Effect of Pravastatin on malondialdehyde-modified low-density lipoprotein levels and coronary plaque regression as determined by 3-dimensional intravascular ultrasound

被引:56
作者
Tani, S [1 ]
Watanabe, I
Anazawa, T
Kawamata, H
Tachibana, E
Furukawa, K
Sato, Y
Nagao, K
Kanmatsuse, K
Kushiro, T
机构
[1] Nihon Univ, Surugadai Hosp, Dept Cardiol, Tokyo, Japan
[2] Nihon Univ, Surugadai Hosp, Dept Emergency & Crit Care Med, Tokyo, Japan
关键词
D O I
10.1016/j.amjcard.2005.05.069
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We hypothesized that, a reduction in atherogenic malondiadehyde-modified low-density lipoprotein (MOA-LDL) levels, which may antagonize the action of athero-protective high-density lipoprotein cholesterol, leads to coronary plaque regression. This study investigated the effects of pravastatin on the serum levels of MDA-LDL and coronary atherosclerosis. In a 6-month prospective study, 75 patients with stable coronary artery disease were randomly assigned to a pravastatin-treatment group (n = 52) or a control group (n = 13). Volumetric analyses were performed in matched coronary artery segments by 3-dimensional intravascular ultrasound. Pravastatin therapy for 6 months resulted in a decrease in coronary plaque volume (14.4%, p < 0.0001) and a corresponding reduction in serum MDA-LDL levels (12.7%, p 0.0001). In the pravastatin treatment group, the percentage of change in plaque volume correlated with changes in the MDA-LDL and high-density lipoprotein cholesterol levels (r = 0.52 and -0.55, respectively, p < 0.0001) but not with the changes in any other lipid levels. Multivariate regression analysis revealed that a reduced MDA-LDL level is an independent predictor of plaque regression, as was an increase in high-density lipoprotein cholesterol. In conclusion, these results suggest that the reduction in the MDA-LDL levels induced by pravastatin may serve as A novel marker of coronary atherosclerosis regression. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:1089 / 1094
页数:6
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