Hormonsubstitution in der Menopause : Einfluss auf Lipide und kardiovaskuläres Risiko

After the menopause the risk for cardiovascular diseases increases to a similar extent in females compared to males. An increase in low density lipoproteins (LDL) as most frequent change in blood lipoprotein composition is in part responsible. Estrogens and gestagens affect the lipoproteins profile differently. Estrogens at doses for substitution lead to a minor decrease of LDL accompanied by an increase in protective high density lipoproteins (HDL). Under estrogen therapy triglycerides rise apparently with little effect on atherogenicity. A multitude of epidemiologic studies point to a decrease of cardiovascular morbidity and mortality under estrogen substitution. This is in part explained by the more favorable lipoprotein profile (decreased LDL, increased HDL). The available data have not remained unchallenged (Framingham Study) and a prospective randomized trial of the effects of estrogen substitution on cardiovascular risk has not been undertaken. Oral administration of estrogens shows a trend for higher effects on lipid-profile improvement when compared to the transdermal route. Gestagens have an effect opposed to the action of estrogens, notably those with an androgenic component (such as norethisterone) reducing HDL and triglycerides and raising LDL. This effect is however-if present-small. Women with hypercholesterolemia or at risk for ischemic heart disease should only receive minimal doses of gestagens. In hysterectomized patients gestagens are not needed. A hypertriglyceridemia can be aggravated by estrogens. A careful dosing scheme should be used in these patients. A history of thrombotic episodes precludes estrogen prescription. Because of the high cardiovascular morbidity and mortality in postmenopausal women the improvement of the lipoprotein profile may be of great significance.