[Hormone replacement therapy and cardiovascular risk].
Coronary artery disease is the main cause of death and morbidity in both genders, in Italy as well as in other Western populations. Nonetheless, striking sex differences in the incidence of coronary artery disease exist, with a relative protection in fertile women. This protection is mostly lost in the post-menopause. Several lines of evidence indicate that this relative protection is due to the effects of ovarian hormones. In the last 10 years the great opportunity to prevent or reduce the occurrence of coronary artery disease in post-menopausal women by hormone replacement therapy has been appreciated. This review examines the effects of hormone replacement therapy on cardiovascular risk and its possible mechanisms. Epidemiological and observational evidence supports the notion of protective effects of estrogens. This may occur through favorable changes on lipid risk factors (a decrease in plasma levels of total and LDL-cholesterol and an increase in HDL-cholesterol), on the vessel wall (endothelial and smooth muscle cells) and on the development of atherosclerosis. Active investigational areas are the search for molecular mechanisms through which estrogens-with or without progestogens-modulate the vascular response to vasoactive agents, endothelial and smooth muscle cell biology, hemostasis and glucose metabolism. There is, however, a lack of adequate prospective studies to evaluate the effects of estrogens-alone or in combination with progestogens-on hard end-points such as total and cardiovascular mortality and morbidity. In addition to this, there is still substantial disagreement on the possible risks, mostly breast cancer, of hormone replacement therapy. At the moment, the evaluation on the opportunity to start hormone replacement therapy in post-menopausal women has to be strictly personalized, by adequately balancing potential risks and probable benefits.
Maffei
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S
Laboratorio per lo Studio della Trombosi e dell'Aterosclerosi, C.N.R, Pisa.
De Caterina
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R
D001161:Arteriosclerosis / Q000517:prevention & control; D001943:Breast Neoplasms / Q000139:chemically induced; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D016889:Endometrial Neoplasms / Q000139:chemically induced; D015914:Estrogen Replacement Therapy / Q000009:adverse effects; D004967:Estrogens / Q000008:administration & dosage / Q000009:adverse effects; D005260:Female; D006801:Humans; D008875:Middle Aged; D017698:Postmenopause; D011372:Progestins / Q000008:administration & dosage / Q000009:adverse effects; D011446:Prospective Studies; D012307:Risk Factors; D013997:Time Factors
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004967:Estrogens; D011372:Progestins; D002784:Cholesterol