Direct in vivo evidence of a vascular statin: a single dose of cerivastatin rapidly increases vascular endothelial responsiveness in healthy normocholesterolaemic subjects

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Abstract
Aims HMG‐CoA reductase inhibitors (statins) have been demonstrated to have in vitro vascular effects. The aim of this study was to determine whether statins actually have in vivo vascular effects independent of their cholesterol‐lowering effect. Methods We investigated the effect of a single dose of cerivastatin on vascular endothelial function by measuring flow‐mediated dilatation of the brachial artery on ultrasound in 30 healthy volunteers with normal serum cholesterol concentrations. They were randomized to either placebo group (n = 15) or cerivastatin group (n = 15), and flow‐mediated dilatation and endothelium‐dependent dilatation were evaluated at before and 1 h, 3 h, 6 h, and 12 h after administration of placebo or cerivastatin. Results There were no differences in total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, malondialdehyde‐LDL, and high‐sensitivity C‐reactive protein before and after administration of placebo or cerivastatin. Cerivastatin significantly increased flow‐mediated dilatation at 3 h (P < 0.001), and this increase rapidly returned to the baseline level 6 h after administration. Endothelium‐­independent dilatation of brachial artery was not altered. Conclusions A single dose of cerivastatin increased vascular endothelial responsiveness. Our data suggest that cerivastatin has a direct effect on the blood vessels that is independent of its lipid‐lowering effect, and thus can be considered as a vascular statin.