Dehydroepiandrosterone and Coronary Atherosclerosis

Abstract

Tissue culture, animal model, and epidemiologic studies suggest that dehydroepiandrosterone (DEHA) may inhibit atherosclerosis through its potent antiproliferative effects. To examine the relation between DHEA and a direct measure of coronary atherosclerosis, plasma DHEA, and DHEA sulfate (DHEAS) levels were determined in 206 middle-aged patients undergoing coronary angiography. Plasma DHEAS levels were lower in subjects with at least one > or = 50% stenosis than in those with no stenosis > 50% (p = 0.05) and was inversely associated with the number of diseased coronary vessels and the extent of coronary atherosclerosis (p = 0.05 and 0.01, respectively). Cardiac allograft vasculopathy is dominated by abnormal cellular proliferation and, therefore, may be uniquely influenced by DHEA. To study this, 61 cardiac allograft recipients with at least one annual follow-up cardiac catheterization were studied. Plasma levels of total and free DHEA were inversely related to the development of accelerated coronary allograft vasculopathy (p = 0.005 and 0.003, respectively). Furthermore, the time to development of accelerated allograft vasculopathy was shorter in subjects with low levels of total and free DHEA (p = 0.062 and 0.046, respectively). These data suggest that low plasma levels of DHEA may facilitate, and high levels may retard, the development of coronary atherosclerosis and coronary allograft vasculopathy.