[Estrogens and risks for onset of atherosclerosis]

There are many evidences suggesting that estrogens prevent atherosclerosis and its consequences such as coronary heart disease (CHD) in women. The risk for CHD is less in premenopausal women when compared with age-matched men, but the protective effect of estrogens is lost with menopause. A part of this beneficial effect may be ascribed to the ability of estrogens to favorably alter the plasma lipoproteins profile, i.e. increase HDL and decrease LDL and Lp(a). However, the changes in the lipid profile do not fully account for the protective effect afforded by estrogens, indicating that other mechanisms are likely to be involved. One of these mechanisms may include estrogens ability to prevent oxidative modification of LDL. A number of animal and human studies strongly suggest also a direct effect on the vascular endothelium, decreasing the expression of adhesion molecules involved in monocyte adhesion such as VCAM-1. It seems that estrogens also cause by increasing the synthesis of NO a decrease in chemokines involved in monocyte migration into the subendothelial space (TNF alpha, IL-1 and MCP-1) and growth factors influencing the migration of smooth muscle cells (PDGF). They also decrease fibrinogen and homocysteine, and these substances when increased are considered independent risk factors for CHD. However, the results of the first randomised controlled trial of hormone replacement therapy (HRT) with estrogens concerning the CHD published recently differ from previous observational epidemiological studies in both primary and secondary intervention, which showed beneficial effect of HRT. The final answer about the effects of HRT on CHD is expected from several ongoing trials.