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7086503 
Journal Article 
Statin treatment for coronary artery plaque composition based on intravascular ultrasound radiofrequency data analysis 
Nozue, T; Yamauchi, T; Muramatsu, T; Hibi, K; Sozu, T; Terashima, M; Michishita, I; Yamamoto, S; Tohyama, S; Umezawa, S; Kunishima, T; Sato, A; Miyake, S; Takeyama, Y; Morino, Y; , 
2012 
Yes 
American Heart Journal
ISSN: 0002-8703
EISSN: 1097-6744 
MOSBY-ELSEVIER 
NEW YORK 
191-U285 
Background Systemic therapy with statin has been shown to lower the risk of coronary events; however, the in vivo effects of statin therapy on plaque volume and composition are less understood.Methods We conducted a prospective, open-labeled, randomized, multicenter study in 11 centers in Japan. A total of 164 patients were randomized to receive either 4 mg/d of pitavastatin (intensive lipid-lowering therapy) or 20 mg/d of pravastatin (moderate lipid-lowering therapy). Analyzable intravascular ultrasound data were obtained for 119 patients at baseline and at 8-month follow-up. The primary end point was the difference of volume changes in each of the 4 main plaque components (fibrosis, fibrofatty, calcium, and necrosis), assessed by virtual histology intravascular ultrasound, between the 2 groups.Results The mean low-density lipoprotein cholesterol level at follow-up was significantly lower in the pitavastatin than in the pravastatin group (74 vs 95 mg/dL, P < .0001). During the 8-month follow-up period, statin therapy reduced the absolute and relative amount of fibrofatty component (pitavastatin: from 1.09 to 0.81 mm(3)/mm, P = .001; pravastatin: from 1.05 to 0.83 mm(3)/mm, P = .0008) and increased in the amount of calcium (pitavastatin: from 0.42 to 0.55 mm(3)/mm, P < .0001; pravastatin: from 0.44 to 0.55 mm(3)/mm, P = .005), whereas volume changes in both plaque components were not statistically different between the 2 groups.Conclusions Both pitavastatin and pravastatin altered coronary artery plaque composition by significantly decreasing the fibrofatty plaque component and increasing the calcified plaque component. (Am Heart J 2012;163:191-199.e1.)