Abstract 148: Intensive Lipid Lowering Therapy Using Rosuvastatin Associates with Greater Atherosclerotic Aortic Plaques Regression - A Magnetic Resonance Imaging Study
Whether intensive lipid-lowering therapy yields greater regression of atherosclerotic plaques remains inconclusive. We therefore performed a prospective, randomized trial comparing standard (achieving LDL-C levels recommended by the Japanese guideline) and intensive (achieving further 30% lower levels than the former) rosuvastatin therapy for 1 year with primary outcome of aortic plaques evaluated by MRI. Sixty dyslipidemic patients, who were eligible for statins therapy, were randomized to standard or intensive group, and dose of rosuvastatin were titrated to achieve the respective target LDL-C. Average doses of rosuvastatin throughout the study were 2.9±3.1 and 6.5±5.1 mg/day in standard and intensive group, respectively. Although both treatments significantly reduced serum LDL-C and hsCRP levels, reduction of LDL-C levels was greater in intensive group than in standard group (-46 vs. -34%). Intensive therapy improved endothelial function as evaluated by FMD in brachial artery compared to standard therapy (95 vs. 22%). MRI study revealed that both thoracic and abdominal plaques were significantly regressed in both groups with greater regression in thoracic plaques in intensive group compared to standard group (-9.1 vs. -3.2%) (Figure A). Correlation analysis revealed no significant association of plaque regression with the doses of rosuvastatin and the changes in serum lipids/FMD. In contrast, thoracic plaque regression correlated with hsCRP reduction (Figure B). Multivariate analysis demonstrated that this association still remain significant even after adjustment of the doses at flow-up, serum lipids and FMD. In conclusions, the present study demonstrated that intensive lipid-lowering using rosuvastatin led to additive plaques regression compared to standard therapy. Therefore, rosuvastatin may provide long term benefit in patients with increased risk through its LDL-C lowering and anti-inflammatory effects.
- © 2012 by American Heart Association, Inc.