Effect of atorvastatin on lipogenic, inflammatory and thrombogenic markers in women with the metabolic syndrome.

Division of Cardiology, University of Florida College of Medicine, Jacksonville FL, USA. Electronic address: gladys.velarde@jax.ufl.edu. Division of Cardiology, University of Florida College of Medicine, Jacksonville FL, USA. Division of Cardiovascular Medicine, University of Texas Health Science Center at Houston, Houston TX, USA. Division of Cardiology, University of Florida College of Medicine, Jacksonville FL, USA; Center for Health Equity and Quality Research, University of Florida College of Medicine, Jacksonville, FL, USA. Department of Internal Medicine, University of Rochester Medical Center, Rochester NY, USA.

Nutrition, metabolism, and cardiovascular diseases : NMCD. 2021;(2):634-640
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Abstract

BACKGROUND AND AIM Specific drug therapy to target the underlying proinflammatory and prothrombotic state in patients with metabolic syndrome (MS) is lacking. We sought to study the effect of high-intensity atorvastatin on markers of lipogenesis, inflammation and thrombogenesis, in women with MS in the absence of cardiovascular disease or diabetes. METHODS AND RESULTS This randomized double-blinded controlled trial included 88 women with MS (according to National Cholesterol Education Panel Adult Treatment Panel III criteria) and low atherosclerotic cardiovascular risk. Participants were randomized to receive atorvastatin 80 mg or matching placebo. Thrombogenic, lipogenic and inflammatory markers were collected at the time of enrollment, after a 6-week dietary run-in phase (time of randomization), and at 6- and 12-weeks after randomization. At 6 weeks post-randomization, there was significant reduction in total cholesterol, low density lipoprotein cholesterol, triglycerides, apolipoprotein-B (Apo-B) and Apo-B/Apo-A1 ratio in the atorvastatin arm compared to placebo. This difference persisted at 12-weeks post randomization. There was no significant difference in fasting blood glucose, high-density lipoprotein cholesterol, high sensitivity C-reactive protein, serum leptin, Apo-A1, intercellular adhesion molecule 1 and platelet activity. A significant increase in vascular adhesion molecule 1 at 6 and 12 weeks was seen within the atorvastatin arm. No difference was observed in blood pressure and waist circumference. CONCLUSIONS In conclusion, high-intensity atorvastatin has an early and significant impact on lipoproteins and apolipoproteins but did not lower inflammatory, thrombogenic or biomarkers of platelet activity and aggregation in women with MS. The use of statins for primary prevention in these patients should be further explored.

Methodological quality

Publication Type : Randomized Controlled Trial

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