Pathological and imaging reports have demonstrated that NA is more common and occurs earlier in DES compared with bare-metal stents (BMS). 2,3 Clinical imaging studies of DES-related in-stent restenosis (ISR) by optical coherence tomography (OCT) have identified that >75% of patients presenting with unstable angina have thin-cap or disrupted neointima with overlying thrombi. 4 However, although systematic in vivo imaging data are not available for BMS, it is reported that more than one third of these patients present with acute coronary syndromes 5 and have evidence of atherosclerotic plaque within aspirates of definite stent thrombosis. 6 Taken together, there remains a need to characterizeBackground-Re-endothelialization is delayed after drug-eluting stent (DES) implantation. In this setting, neointima is more prone to become lipid laden and develop neoatherosclerosis (NA), potentially increasing plaque vulnerability. Methods and Results-Optical coherence tomography and near-infrared spectroscopy with intravascular ultrasound were used to characterize NA in 65 (51 DES and 14 bare-metal stents) consecutive symptomatic patients with in-stent restenosis. , and III (peri-strut NA). Type I thin-cap neoatheroma was more common in DES (20% versus 3%; P=0.01) and in areas of the stented segment without significant in-stent restenosis (71%). Periprocedural myocardial infarction occurred only in DES (11 versus 0; P=0.05), of which 6 (55%) could be attributed to segments with >70% in-stent restenosis. By logistic regression, prior DES was the only independent predictor of both NA (odds ratio, 7.0; 95% confidence interval, 1.7-27; P=0.006) and periprocedural myocardial infarction (odds ratio, 1.8; 95% confidence interval, 1.1-2.4; P=0.05). Conclusions-In-stent thin-cap neoatheroma is more prevalent, is distributed more diffusely across the stented segment, and is associated with increased periprocedural myocardial infarction in DES compared with bare-metal stents. These findings support NA as a mechanism for late DES failure. (Circ Cardiovasc Interv. 2013;6:507-517.)