Effects of short-term glucocorticoids on cardiovascular biomarkers

被引:89
作者
Brotman, DJ
Girod, JP
Garcia, MJ
Patel, JV
Gupta, M
Posch, A
Saunders, S
Lip, GYH
Worley, S
Reddy, S
机构
[1] Cleveland Clin Fdn, Dept Gen Internal Med, Cleveland, OH 44195 USA
[2] Cleveland Clin Fdn, Dept Cardiovasc Med, Cleveland, OH 44195 USA
[3] Cleveland Clin Fdn, Dept Diabet Endocrinol & Metab, Cleveland, OH 44195 USA
[4] Cleveland Clin Fdn, Dept Biostat & Epidemiol, Cleveland, OH 44195 USA
[5] Univ Pittsburgh, Med Ctr, Dept Cardiol, Pittsburgh, PA 15203 USA
[6] City Hosp, Univ Dept Med, Haemostasis Thrombosis & Vasc Biol Unit, Birmingham B18 7QH, W Midlands, England
关键词
D O I
10.1210/jc.2004-2379
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:3202 / 3208
页数:7
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