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.