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Effects of hormone replacement therapy on hemostatic cardiovascular risk factors

L F Andersen1, J Gram, S O Skouby

  • 1Diabetes Centre, Department of Gynecology and Obstetrics, Rigshospitalet, and the Department of Gynecology and Obstetrics, Frederiksberg Hospital, Copenhagen, Denmark.

Insights

Hormone replacement therapy favorably impacts cardiovascular risk factors in postmenopausal women by lowering fibrinogen and other markers. Different HRT regimens showed similar effects on hemostatic factors over one year.

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Hematology

Background:

  • Observational studies suggest hormone replacement therapy (HRT) reduces cardiovascular events in postmenopausal women.
  • The precise mechanisms underlying this cardiovascular protection remain incompletely understood.
  • HRT's effects on established hemostatic risk factors require further investigation.

Purpose of the Study:

  • To investigate the effects of HRT on hemostatic risk factors in healthy postmenopausal women over a 1-year period.
  • To compare the impact of cyclic versus continuous HRT regimens on these risk factors.

Main Methods:

  • Sixty postmenopausal women were randomized to continuous or cyclic HRT regimens.
  • Blood samples were collected at baseline and during cycles 3, 6, and 12.
  • A reference group of 30 women was observed for 12 months.

Main Results:

  • One-year HRT significantly decreased fibrinogen, tissue-type plasminogen activator, plasminogen activator inhibitor-1, and lipoprotein(a).
  • Fibrinogen levels were significantly lower in the HRT group compared to the reference group.
  • No significant differences in hemostatic effects were observed between cyclic and continuous HRT regimens.

Conclusions:

  • One-year HRT favorably influences several cardiovascular risk factors, notably lowering fibrinogen.
  • The observed hemostatic effects of HRT were consistent across both cyclic and continuous administration regimens.
  • HRT may offer cardiovascular benefits through modulation of hemostatic pathways.
Abstract

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