Increased Thin-Cap Neoatheroma and Periprocedural Myocardial Infarction in Drug-Eluting Stent Restenosis

Abstract

Background—: 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. Median duration poststent implantation was 33 months. Optical coherence tomography–verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-metal stents (68% versus 36%; P =0.02), and demonstrated significantly higher prevalence of thin-cap neoatheroma (47% versus 7%; P =0.01) in DES. Near-infrared spectroscopy assessment demonstrated that the total lipid core burden index (34 [interquartile range, 12–92] versus 9 [interquartile range, 0–32]; P P 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.