Acute administration of 17beta-estradiol reduces endothelin-1 release during pacing-induced ischemia.

Objectives: To assess whether acute administration of 17beta-estradiol reduces pacing-induced cardiac release of endothelin-1 in female menopausal patients with coronary artery disease.

Background: Endothelin-1 is a potent vasoactive peptide which plays a pathogenetic role in myocardial ischemia and adverse clinical events in patients with coronary artery disease. Estrogens decrease plasma levels of endothelin-1 and improve stress-induced myocardial ischemia in menopausal women with coronary artery disease.

Effect of estradiol 17beta upon coronary artery vasoconstrictor response to methylergometrine maleate in female menopausal patients.

Background: Estrogens produce several beneficial effects upon the cardiovascular system. Amongst these, an endothelium-independent effect has been convincingly demonstrated only in vitro, while there is no evidence for such an effect in vivo. The aim of the present study was to evaluate the effect of acute administration of estradiol 17beta upon coronary artery reactivity to methylergometrine in 16 menopausal patients with coronary artery disease.

Interleukin-6 and flow-mediated dilatation as markers of increased vascular inflammation in women receiving hormone therapy.

Objective: The lack of a beneficial long-term cardiovascular effect of hormone therapy and the early incidence of cardiovascular adverse events observed in recent randomized studies have been related to a heightened inflammatory effect of hormone therapy.

Design: We evaluated the effect of different postmenopause therapies on inflammatory markers and endothelial function in 205 postmenopausal women before and after therapy.

Results: all postmenopausal women, estrogens alone increased plasma levels of C-reactive protein (CRP) but decreased all other markers of inflammation including interleukin-6 (IL-6) (CRP: +75% +/- 11%, intracellular adhesion molecule: -21% +/- 4%, vascular cell adhesion molecule: -15% +/- 6%, E-selectin: -18% +/- 4%, s-thrombomodulin -10.

Different effect of hormone replacement therapy, DHEAS and tibolone on endothelial function in postmenopausal women with increased cardiovascular risk.

Menopause is associated with an increased cardiovascular risk and with a decrease in endothelial function. Hormone replacement therapy (HRT) improves endothelial function in post-menopausal women (PMW) without established atherosclerosis. New alternative treatments, among which tibolone (T) and DHEAS have been suggested to reduce postmenopausal cardiovascular risk.

Value of C-reactive protein levels and IL-6 in predicting events levels in women at increased cardiovascular risk.

Background: Elevated C-reactive protein (CRP) levels due to of heightened vascular inflammatory state in vascular conditions are often associated with elevated interleukin-6 (IL-6) levels since during inflammation CRP production in the liver is induced by IL-6. It has been suggested that CRP may be a predictors of unfavourable outcome in postmenopausal women (PMW) receiving hormone replacement therapy. Because of the possible metabolic effect of hormone replacement therapy (HRT) on CRP, the relative predictive importance of CRP and IL-6 levels in PMW receiving HRT remains to be elucidated.

The metabolic syndrome in women: implications for therapy.

It is becoming increasingly clear that hypertension and metabolic risk factors in women are inter-related and often share underlying causes. Menopause acts explicitly as a risk factor by reducing the direct beneficial effect of ovarian hormones upon cardiovascular functions and indirectly by negatively influencing other risk factors for coronary artery disease--i.e.

Metabolic and vascular effect of progestins in post-menopausal women. Implications for cardioprotection.

Estrogen therapy causes changes in a variety of cardiovascular risk factors, including insulin resistance, lipoprotein profile, haemostasis, coronary atherosclerosis and vascular reactive, that suggest a potential cardioprotective effect in postmenopausal women. With respect to the role of adjunctive progestins, currently available data suggest that the cardiovascular effects may differ depending on the type, dosage and route of administration of the progestin. Androgenic progestins antagonise the favourable cardiovascular effect of estrogens, whilst non-androgenic progestins do not impair, or may even enhance, the beneficial effect of estrogens.

Hormone replacement therapy and cardioprotection: the end of the tale?

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.

In patients with coronary artery disease endothelial function is associated with plasma levels of C-reactive protein and is improved by optimal medical therapy.

Background: Endothelial function is impaired in patients with coronary artery disease (CAD); in these patients plasma levels of C-reactive protein (CRP) and impaired endothelial function are related to future cardiac events. The aim of the present study was to evaluate the effects of medical therapy on endothelial function and CRP in patients with CAD.

Methods: Seventy-three patients (52 men, 21 women, mean age 66 +/- 9 years) with CAD and 32 control subjects (25 men, 7 women, mean age 65 +/- 11 years) were enrolled in the study.

Report of erectile dysfunction after therapy with beta-blockers is related to patient knowledge of side effects and is reversed by placebo.

Aims: Patients with cardiovascular diseases frequently complain of erectile dysfunction especially when treated with beta-blockers. In order to assess whether the effect of beta-blockers on erectile dysfunction is in part related to patient knowledge of the drug side effects, 96 patients (all males, age 52+/-7 years) with newly diagnosed cardiovascular disease and not suffering from erectile dysfunction entered a two phase, single cross over study.

Methods And Results: During the first phase of the study patients received atenolol 50mg o.

Increased levels of C-reactive protein after oral hormone replacement therapy may not be related to an increased inflammatory response.

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).

Dydrogesterone does not reverse the effects of estradiol on endothelium-dependant vasodilation in postmenopausal women: a randomised clinical trial.

Objectives: The purpose of this study was to evaluate endothelium-dependent flow-mediated dilation (FMD) in the brachial artery and the plasma levels of endothelin-1 in postmenopausal women at risk for coronary artery disease before and after treatment with both estradiol and estradiol plus dydrogesterone.

Methods: Sixteen postmenopausal women (PMW) (mean age 58+/-9 years) with more than two risk factors for coronary artery disease, were randomized to receive either oral estradiol (2 mg) for 28 days or oral estradiol (2 mg) for 14 days and oral estradiol (2 mg) and dydrogesterone (10 mg) for 14 days, in a double-blind, placebo-controlled, single cross-over study. Patients were crossed-over the complementary treatment 7 days after completing the first treatment.