Abstract 12822: Continuous Smoking Promotes Neoatherosclerosis Formation in Stent Restenotic Neointimal Tissue After Drug-Eluting Stent Implantation
Introduction: Despite the advance of drug-eluting stents (DES), late adverse events such as very late stent thrombosis (VLST) and late target lesion revascularization are of concern. Although continuous smoking is an independent risk factor of VLST, the pathogenic impact on in-stent restenotic neointimal tissue components after DES implantation remains unclear.
Hypothesis: We assessed the hypothesis that continuous smoking after DES implantation might promote neoatherosclerosis formation in restenosis lesions.
Methods: We enrolled 47 consecutive patients with in-stent restenosis requiring revascularization after DES implantation between January 2008 and March 2015. In advance, we excluded the patients with recurrent restenosis, thrombotic lesions, and total occlusion. For evaluation of in-stent tissue components, integrated backscatter intravascular ultrasound (IB-IVUS) was performed. Patients were divided into current smokers and nonsmokers including both previous smokers and never-smokers.
Results: Of these patients, 12 (25.5%) were current smokers. On volumetric IB-IVUS analyses, current smokers had a significantly higher percentage of lipid tissue volume within the neointima and a significantly lower percentage of fibrous tissue volume than nonsmokers (42.9 ± 19.4 vs. 26.3 ± 12.8%; p = 0.03, and 55.1 ± 19.2 vs. 70.9 ± 11.9%; p = 0.04, respectively). Moreover, continuous smoking was positively correlated with the percentage of lipid volume on multiple linear regression analysis after adjustment for confounding factors (β = 0.35, p = 0.03). Interval from stent implantation was similar between current smokers and nonsmokers (44.6 ± 38.2 vs. 37.5 ± 29.1 months; p = 0.58).
Conclusions: Continuous smoking was associated with larger lipid tissue volume within the neointima after DES placement, suggesting the development of neoatherosclerosis and vulnerable neointima. Thus continuous smoking might lead to future adverse coronary events.
Author Disclosures: Y. Uchida: None. S. Ichimiya: None. H. Ishii: None. K. Mizutani: None. R. Yamaguchi: None. H. Oishi: None. Y. Miki: None. M. Fujimoto: None. T. Kawamiya: None. H. Mihara: None. H. Ichimiya: None. S. Hayano: None. S. Suzuki: None. J. Watanabe: None. M. Kanashiro: None. T. Amano: None. T. Matsubara: None. T. Murohara: None.
- © 2015 by American Heart Association, Inc.