Menopause and hormone therapy: from vascular endothelial function to cardiovascular disease.

C ardiovascular diseases (CVD), including coronary artery, cerebrovascular and peripheral vascular disease, are the major causes of morbidity and mortality in both men and women, although female sex has long been considered to be a “protective factor” against CVD. Indeed, the incidence of CVD is low in premenopausal women but increases with age, especially after menopause; women develop CVD about a decade later than men. This has been attributed to the cardioprotective effects of endogenous oestrogen, whose levels decline after menopause. Hormone therapy (HT), i.e. oestrogen only or oestrogen/progestogen treatment, still remains the most important means for treating menopausal symptoms. Until about a decade ago, it was thought that HT could contribute to the prevention of cardiovascular (CV) events in post-menopausal women, as observational studies had shown that women who used HT had a 35-50% lower risk of coronary artery disease (CAD) than nonusers, while numerous basic research, animal and human studies had also demonstrated that oestrogen exerts protective effects on the CV system. Surprisingly, more recent randomised trials have shown no clinical benefit of HT in primary or secondary CVD prevention, thus creating great confusion about the effects of HT on CVD. Menopause and Hormone Therapy: From Vascular Endothelial Function to Cardiovascular Disease