DEHYDROEPIANDROSTERONE AND CARDIAC ALLOGRAFT VASCULOPATHY

Background: Tissue culture, animal model, and epidemiologic studies su ggest that dehydroepiandrosterone may inhibit atherosclerosis through its potent antiproliferative effects. Because cardiac allograft vascul opathy is predominantly a proliferative abnormality of intimal and med ial smooth muscle cells, plasma levels of dehydroepiandrosterone may p lay an important role in the development of this disease. Methods: Six ty-one cardiac allograft recipients who survived for 1 year or more an d had at least one annual follow-up cardiac catheterization were inclu ded in the study. Plasma levels of dehydroepiandrosterone, dehydroepia ndrosterone sulfate, and free dehydroepiandrosterone (dehydroepiandros terone not bound to sex hormone-binding globulin) were measured in all 61 subjects and compared with the presence or absence of cardiac allo graft vasculopathy as defined by angiography. Results: Plasma levels o f total and free dehydroepiandrosterone were lower in subjects in whom cardiac allograft vasculopathy developed (p = 0.005 and 0.003, respec tively). Furthermore, the time to development of cardiac allograft vas culopathy was shorter in subjects with low levels of total and free de hydroepiandrosterone (p = 0.052 and 0.046, respectively). This relatio nship was maintained after adjusting for age, gender, cholesterol, pre dnisone use, and blood pressure. Conclusions: Low plasma levels of deh ydroepiandrosterone may facilitate and high levels may retard the deve lopment of cardiac allograft vasculopathy.