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Sex hormone replacement therapy and modulation of vascular function in cardiovascular disease.
Expert Rev Cardiovasc Ther. 2007 Jul; 5(4):777-89.ER

Abstract

Epidemiological and experimental studies suggest vascular protective effects of estrogen. Cardiovascular disease (CVD) is less common in premenopausal women than in men and postmenopausal women. Cytosolic/nuclear estrogen receptors (ERs) have been shown to mediate genomic effects that stimulate endothelial cell growth but inhibit vascular smooth muscle proliferation. However, the Heart and Estrogen/Progestin Replacement Study (HERS), HERS-II and Women's Health Initiative clinical trials demonstrated that hormone replacement therapy (HRT) may not provide vascular benefits in postmenopausal women and may instead trigger adverse cardiovascular events. HRT may not provide vascular benefits because of the type of hormone used. Oral estrogens are biologically transformed by first-pass metabolism in the liver. By contrast, transdermal preparations avoid first pass metabolism. Also, natural estrogens and phytoestrogens may provide alternatives to synthetic estrogens. Furthermore, specific ER modulators could minimize the adverse effects of HRT, including breast cancer. HRT failure in CVD could also be related to changes in vascular ERs. Genetic polymorphism and postmenopausal decrease in vascular ERs or the downstream signaling mechanisms may reduce the effects of HRT. HRT in the late postmenopausal period may not be as effective as during menopausal transition. Additionally, while HRT may aggravate pre-existing CVD, it may thwart its development if used in a timely fashion. Lastly, the vascular effects of progesterone and testosterone, as well as modulators of their receptors, may modify the effects of estrogen and thereby provide alternative HRT strategies. Thus, the beneficial effects of HRT in postmenopausal CVD can be enhanced by customizing the HRT type, dose, route of administration and timing depending on the subject's age and cardiovascular condition.

Authors+Show Affiliations

Brigham and Women's Hospital, Division of Vascular Surgery, 75 Francis Street, Boston, MA 02115, USA. vkoledova@partners.orgNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

17605655

Citation

Koledova, Vera V., and Raouf A. Khalil. "Sex Hormone Replacement Therapy and Modulation of Vascular Function in Cardiovascular Disease." Expert Review of Cardiovascular Therapy, vol. 5, no. 4, 2007, pp. 777-89.
Koledova VV, Khalil RA. Sex hormone replacement therapy and modulation of vascular function in cardiovascular disease. Expert Rev Cardiovasc Ther. 2007;5(4):777-89.
Koledova, V. V., & Khalil, R. A. (2007). Sex hormone replacement therapy and modulation of vascular function in cardiovascular disease. Expert Review of Cardiovascular Therapy, 5(4), 777-89.
Koledova VV, Khalil RA. Sex Hormone Replacement Therapy and Modulation of Vascular Function in Cardiovascular Disease. Expert Rev Cardiovasc Ther. 2007;5(4):777-89. PubMed PMID: 17605655.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sex hormone replacement therapy and modulation of vascular function in cardiovascular disease. AU - Koledova,Vera V, AU - Khalil,Raouf A, PY - 2007/7/4/pubmed PY - 2007/9/5/medline PY - 2007/7/4/entrez SP - 777 EP - 89 JF - Expert review of cardiovascular therapy JO - Expert Rev Cardiovasc Ther VL - 5 IS - 4 N2 - Epidemiological and experimental studies suggest vascular protective effects of estrogen. Cardiovascular disease (CVD) is less common in premenopausal women than in men and postmenopausal women. Cytosolic/nuclear estrogen receptors (ERs) have been shown to mediate genomic effects that stimulate endothelial cell growth but inhibit vascular smooth muscle proliferation. However, the Heart and Estrogen/Progestin Replacement Study (HERS), HERS-II and Women's Health Initiative clinical trials demonstrated that hormone replacement therapy (HRT) may not provide vascular benefits in postmenopausal women and may instead trigger adverse cardiovascular events. HRT may not provide vascular benefits because of the type of hormone used. Oral estrogens are biologically transformed by first-pass metabolism in the liver. By contrast, transdermal preparations avoid first pass metabolism. Also, natural estrogens and phytoestrogens may provide alternatives to synthetic estrogens. Furthermore, specific ER modulators could minimize the adverse effects of HRT, including breast cancer. HRT failure in CVD could also be related to changes in vascular ERs. Genetic polymorphism and postmenopausal decrease in vascular ERs or the downstream signaling mechanisms may reduce the effects of HRT. HRT in the late postmenopausal period may not be as effective as during menopausal transition. Additionally, while HRT may aggravate pre-existing CVD, it may thwart its development if used in a timely fashion. Lastly, the vascular effects of progesterone and testosterone, as well as modulators of their receptors, may modify the effects of estrogen and thereby provide alternative HRT strategies. Thus, the beneficial effects of HRT in postmenopausal CVD can be enhanced by customizing the HRT type, dose, route of administration and timing depending on the subject's age and cardiovascular condition. SN - 1744-8344 UR - https://www.unboundmedicine.com/medline/citation/17605655/Sex_hormone_replacement_therapy_and_modulation_of_vascular_function_in_cardiovascular_disease_ DB - PRIME DP - Unbound Medicine ER -