[Postmenopause, plasma lipoproteins, and hormone replacement therapy]
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Updated: Nov 9, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
A Insúa1, F Massari, J R Zanchetta
1Instituto de Investigaciones Metabólicas, Buenos Aires, Argentina.
Abstract:
The incidence of coronary heart disease (CHD) rises after menopause. Hormonal replacement therapy (HRT) reduces cardiovascular morbidity and mortality. Plasma lipoproteins are modified by oral estrogen treatment: LDL are lowered while HDL and VLDL are augmented. The cardioprotective effect of oral HRT may be partially due to the reduction in the LDL/HDL ratio. Optimal changes in lipid profile are achieved with doses that usually prevent bone mass loss. Progestogens tend to blunt the increment of HDL induced by estrogens, but this depends on the type of agent and its dose. Unlike oral estrogen, HRT by the transdermal route does not always modify the lipid profile. When it does, changes are similar to those observed under the oral route in that the LDL/HDL ratio is diminished, but VLDL do not rise. Possible explanations for this discrepancy are discussed. At present there is no clear evidence that combined estrogen/progestogen treatment or transdermal estrogen alone could reduce CHD's incidence. Women with an intact uterus should receive a progestogen in addition to estrogen for prevention of endometrial carcinoma. Estrogen alone is preferable for hysterectomized women. When beneficial and adverse effects of HRT are considered simultaneously, the overall result is considered favorable, principally as a consequence of its cardioprotective properties.
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