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Menopause and the Risk of Cardiovascular Diseases Current Topics in Menopause 127 diseases account for 43% of deaths in men and 54% in women in Europe [2]. Specifically, coronary heart disease represents 21% of deaths in men and 22% in women, whereas stroke is a more frequent cause of death in women than in men (17% and 11%, respectively), as well as the other cardiovascular diseases (15% in women and 11% in men). Thus, stroke represents the third cause of death in men and the second in women. Despite unequivocal epidemiological observation the cardiovascular risk in females is underestimated because women are perceived as protected against cardiovascular disease [3]. However, the incidence of cardiac events is lower during the fertile age but increases after menopause and the misperception of the actual risk in this period may leave most women without appropriate preventive measures [4]. Sex hormones exert significant effects on the cardiovascular system. Ovarian hormone deficiency associated with menopause may play an important role in the development of cardiovascular disease in women. As the loss of ovarian hormones at menopause has an adverse impact on many cardiovascular risk factors, several observational studies were conducted in the 1980s in order to verify a potential association between the administration of exogenous estrogens and risk reduction of cardiovascular diseases. However, the reduced risk of cardiovascular diseases associated with hormone replacement therapy (HRT), reported in the observational studies, has not been subsequently confirmed in the randomized clinical trials. Therefore, at the present time, HRT is not recommended for postmenopausal women for the prevention of cardiovascular diseases. However, the possibility to consider HRT in women who experience menopausal symptoms that significantly affect their quality of life in relation to age, time since menopause began, route of administration and dosages is taken into consideration in recent Statements or Guidelines of Scientific Societies [5]. Although the majority of both men and women with ischemic heart disease have the typical symptoms of chest pain, more women than men show atypical clinical manifestations and the disease may go unrecognized for many years. Therefore, it is extremely important to carefully assess the risk of cardiovascular diseases in women in the peri- and postmenopausal period in order to develop appropriate
128 Current Topics in Menopause Marco Stramba-Badiale prevention strategies [6]. Furthermore, efficacy and safety of cardiovascular therapy should be evaluated in clinical studies which enroll a significant proportion of women [7]. EFFECTS OF SEX HORMONES ON THE CARDIOVASCULAR SYSTEM Cardiac receptors for estrogen, progesterone and androgens have been described in animals and humans, and their potential functional relevance has been demonstrated [8, 9]. It has been shown that sex hormones are involved in the transcription of hormone-sensitive genes such as NO synthases and that they interfere with various membrane-associated and cytoplasmic signalling pathways [8-10]. Experimental studies have also suggested that metabolites of estradiol exert direct effects on vascular cells [11], thus reducing infarct size and improving cardiac remodelling. Myocardial hypertrophy in female ovariectomized mice with aortic stenosis is reduced by estrogens administration [12]. It has been shown that polymorphisms in the gene that encodes the estrogen alpha receptor are associated with an increased rate of myocardial infarction in men and in women [9] and men with defects in this receptor develop early atherosclerosis [13]. In women and men, estrogens induce fast vasodilation, improve endothelialmediated vasodilation, and modulate proliferation or apoptosis of vascular smooth muscle cells and endothelial cells. Endogenous estrogens also reduce adhesionmolecule expression and increase the synthesis of vascular endothelial growth factor, which promotes angiogenesis and stimulates re-endothelialization after injury [8, 10, 14]. It has been shown that estrogen increases NO synthesis by increasing the activity of endothelial NO synthase [9]. Finally, endogenous, but not exogenous, estrogen inhibits angiotensinogen synthesis in the liver and angiotensin AT1 receptor expression in the myocardium, leading to an increased inhibition of the renin angiotensin system which may contribute to cardiovascular protection in premenopausal women [9]. On the basis of these observations it is plausible that a reduction in sex hormones in postmenopausal women might be associated with detrimental effects on the cardiovascular system.
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