Estrogens, Progestins, and Heart Disease

Vogel, Robert A.; Corretti, Mary C.

doi:10.1161/01.cir.97.13.1223

Cited by 41 publications

(6 citation statements)

References 50 publications

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“…The differences of these factors clearly affect flow-mediated dilation. 31,32 To avoid these kinds of issues and unmeasured bias, we decided to perform a crossover design in the present study. Furthermore, the abovementioned study did not provide the effects of HT and tibolone on lipoprotein levels.…”

Section: Discussionmentioning

confidence: 99%

Significant Differential Effects of Hormone Therapy or Tibolone on Markers of Cardiovascular Disease in Postmenopausal Women

Koh

Ahn

Jin

et al. 2003

ATVB

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Objective-The objective was to compare the effects of tibolone and hormone therapy (HT) on lipid profile, vasodilation, and factors associated with inflammation and hemostasis. Methods and Results-Fifty-three women received micronized progesterone (MP, 100 mg) with conjugated equine estrogen (CEE, 0.625 mg) or tibolone (2.5 mg) daily for 2 months, with a 2-month washout period. Key Words: hormone therapy Ⅲ tibolone Ⅲ endothelial function Ⅲ inflammation Ⅲ hemostasis P rospective cohort surveys suggest that hormone therapy (HT) decreases the risk of coronary artery disease in relatively young and healthy postmenopausal women. 1,2 In contrast, 2 recent randomized studies, the Heart and Estrogen/ Progestin Replacement Study (HERS) 3 and the Women's Health Initiative (WHI), 4 reported that HT did not reduce the risk of cardiovascular events and, furthermore, demonstrated some trends toward an increased risk of cardiovascular events. The increased risk of coronary heart disease (CHD) was surprising, given that LDL cholesterol levels decreased and that HDL cholesterol levels increased. The reasons may result from the effects of HT on an increase in triglyceride and C-reactive protein (CRP) levels and thromboembolism risk through activating coagulation pathways, evidenced by decreased antithrombin III and increased prothrombin fragment 1ϩ2 (F1ϩ2). 5,6 Tibolone, a synthetic steroid with estrogenic, androgenic, and progestogenic properties, relieves climacteric symptoms and prevents postmenopausal bone loss. Furthermore, compared with HT, tibolone has no effect on breast cancer incidence and does not promote endometrial hyperplasia or rare vaginal bleeding. 7 Tibolone has some beneficial effects, such as reduction of triglyceride, total cholesterol, LDL cholesterol, and lipoprotein(a) levels, reducing the risk of CHD. 7 Nonetheless, its antiatherosclerotic effects have been questioned because of consistent reductions in the levels of HDL cholesterol, which has antiatherosclerotic properties. However, recent animal studies have demonstrated that the use of tibolone results in significantly less atherosclerosis than does use of placebo 8 or, at least, that use of tibolone compared with control results in no increase in coronary atherosclerosis, 9 despite a marked reduction of HDL choles-

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Section: Discussionmentioning

confidence: 99%

Significant Differential Effects of Hormone Therapy or Tibolone on Markers of Cardiovascular Disease in Postmenopausal Women

Koh

Ahn

Jin

et al. 2003

ATVB

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“…20 Moreover, given its pivotal role in the atherogenic process, endothelial dysfunction may be regarded as the "ultimate risk of the risk factors" indicating the existence of a specific atherogenic vascular milieu ( Figure 2). …”

