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| Effects of Statins on Clinical Restenosis and Neointimal Hyperplasia after Successful Coronary Artery Stenting
: An Intravascular Ultrasound Study
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| The Heart Center of Chonnam National University Hospital, Chonnam National University Research Institute of Medical Science, Gwangju, Korea |
| Young Joon Hong, Myung Ho Jeong, Weon Kim, Sang Yup Lim, Sang Hyun Lee, Seo Na Hong, Kyung Ho Yun, Kye Hun Kim, Dong Goo Kang, Yeon Sang Lee, Ju Han Kim, Young Keun Ahn, Jeong Gwan Cho, Jong Chun Park, and Jung Chaee Kang |
Background: Statins are effective lipid lowering agents, and imaging studies have demonstrated their ability to slow progression and promote regression of atherosclerosis. However, few studies performed to date have used intravascular ultrasound (IVUS) to examine the effects of statin therapy on the regression of atherosclerosis.
Objectives: We examined the effects of statin therapy on neointimal hyperplasia after successful stent implantation in patients with coronary artery disease.
Methods: This study included 108 patients who underwent stent implantation for angiographically significant stenosis. Patients were divided into two groups according to statin therapy (statin group; n=62, 54.7±10.7 years, male 87.1%, non-statin group; n=46, 57.5±11.2 years, male 78.3%). All patients underwent angiographic and intravascular ultrasound (IVUS) follow-up at six months.
Results: There were no significant differences in clinical and angiographic results between both groups. At six-months follow-up, the restenosis rate was 22.6% in the statin group and 28.3% in non-restenosis group and repeat revascularization was performed in 21% in statin group and 23.9% in non-statin group (p=0.500, 0.716, respectively). Pre-interventional and post-interventional IVUS findings are similar in both groups. At six-months follow-up, the extracellular matrix cross-sectional area (EEM CSA) at lesion site was significantly larger in the statin group (14.9±3.7mm2 vs. 13.7±3.2mm2, p=0.050) and the remodeling index was significantly higher in the statin group than that in the non-statin group (1.10±0.15 vs. 0.90±0.17, p=0.015). At six-month follow-up, the NIH CSA in the minimal lumen CSA was smaller in the statin group (2.0±1.4mm2 vs. 2.6±1.8mm2, p=0.072) and the lumen CSA was larger in the statin group (5.5±1.6mm2 vs. 4.9±1.5mm2, p=0.077), but, these did not statistically significant.
Conclusions: Statin therapy may induce positive remodeling of vascular segments containing atherosclerotic plaques and may showe a trend to reduce neointimal hyperplasia after stent implantation.
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