학술대회 안내 사전등록 안내 초록등록 안내 초록등록/관리 숙박및교통 안내


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ǥ : ȣ - 500017   114 
Low-dose Simvastatin Induces Positive Vascular Remodeling without Significant Plaque Regression at Non-stented Vascular Segments Containing Atherosclerotic Plaques: Intravascular Ultrasound Study
전남대학교병원 심장센터, 광주원광대학병원
이 석, 정명호, 홍영준, 황선호, 윤남식, 이상록, 홍서나, 김계훈, 박형욱, 김주한, 안영근, 조정관, 박종춘, 강정채, 박옥규
Background The purpose of this study was to assess the effects of low-dose simvastatin therapy on the plaque regression and vascular remodeling in normocholesterolemic patients. Methods and Results This study included 108 normocholesterolemic patients who underwent intravascular ultrasound study (IVUS)-guided stenting. Patients were divided into two groups according to the simvastatin therapy (simvastatin group; n=62, non-simvastatin group; n=46). 20 mg of simvastatin was taken to simvastatin group. 6-month follow-up quantitative coronary angiography and IVUS data were analyzed at stented and at non-stented segments at 10 mm proximal or distal to the stent edge. At 6-month after stenting, binary in-stent restenosis was present in 18% (11/62) of simvastatin group and in 22% (10/46) of non-simvastatin group (p=NS). In-stent neointima area did not differ significantly between the 2 groups at 6-month follow-up. At non-stented segments, there was no significant difference in plaque volume change between the 2 groups at 6-month follow-up, however, this was compensated by an increase in vessel volume, resulting in an increase in lumen volume in simvastatin group, but not in non-simvastatin group (vessel volume change; 3.2±0.5 mm3 vs -0.6±0.3 mm3, p=0.025, lumen volume change; 4.1±0.7 mm3 vs -2.2±0.5 mm3, p=0.005). The remodeling index was significantly higher in the simvastatin group compared to non-simvastatin group at 6-month follow-up (1.04±0.45 vs 0.97±0.37, p=0.015). Conclusion In normocholesterolemic patients undergoing coronary stenting, low-dose simvastatin therapy does not inhibit intimal hyperplasia at stented segments, but it induces positive vascular remodeling without significant plaque regression at non-stented vascular segments containing atherosclerotic plaques.


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