Cardiovascular protection by estrogen: a hemodynamic mechanism?

Cardiovascular risk is higher in men than in women, and also more prevalent in postmenopausal than in premenopausal women, especially if not treated by estrogens. These differences may be due, in part, to a cardioprotective action of sex hormones, mainly estrogens. However, only a limited part of this protection may be attributed to metabolic modifications induced by replacement therapy with estrogen. Therefore, it remains to be determined which other cardioprotective mechanisms influenced by sex steroids might be involved. It has been demonstrated that the menopause is associated with an increase in uterine arterial pulsatility index, reflecting increased peripheral resistance, while the administration of estrogens has an opposite effect at this level. In Doppler studies, estrogen replacement therapy was also associated with an increase in stroke volume and flow acceleration in the aorta. This suggests a positive inotropic effect of estrogens. Using technetium scanning, it was found that women at an early phase of menopause have a stronger myocardial contractility than women of a similar age whose menopause is of longer duration. These effects of estrogens on hemodynamic characteristics might be controlled by vasoregulatory hormones such as endothelin(s) or endothelial-derived relaxing factor (EDRF), now identified as nitric oxide (NO). Indeed, sex-associated differences in endothelin have been observed. Such are some of the mechanisms by which estrogen administration might effect a cardiovascular protection. At the present time, however, conclusive data are not available.