Author + information
- Received January 10, 1990
- Revision received March 7, 1990
- Accepted April 4, 1990
- Published online October 1, 1990.
- David M. Herrington, MD, MHS*,1,2,
- Gary B. Gordon, MD, PhD1,3,
- Stephen C. Achuff, MD, FACC1,
- Jorge F. Trejo, MD1,
- Harlan F. Weisman, MD, FACC1,
- Peter O. Kwiterovich Jr., MD1 and
- Thomas A. Pearson, MD, PhD, FACC1
- ↵*Present address and address for reprints: David M. Herrington. MD. MHS. Division of Cardiology. The Bowman Gray School of Medicine, 300 South Hawthorne Road, Winston-Salem. North Carolina 27103.
Serum levels of DHEA sulfate are inversely associated with cardiovascular death in men, and urinary dehydroepiandrosterone (DHEA) levels are inversely associated with clinical manifestations of coronary artery disease. These observations may be related to the antiproliferative effects of DHEA, resulting in inhibition of atherosclerotic intimai hyperplasia. To examine the relation between these steroids and a direct measure of coronary atherosclerosis, plasma DHEA and DHEA sulfate levels were determined in 206 middle-aged patients (103 men, 103 women) undergoing elective coronary angiography.
Plasma DHEA sulfate levels were lower in men with at least one stenosis ≥50% compared with those without any stenosis ≥50% (4.9 ± 2.7 versus 6.1 ± 3.5 nmol/ml, p = 0.05). Levels of DHEA sulfate were also inversely related to the number of diseased coronary vessels (r = −0.20, p = 0.05) and a continuous measure of the extent of coronary atherosclerosis (r = −0.25, p = 0.01) in men. The association between DHEA sulfate levels and extent of coronary artery disease was independent of age and other conventional risk factors for coronary disease. In women, there was no association between plasma DHEA or DHEA sulfate levels and coronary disease.
These data demonstrate a consistent, independent, inverse, dose-response relation between plasma DHEA sulfate levels and angiographically defined coronary atherosclerosis in men. Plasma DHEA sulfate may be another important and potentially modifiable risk factor for the development and progression of coronary atherosclerosis.
- Received January 10, 1990.
- Revision received March 7, 1990.
- Accepted April 4, 1990.
- American College of Cardiology Foundation