Cardiovascular implications of estrogen replacement therapy

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Abstract
Estrogen appears to protect against the development of cardiovascular disease, the leading cause of death in women, by a number of mechanisms. The protective effect is believed to be mediated principally by beneficial changes in cholesterol levels. Estrogen decreases low-density lipoprotein (LDL) cholesterol and increases high-density lipoprotein (HDL) cholesterol levels by mechanisms that include the possible induction of LDL receptors and the destruction of hepatic lipase, which degrades HDL cholesterol. However, estrogen also appears to have a direct beneficial effect on vessel-wall physiology. One of these effects may be an increase in local prostacyclin production. The type of estrogen used in hormone replacement therapy and the route of administration determine the positive and negative effects of estrogen on the cardiovascular system. In general, synthetic estrogens, because they are manyfold more potent than natural estrogens, should not be used. Most studies show a 50% or greater reduction in cardiovascular disease and related mortality with postmenopausal estrogen administration. There is no evidence that postmenopausal estrogen replacement adversely affects carbohydrate metabolism, blood pressure, or coagulation. By use of a mathematical model to study the overall effects of estrogen therapy, it can be shown that more lives can be saved from the reduction in cardiovascular disease with estrogen use than from the reduction in death from osteoporosis or any other disease state affected by estrogen. Serious consideration has to be given to the cardiovascular effects of added progestogen, which may attenuate or eliminate the beneficial effects of estrogen on HDL2 cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

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