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Effects of Short-Term Glucocorticoids on Cardiovascular Biomarkers

Departments of General Internal Medicine (D.J.B., J.P.G., S.S.), Cardiovascular Medicine (M.J.G.), Endocrinology, Diabetes, and Metabolism (M.G., A.P., S.R.), and Biostatistics and Epidemiology (S.W.), Cleveland Clinic Foundation, Cleveland, Ohio 44195; Department of Cardiology (J.P.G.), University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15203; and Haemostasis Thrombosis and Vascular Biology Unit (J.V.P., G.Y.H.L.), University Department of Medicine, City Hospital, Birmingham B18 7QH, United Kingdom

Address all correspondence and requests for reprints to: Daniel J. Brotman, M.D., F.A.C.P., Director, Hospitalist Program, Department of Medicine, Johns Hopkins Hospital, Jefferson 242, 600 North Wolfe Street, Baltimore, Maryland 21287. E-mail: dbrotma1{at}jhmi.edu.

Context: Glucocorticoids are known to acutely increase blood pressure, suppress inflammation, and precipitate insulin resistance. However, the short-term effects of glucocorticoids on other cardiovascular risk factors remain incompletely characterized.

Objective: Our objective was to determine the effects of a short course of dexamethasone on multiple cardiovascular biomarkers and to determine whether suppression of morning cortisol in response to low-dose dexamethasone is correlated with cardiovascular risk markers in healthy volunteers.

Design: We conducted a randomized, double-blind, placebo-controlled study.

Setting: The study took place in a tertiary care hospital. Study subjects: Twenty-five healthy male volunteers, ages 19–39 yr, participated in the study.

Intervention: Subjects received either 3 mg dexamethasone twice daily or placebo for 5 d. Subjects also underwent a low-dose (0.5 mg) overnight dexamethasone suppression test.

Measures: Parameters examined before and after the 5-d intervention included heart rate, blood pressure, weight, fasting lipid variables, homocysteine, renin, aldosterone, insulin resistance (homeostasis model assessment), high-sensitivity C-reactive protein, B-type natriuretic peptide, flow-mediated and nitroglycerin-mediated brachial artery dilatation, and heart rate recovery after exercise. All measurements were done in the morning hours in the fasting state.

Results: Dexamethasone increased systolic blood pressure, weight, B-type natriuretic peptide, and high-density-lipoprotein-cholesterol. Dexamethasone decreased resting heart rate, high-sensitivity C-reactive protein, and aldosterone and tended to attenuate nitroglycerin-mediated vasodilatation. There was no effect on flow-mediated vasodilatation, diastolic blood pressure, triglycerides, low-density-lipoprotein-cholesterol, nonesterified fatty acids, homocysteine, or heart rate recovery. The response of circulating cortisol to low-dose dexamethasone had no significant correlation with any of the cardiovascular risk markers.

Conclusions: Short-term glucocorticoids elicits both favorable and unfavorable effects on different cardiovascular risk factors. Manipulation of specific glucocorticoid-responsive physiological pathways deserves further study.

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