What is the role of estrogen therapy in cardiovascular disease prevention?

Updated: Oct 16, 2018
  • Author: Janice L Bacon, MD; Chief Editor: Richard Scott Lucidi, MD, FACOG  more...
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Cardiovascular disease is the leading cause of death in postmenopausal women and menopause increases the risk of CVD independent of patient age.

Results from epidemiologic studies in the 1980s and 1990s, such as the Nurses' Health Study, suggested that hormone therapy was protective against coronary heart disease (CHD) and related mortality. [32, 33] Data from retrospective studies also supported the notion that hormone therapy was cardioprotective. [34]  Reappraisal of older studies, such as the WHI, as well as newer investigations consider results and risks associated with the use of HT in younger women (< age 60) or less than 10 years from menopause be separately considered from those of women >age 60  or >10 years from the onset of menopause

For younger women (< age 60 or < 10 years form menopause onset, the effects of E or E+P on initiated less than 10 years from menopause onset lowered the CHD risks in postmenopausal women. It also lowered the risk of stroke and all-cause mortality. An increased risk of VTE was noted. This was most recently upheld by a 2015 Cochrane Review and had first been put forth by an earlier meta-analysis. [116] The WHI, for CEE use alone in younger women with < 10 years since menopause onset showed also less CVD risks except VTE. ( A slightly higher risk in women ages 50-59 was present but not statistically significant). [116, 122]

Hormone therapy initiated in older women ( >age 60 ) or greater than 10 years showed a greater risk of CVD as the time since menopause  increased. The type of progestin (MPA versus micronized progesterone) could also contribute to a greater CVD risk. No reduction in all-cause mortality was noted. Effects on stroke noted increased risk in older women and variable results in younger women with a lesser risk in lower doses of therapy (oral or transdermal). Patient medical disorders and familial risks of CVD and VTE should also be factored in before implementing HT.

Standard doses of HT resulted in an increased risk of VTE at hormone initiation. This risk could be reduced with lower doses of estrogen or transdermal applications. NO increase in VTE was noted in women using vaginal preparations for genitourinary symptoms.

Therefore, while HT cannot be recommended for cardioprotection, as was formerly touted, the potential risks have been more carefully delineated and will assist calculation of safety in more patients.

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