Estrogen replacement has been found to reduce the risk of heart disease by as much as 50% in postmenopausal females. The mechanism of action of this cardioprotective effect of estrogen, however, is not clear. The use of replacement hormones has recently been associated with the enhancement of endogenous fibrinolytic potential, i.e., blood thinning factors. This enhanced fibrinolytic potential may contribute to the inverse relation between hormonal replacement and coronary heart disease. These effects are consistent whether oral estrogen monotherapy, estrogen plus progesterone or transdermal estradermal estradiol is administered. For study purposes, we will randomize each woman to take one month of either oral or transdermal estrogen or placebo. The primary goal is to evaluate the effects of estrogen on blood thinning and clotting factors (i.e.tPA antigen, PAI-1 antigen D-dimer, von Willebrand factor, and fibrinogen). Our second goal will be to assess the effects of using 2 different routes of hormonal replacement (oral and transdermal estrogen) on fibrinolytic and hemostatic potential in postmenopausal women. The third goal is to determine the fibrinogen phenotype and acute phase reactants that are found after estrogen therapy.
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