Abstract
Objective: Analysis of contemporary knowledge of influences of hormone replacement therapy on cardiovascular system. Method: Informations were collected from fulltexts which were chosen in database Medline and Ovid.
Conclusion: Hormone replacement therapy (HRT) has positive influence on some risk factors of cardiovascular disease. Changes in the lipoprotein spectrum are well known.
Oral estrogens cause a decrease of low density lipoprotein cholesterol (LDL-C) and, especially an increase of high density lipoprotein cholesterol (HDL-C) levels, which both have potentially favourable effects; they also cause a triglyceride level increase, which probably has no clinical relevance except in cases with basal hypertriglyceridemia. Transdermal estradiol causes generally a minor dicrease in LDL-C and minor increase HDL-C levels, with no increase or even decrease in triglyceride levels.
The addition of androgenic progestins at conventionally used doses, while not interfering with LDL-C variations, causes a HDL-C decrease, which contrasts he effect of oral estrogens and completely reverses the effect of transdermal estradiol. On the contrary, the addition of a non-adrogenic progestin does not interfere with any of the estrogen induced lipid profile modifications.
Transdermal estradiol does not cause change of insulinoresistance. Estrogen substitution protects gynoid distribution of body fat that is conected with lower risk of ischemic heart disease.
Estrogens have posibility to dilate vessels. Decreasing of levels of cytoadhesive moleculs was verificate during HRT so as lowering of homocysteine level to premenopausal levels.
Newly uncovered changes like the significant increase of CRP conected with oral estrogene therapy could explain increasing of cardiovascular risk on the beginning of HRT especially in group of women with history of ischemic heart disease.