Department of Endocrinology (F.C.W.W.), Manchester Royal Infirmary, University of Manchester, Manchester M13 9WL, United Kingdom; and Institute of Clinical Chemistry (A.v.E.), University of Zurich and University Hospital of Zurich, CH-8091 Zurich, Switzerland
Correspondence: Address all correspondence and requests for reprints to: Dr. F. C. W. Wu, Department of Endocrinology, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, England, United Kingdom. E-mail: frederick.wu{at}man.ac.uk
A significant and independent association between endogenoustestosterone (T) levels and coronary events in men and womenhas not been confirmed in large prospective studies, althoughcross-sectional data have suggested coronary heart disease canbe associated with low T in men. Hypoandrogenemia in men andhyperandrogenemia in women are associated with visceral obesity;insulin resistance; low high-density lipoprotein (HDL) cholesterol(HDL-C); and elevated triglycerides, low-density lipoproteincholesterol, and plasminogen activator type 1. These genderdifferences and confounders render the precise role of endogenousT in atherosclerosis unclear. Observational studies do not supportthe hypothesis that dehydroepiandrosterone sulfate deficiencyis a risk factor for coronary artery disease.
The effects of exogenous T on cardiovascular mortality or morbidityhave not been extensively investigated in prospective controlledstudies; preliminary data suggest there may be short-term improvementsin electrocardiographic changes in men with coronary arterydisease. In the majority of animal experiments, exogenous Texerts either neutral or beneficial effects on the developmentof atherosclerosis. Exogenous androgens induce both apparentlybeneficial and deleterious effects on cardiovascular risk factorsby decreasing serum levels of HDL-C, plasminogen activator type1 (apparently deleterious), lipoprotein (a), fibrinogen, insulin,leptin, and visceral fat mass (apparently beneficial) in menas well as women. However, androgen-induced declines in circulatingHDL-C should not automatically be assumed to be proatherogenic,because these declines may instead reflect accelerated reversecholesterol transport. Supraphysiological concentrations ofT stimulate vasorelaxation; but at physiological concentrations,beneficial, neutral, and detrimental effects on vascular reactivityhave been observed. T exerts proatherogenic effects on macrophagefunction by facilitating the uptake of modified lipoproteinsand an antiatherogenic effect by stimulating efflux of cellularcholesterol to HDL.
In conclusion, the inconsistent data, which can only be partlyexplained by differences in dose and source of androgens, militateagainst a meaningful assessment of the net effect of T on atherosclerosis.Based on current evidence, the therapeutic use of T in men neednot be restricted by concerns regarding cardiovascular sideeffects. Available data also do not justify the uncontrolleduse of T or dehydroepiandrosterone for the prevention or treatmentof coronary heart disease.
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