Can menopause be considered an independent risk factor for cardiovascular disease?

Following the menopause, women develop coronary artery disease at the same rate as men. The best documented change observed in the risk factors linked to ovarian exhaustion is an alteration in lipid composition. More recent studies, however, suggest that the increased cardiovascular morbidity and mortality after menopause cannot be fully explained by changes in plasma lipoproteins, and support the concept that ovarian hormone deprivation has a widespread impact on the cardiovascular system, with a direct harmful effect on vessel-wall physiology. After the menopause, subjects free from cardiovascular diseases show vascular hyperactivity and a poor vasodilator reserve; the rate of increase in the incidence of arterial hypertension in women is higher than that observed among males of the same age; altogether, cardiovascular diseases become the number one cause of death among women. A large number of mechanistic studies have shown that estrogens, through either direct or genomic-dependent activities, produce beneficial effects on the factors controlling blood flow and plaque formation. Nevertheless, results from recent randomized clinical trials are challenging the belief that postmenopausal hormone therapy protects against coronary artery disease.