Section: Endothelial Dysfunction and Risk Factorsmentioning

confidence: 99%

Endothelial Dysfunction

Bonetti

Lerman

2003

ATVB

1,914

673

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Abstract-Endothelial dysfunction is a systemic disorder and a key variable in the pathogenesis of atherosclerosis and its complications. Current evidence suggests that endothelial status is not determined solely by the individual risk factor burden but rather, may be regarded as an integrated index of all atherogenic and atheroprotective factors present in an individual, including known as well as yet-unknown variables and genetic predisposition. Endothelial dysfunction reflects a vascular phenotype prone to atherogenesis and may therefore serve as a marker of the inherent atherosclerotic risk in an individual. In line with this hypothesis, dysfunction of either the coronary or peripheral vascular endothelium was shown to constitute an independent predictor of cardiovascular events, providing valuable prognostic information additional to that derived from conventional risk factor assessment. Interventions like risk factor modification and treatment with various drugs, including statins and angiotensin-converting enzyme inhibitors, may improve endothelial function and thereby, potentially prognosis. Hence, given its reversibility and granted the availability of a diagnostic tool to identify patients at risk and to control the efficacy of therapy in clinical practice, endothelial dysfunction may be an attractive primary target in the effort to optimize individualized therapeutic strategies to reduce cardiovascular morbidity and mortality. Key Words: endothelial dysfunction Ⅲ atherosclerosis Ⅲ risk factor Ⅲ cardiovascular event Ⅲ prognosis D uring the last 2 decades, it has become evident that the vascular endothelium is an active paracrine, endocrine, and autocrine organ that is indispensable for the regulation of vascular tone and maintenance of vascular homeostasis (Table 1). Moreover, recent insights into the basic mechanisms involved in atherogenesis indicate that deleterious alterations of endothelial physiology, also referred to as endothelial dysfunction, represent a key early step in the development of atherosclerosis and are also involved in plaque progression and the occurrence of atherosclerotic complications. 1,2 Endothelial dysfunction is characterized by a reduction of the bioavailability of vasodilators, in particular, nitric oxide (NO), whereas endothelium-derived contracting factors are increased. 3 This imbalance leads to an impairment of endothelium-dependent vasodilation, which represents the functional characteristic of endothelial dysfunction. On the other hand, endothelial dysfunction, aside from denoting impaired endothelium-dependent vasodilation, also comprises a specific state of "endothelial activation," which is characterized by a proinflammatory, proliferative, and procoagulatory milieu that favors all stages of atherogenesis. 4 Given this relationship between endothelial dysfunction and atherosclerosis, it is likely that the status of endothelial function may reflect the propensity of an individual to develop atherosclerotic disease, and thus, the presence of endothelial dysfunction ...

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“…[8][9][10] Estrogen may inhibit atherosclerosis and also play an integral role in the maintenance of arterial hemodynamics that prevent ischemia. 11,12 In this study, we report the acute effect of conjugated estrogens on the elastic properties of common carotid artery (CCA) in normotensive, postmenopausal women in an attempt to clarify the possible mechanisms by which hormone replacement therapy exerts its favorable effect on the risk of stroke.…”

Section: Introductionmentioning

confidence: 99%

Conjugated estrogen administration improves common carotid artery elastic properties in normotensive postmenopausal women

Kallikazaros

Tsioufis

Zambaras

et al. 2002

Clinical Cardiology

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SummaryBackground: Various vascular effects of estrogens have been proposed to explain further the beneficial effect of replacement therapy in cardiovascular events.Hypothesis: The study was undertaken to assess the effect of conjugated estrogen on the elastic properties of the large arteries in normotensive, healthy, postmenopausal women.Methods: Toward this end, we investigated the acute effect of conjugated estrogen on the elastic properties of the common carotid artery (CCA) in 20 normotensive, healthy, postmenopausal women (age 54 ± 3 years) at baseline and 20 min after the intravenous administration of 1.25 mg conjugated estrogens. The CCA distensibility was derived by a combination of surface ultrasonographic data and simultaneous blood pressure measurements at the brachial artery. The carotid pulsatility index, a measure of brain impedance, was determined electronically by tracing the CCA Doppler waveform.Results: At baseline, CCA distensibility had a negative correlation with both patients' age and time since menopause (r = Ϫ0.57 and r = Ϫ0.48, p < 0.05 for both cases). After estrogen administration, estradiol and estrone plasma levels were restored to the range of usual premenopausal values. Estrogen induced a significant increase in CCA distensibility by 0.92 ±

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Estrogens, Progestins, and Heart Disease

Cited by 41 publications

References 50 publications

Significant Differential Effects of Hormone Therapy or Tibolone on Markers of Cardiovascular Disease in Postmenopausal Women

Significant Differential Effects of Hormone Therapy or Tibolone on Markers of Cardiovascular Disease in Postmenopausal Women

Endothelial Dysfunction

Conjugated estrogen administration improves common carotid artery elastic properties in normotensive postmenopausal women

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