Our results show that the knowledge and prejudice about side effects of beta-blockers can produce anxiety, that may cause erectile function.

Background-It has been suggested that hormone replacement therapy (HRT) in postmenopausal women is associated with an increased inflammatory response that may trigger acute cardiovascular events. This suggestion is mainly based on the finding of elevated C-reactive protein (CRP) levels after HRT. The aim of the present study was to evaluate a broad spectrum of vascular inflammation markers in 389 postmenopausal women with increased cardiovascular risk at baseline and after either 6 months of HRT (126 women) or no HRT (263 women). Methods and Results-Compared with baseline, CRP levels significantly increased after HRT (0.9Ϯ0.2 versus 1.6Ϯ0.4 mg/L, PϽ0.01); on the contrary, soluble intracellular adhesion molecule-1 decreased from 208Ϯ57 to 168Ϯ37 ng/mL (PϽ0.01) after HRT. Similarly, vascular cell adhesion molecule-1 decreased from 298Ϯ73 to 258Ϯ47 ng/mL (PϽ0.01), plasma E-selectin levels were reduced from 17.8Ϯ5.6 to 14.8Ϯ3.9 ng/mL (PϽ0.01), interleukin-6 levels decreased from 1.51Ϯ0.22 to 1.29Ϯ0.28 pg/mL, and s-thrombomodulin plasma levels decreased from 4.8Ϯ0.7 to 4.3Ϯ0.9 ng/mL (PϽ0.01). No significant changes in either CRP or vascular inflammatory marker were detected in women not taking HRT. Conclusions-The discrepancy between increased plasma levels of CRP and reduced plasma levels of all other markers of inflammation suggests that the increased CRP levels after oral HRT may be related to metabolic hepatic activation and not to an acute-phase response. HRT seems to be associated with an overall decrease in vascular inflammation.

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Postmenopausal hormone therapy is associated with decreased vascular inflammation; however, in patients with a longer time since menopause, postmenopause hormone therapy may increase inflammation and worsen endothelial function. These unfavorable vascular effects may be detected by an elevation in IL-6 levels and by a lack of improvement in endothelial function.

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in women after the age of 50 years in most developed countries. Estrogen deficiency plays a key role in causing CVD in women. Apart from the direct effect of ovarian hormones on the vessel wall, cessation of ovarian function and the consequent reduction of sex steroid hormone levels have important metabolic and pathological implications that negatively influence the cardiovascular system. Therefore, the increased incidence of CVD observed in women after menopause should be considered on a multifactorial basis. Data available for the effects of ERT and HRT in the primary prevention of CVD are mainly observational. However, despite limitations related to this kind of study, it must be noted that their results consistently show a reduction in cardiovascular events in hormone users. Meta-analysis of epidemiological studies found that women who had ever used estrogens had a 34% overall reduction in the relative risk of cardiovascular events compared to those who had never used hormones. Most of the early epidemiological studies were conducted using unopposed estrogen replacement therapy. The number of studies evaluating the effects of estrogen-progestin replacement therapy is limited. Recently, the estrogen-progestin arm of the Women's Health Initiative (WHI) study has been stopped because of an increased incidence of breast cancer, and too early on to give any insight into possible cardiovascular effects. Comments on the cardiovascular effects of HRT from the results of the WHI study are therefore not warranted, as the study did not continue for a duration long enough to enable a calculation of cardiovascular end points. The WHI study included only one single type of estrogen-progestin association; whether different estrogen-progestin combinations, more commonly used outside the United States, may have a different effect is still a matter of speculation. A major difference between observational and randomized studies on the effect of ovarian hormones on cardiovascular function is the time of HRT initiation since menopause, which is significantly shorter in observational studies. In conclusion, the average 35-50% risk reduction in CVD with HRT in primary prevention in postmenopausal women is based on nonrandomized observational data.