Issue: October 2010
October 01, 2010
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CV mortality in women linked to levels of dehydroepiandrosterone sulfate

Issue: October 2010
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Low circulating dehydroepiandrosterone sulfate levels predicted high cardiovascular disease mortality and all-cause mortality in postmenopausal women who underwent coronary angiography for suspected myocardial ischemia, a new study found.

“There are increasing lessons to be learned from these reproductive steroid hormones and the roles they play in the relationship with common diseases such as CVD and cancer,” C. Noel Bairey Merz, MD, medical director of the Women’s Heart Center at Cedars-Sinai Heart Institute, told Endocrine Today. “If dehydroepiandrosterone (DHEA) sulfate is involved in CVD, it potentially represents a therapeutic target pathway to prevent or treat certain CVDs.”

The researchers examined the relationship between circulating DHEA sulfate levels, CVD and mortality risk among 270 postmenopausal women with suspected myocardial ischemia. All were included in the Women’s Ischemia Syndrome Evaluation (WISE) study and were followed annually. The mean DHEA sulfate level was 48.1 mcg/dL.

Linking low levels, mortality

During 6 years of follow-up, 10% of the women died of CVD causes and 12.6% died from all causes. Additionally, 8.2% were hospitalized for heart failure, 5.9% for stroke and 4.8% for myocardial infarction.

More than half of the women who died had levels in the lowest DHEA sulfate tertile (55% of CVD deaths; 53% of all-cause deaths). The researchers noted no difference in CVD mortality or all-cause mortality among women with higher DHEA sulfate levels.

Low levels — 0.02 g/dL to 24.7 g/dL — were associated with two times the risk for CVD mortality (6-year mortality rate: 17% vs. 8%) and all-cause mortality (21% vs. 10%) compared with women with higher levels ranging from 24.8 g/dL to 244 g/dL.

After the researchers adjusted for multiple CVD risk factors, the increased CVD mortality risk remain unchanged (HR=2.55; 95% CI, 1.19-5.45). However, the increased mortality risk was nonsignificant after adjustment for the presence or severity of angiographic obstructive coronary artery disease (HR=1.99; 95% CI, 0.87-4.59). The researchers noted a similar trend for all-cause mortality.

Potential therapeutic target pathway

Previous research has implicated low levels of DHEA sulfate in CVD risk and all-cause mortality; however, these results have not been consistently replicated in women.

In addition, the mechanisms that link DHEA sulfate levels to CVD and mortality risk remain unclear, according to the researchers.

Bairey Merz said the results of this observational study should serve as a “wake-up call to physicians that all of women’s health is not defined by estrogen.

“DHEA [sulfate] is a natural hormone that rises and falls with age and disease,” she said. “The next step is to see if we can alter these reproductive hormones as a mechanism to alter disease.” – by Matthew Brannon

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