Abstract
See related article, pp 694–704 Regardless of age, race, and ethnicity, cardiovascular disease is the number 1 cause of death for women, and its prevalence rises rapidly after menopause.1–4 This postmenopausal increase is believed to result from the loss of endogenous estrogen. Although estrogen replacement therapy (ERT) has long been thought to protect against menopause-associated cardiovascular anomalies, osteoporosis, hot flashes, and thinning of the vaginal epithelium,3–5 findings from the Heart and Estrogen/Progestin Replacement Study and the Women's Health Initiative Study5 do not support the notion that ERT protects the cardiovascular system. Instead, the data indicate just the opposite, that is, increased risk of cardiovascular disease, in addition to the apparent higher risk of breast cancer and deep vein thrombosis.1,2,4 Although results from clinical trials have substantiated the beneficial role of ERT in the management of menopausal symptoms, the unexpected finding of exacerbated cardiovascular function after ERT has made women hesitant to initiate ERT after menopause.1 Further analysis of the clinical trials revealed that the age of a woman and especially the number of years after menopause onset may be primary factors that contribute to the ultimate cardiovascular outcome of ERT. Although estrogen-progesterone therapy was found beneficial in young postmenopausal women, it increased cardiovascular risk when initiated in older postmenopausal women with established coronary artery disease.2,4 It is, thus, recommended that ERT be limited to the shortest duration consistent with treatment goals (eg, relief of menopausal symptoms).1 In contrast to the generalized recommendation for short duration of menopausal hormone treatment,2,4 careful scrutiny of the data from the Women's Health Initiative Estrogen Plus Progestin Trial reveal a reduced coronary heart disease risk after 5 to 6 years of ERT treatment. Accordingly, the …
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