[Cardiovascular effects and estrogen/gestagen substitution therapy].
After the menopause there is a profound increase in cardiovascular diseases which is mainly based on an enhanced development of atherosclerosis caused by an estrogen deficiency. The most important pathomechanisms are the rise in LDL-cholesterol and triglycerides as a result of an impaired elimination of LDL and remnants in the liver, and an enhancement of LDL oxidation in the arterial intima. Moreover, at the site of endothelial lesions the occurrence of vasospasms and platelet aggregation is facilitated in estrogen-deficient women which may lead to ischemia. Epidemiological studies revealed that replacement therapy with natural estrogens reduces the risk of cardio-vascular diseases by 30 to 50%, whereby the protective effect is not impaired by the addition of progestogens. The mechanism of action is only partly based on the favorable effect of estrogens on lipid metabolism. Besides an increase in HDL, estrogens may reduce LDL-cholesterol by means of an enhancement of receptor-mediated elimination of LDL and remnants in the liver. A rise in triglycerides is of no clinical relevance, if based on an estrogen-induced increase in triglyceride synthesis and VLDL-LDL turnover. Even in the case of an unfavorable lipid pattern estrogens may protect from atherosclerosis, as they inhibit LDL oxidation by scavenging free oxygen radicals. Finally, estrogens may cause vasodilation which is partly endothelium - dependent, but presumably is also based on the blockade of calcium influx into smooth muscle cells. This may be of particular importance in women with endothelial lesions, e.g. coronary sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Abteilung für gynäkologische Endokrinologie, Universitäts-Frauenklinik Frankfurt am Main.
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D000328:Adult; D001161:Arteriosclerosis / Q000517:prevention & control*; D008076:Cholesterol, HDL / Q000378:metabolism; D008078:Cholesterol, LDL / Q000378:metabolism; D004967:Estrogens / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D016166:Free Radical Scavengers; D006801:Humans; D008055:Lipids / Q000097:blood; D008875:Middle Aged; D017698:Postmenopause; D011372:Progestins / Q000008:administration & dosage / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects
D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004967:Estrogens; D016166:Free Radical Scavengers; D008055:Lipids; D011372:Progestins
Kardiovaskuläre Effekte und Ostrogen/Gestagen-Substitutionstherapie.