ABSTRACT
Epidemiological data indicate that pre-menopausal women are at lower risk of coronary heart disease than are men of similar age (Clawson, 1941). The increased incidence of atherosclerosis in women who undergo premature menopause has also been well described (Oliver and Boyd, 1959). Finally, there is increasing evidence that treatment with replacement estrogen after menopause will reduce cardiovascular mortality (Gruchow et al., 1988; Matthews et al., 1989). Endogenous and exogenous estrogens have been observed to alter the level of lipids and lipid metabolism in humans. Oxidative modification of low-density lipoproteins (LDL) may be atherogenic and is inhibited by 17β estradiol in postmenopausal women, suggesting a beneficial effect of an estrogen-replacement therapy on cardiovascular disease (Sack et al., 1994). The changes in serum lipids noted in human patients, however, fail to fully account for the discrepancy in the incidence of coronary disease between men and pre-menopausal women (Bush et al., 1987). It is also clear that the plasma lipidindependent antiatherogenic effect of estradiol in rabbits is not mediated through a change in aortic permeability to LDL (Haarbo et al., 1994). The demonstration of a functional estrogen receptor in
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