4.7 Article

Effect of Intensive Versus Moderate Lipid-Lowering Therapy on Epicardial Adipose Tissue in Hyperlipidemic Post-Menopausal Women A Substudy of the BELLES Trial (Beyond Endorsed Lipid Lowering with EBT Scanning)

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
卷 61, 期 19, 页码 1956-1961

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2012.12.051

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atherosclerosis; epicardial adipose tissue; statins

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Objectives This study sought to evaluate the effect of intensive and moderate statin therapy on epicardial adipose tissue (EAT). Background EAT has been associated with coronary artery disease severity and outcome. It is currently unknown whether EAT volume changes over time when patients are exposed to statin therapy. Methods Subanalysis of a randomized study of atorvastatin 80 mg/day versus pravastatin 40 mg/day for 1 year in a clinical trial designed to assess the progression of coronary artery calcium (CAC) in hyperlipidemic post-menopausal women. Patients underwent cardiac computed tomography scans at the start and end of the trial period. Results Of 420 patients, 194 received atorvastatin and 226 pravastatin; the median low-density lipoprotein change was -53.3% and -28.3% with atorvastatin and pravastatin, respectively (p < 0.001). Baseline EAT correlated with age, body mass index, hypertension, diabetes mellitus, high-density lipoprotein, triglyceride levels, and CAC (p < 0.001). At the end of follow-up, EAT regressed more in the atorvastatin than in the pravastatin group (median, -3.38% vs. -0.83%, p = 0.025). The EAT percent change from baseline was significant in the atorvastatin, but not the pravastatin group (p < 0.001 and p = 0.2, respectively). There was no correlation between lipid lowering and EAT regression. CAC progressed significantly in both groups from baseline. Conclusions In hyperlipidemic post-menopausal women, statin therapy induced EAT regression, although intensive therapy was more effective than moderate-intensity therapy. This effect does not seem linked to low-density lipoprotein lowering and may be secondary to other actions of statins such as anti-inflammatory effects. (C) 2013 by the American College of Cardiology Foundation

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