Epidemiological, experimental and clinical data verify that the risk of atherosclerotic cardiovascular disease is increased by a long-term estrogen deficiency. This is, among other beneficial effects of estrogens on arteries, caused by alteration of lipid and lipoprotein metabolism [e.g. decrease in total cholesterol, LDL-cholesterol and lipoprotein (a) and decrease in HDL2 cholesterol in serum and decrease in the accumulation of cholesterol in the arterial wall]. The beneficial cardioprotective effects of estrogens are attenuated by estrogen overdosing (causing hypertriglyceridemia), the use of synthetic instead of natural estrogen products (increased incidence of adversary effects) and especially by use of inappropriate progestins. The effect of progestins may be minimized by selecting a lower dose of a more metabolically inert products (especially progestins of the third generation). Mild to moderate hypercholesterolemia may improve with oral estrogen, and this strategy may be used as an adjunct for treatment. The replacement treatment of menopause is not yet widespread in Czechoslovakia. The new forms of treatment, not causing menstrual bleeding (continual medication, tamoxifen) may achieve more interest in the therapy. Hypogonadal men are known to have a more advanced development of atherosclerosis. The appropriate replacement is done by administration of such testosterone derivatives which enable the conversion to estrogens.

Keywords: Androgens /physiology/; Arteriosclerosis /physiopathology/; Estrogens /physiology/; Female; Humans; Lipid Metabolism; Male; Progestins /physiology/