Abstract 12732: Coronary Stent Fracture Promotes Neoatherosclerosis Formation in-Stent Restenotic Neointimal Tissue After Drug-Eluting Stent Implantation
Introduction:Drug-eluting stent (DES) reduced the rates of in-stent restenosis and subsequent target lesion revascularization. However, stent fracture (SF) after DES implantation has become an important concern because of its potential association with restenosis and stent thrombosis. In addition, the pathogenic impact of SF on in-stent restenotic neointimal tissue components after DES implantation remains unclear.
Hypothesis:We assessed the hypothesis that SF after DES implantation might promote neoatherosclerosis formation in restenosis lesions.
Methods:We enrolled 41 consecutive patients with in-stent restenosis requiring revascularization after DES implantation between January 2008 and March 2014. 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. SF was defined as complete or partial separation of stent segments observed by using plain fluoroscopy or intravascular ultrasound.
Results:SF was observed in 14 (34.1%) of enrolled patients. On volumetric IB-IVUS analyses, patients with SF had a significantly higher percentage of lipid tissue volume within the neointima and a significantly lower percentage of fibrous tissue volume than those without (37.3 ± 18.9 vs. 23.3 ± 12.2%; p = 0.02, and 61.2 ± 18.3 vs. 73.3 ± 11.9%; p = 0.04, respectively). Interval from stent implantation was similar in both groups (42.3 ± 23.8 vs. 34.5 ± 29.0 months; p = 0.43). Moreover, SF was positively correlated with the percentage of lipid volume on multiple linear regression analysis after adjustment for confounding factors (β = 0.46, p = 0.01).
Conclusions:SF was associated with larger lipid tissue volume within the neointima after DES placement, suggesting the development of neoatherosclerosis and vulnerable neointima. Thus SF might lead to future adverse coronary events.
Author Disclosures: Y. Uchida: None. S. Ichimiya: None. H. Oishi: None. T. Aoki: None. Y. Miki: None. T. Kawamiya: None. H. Ichimiya: None. J. Watanabe: None. M. Kanashiro: None. S. Hayano: None. S. Suzuki: None. H. Ishii: None. T. Amano: None. T. Matsubara: None. T. Murohara: None.
- © 2014 by American Heart Association, Inc.