Gaspard U J
Service de Gynécologie, Centre Hospitalier Universitaire de Liège, Domaine Universitaire du Sart Tilman, Belgique.
J Gynecol Obstet Biol Reprod (Paris). 1996;25(7):671-6.
Cardiovascular diseases (CVD) are a major cause of female mortality. The occurrence of menopause and estrogen deficiency is a well defined risk factor for CVD. Both retrospective and prospective epidemiological studies indicate that estrogen as well as estrogen-progestin hormone replacement therapy is associated with a reduced incidence of mortality and morbidity due to myocardial infarction or (probably) to stroke by about 50% without any obvious change in venous thromboembolism, when compared to absence of hormone use. A favorable effect of estrogens on the lipid profile could explain about 1/3 of this reduction of risk. Among other potential non-lipid effects of estrogens associated with a positive cardiovascular action, an improvement of insulin secretion together with a decrease in insulin resistance have been noted, this effect being however less obvious if the progestin used has androgenic properties. An improvement of the coagulation-fibrinolysis balance is plausible under treatment, as well as direct action of estrogen on the arterial wall (alteration of both endothelium-dependent and endothelium-independent factors such as a calcium-antagonist effect), leading to an improvement of arterial flow at the coronary, cerebral and peripheral levels. Hormone replacement therapy would be a primary and-potentially-secondary prevention of cardiovascular diseases. However, large prospective, controlled and randomized therapeutic trials that are now underway, are mandatory to definitively establish the cardioprotective effect of hormone replacement therapy.
