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Joslin Diabetes Center (P.A.E., E.T., E.S.H.) and Microcirculation Laboratory (A.C., L.K., A.V.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston Massachusetts 02215
Address all correspondence and requests for reprints to: Aristidis Veves, M.D., Microcirculation Laboratory, Palmer 317, Beth Israel Deaconess Medical Center, West Campus, One Deaconess Road, Boston, Massachusetts 02215. E-mail: aveves{at}bidmc.harvard.edu.
We have investigated the effect of atorvastatin on the endothelial function of patients with diabetes and subjects at risk for type 2 diabetes in a 12-wk, prospective, randomized, placebo-controlled, double-blind clinical trial. The flow- mediated dilation (FMD; endothelium dependent) and nitroglycerin-induced dilation (endothelium independent) in the brachial artery and the vascular reactivity at the forearm skin were measured. FMD improved in the atorvastatin-treated, at-risk subjects [median (25–75 percentile), 7.2% (2.9–9.6%) at exit visit vs. 6.6% (2.9–9.5%) at baseline; P < 0.05]. A similar improvement of FMD was found in atorvastatin-treated diabetic patients [median (25–75 percentile), 5.6 (3.9–7.9) at exit visit vs. 4.2 (3.2–7.2) at baseline; P = 0.07]. No changes were observed in nitroglycerin-induced dilation and the microcirculation reactivity measurements in either group. In the at-risk group, there was a decrease in the C-reactive protein [median (25–75 percentile), 0.12 mg/dl (0.07–0.27 mg/dl) at exit visit vs. 0.24 mg/dl (0.07–0.35 mg/dl) at baseline; P < 0.05] and TNF
[median (25–75 percentile), 2.6 pg/ml (1.8–4.1 pg/ml) at exit visit vs. 4.4 pg/ml (3.6–6.0 pg/ml) at baseline; P < 0.05] in the atorvastatin-treated patients, whereas in the diabetes group, a decrease in endothelin-1 (mean ± SD, 0.97 ± 0.29 pg/ml at exit visit vs. 1.19 ± 0.42 pg/ml at baseline; P < 0.05) and plasminogen activator inhibitor-1 [median (25–75 percentile), 18 ng/ml (9–24 ng/ml) at exit visit vs. 27 ng/ml (7–41 ng/ml) at baseline; P < 0.05] were observed. We conclude that atorvastatin improves endothelial function and decreases levels of markers of endothelial activation and inflammation.
This work was supported by a clinical research grant from Pfizer Inc. (to A.V.) and, in part, by Grant RR 01032 to the Beth Israel Deaconess Medical Center General Clinical Research Center from the National Institutes of Health, a William Randolph Hearst Fellowship provided by the William Randolph Hearst Foundation, and a Mary K. Iacocca Fellowship provided by the Iacocca Foundation.
Abbreviations: CRP, C-reactive protein; cv, coefficient of variation; FMD, flow-mediated dilation; HDL, high-density lipoprotein; LDL, low-density lipoprotein; PAI, plasma activator inhibitor; tPA, tissue plasminogen activator.
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