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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen replacement therapy (ERT) is used not only for the short-term control of menopausal symptoms but long-term for disease prevention. This study examined the influence of selected clinical conditions on the use of ERT and the duration of ERT use among women enrolled in a state Medicaid program. We identified 60,531 women, aged >/=45 years, who were enrolled in Maryland Medicaid continuously for at least 2 of 3 years. ERT use was determined through prescription claims submitted for reimbursement. The presence or risk of selected clinical conditions (e.g., osteoporosis, heart disease, estrogen-sensitive cancers) was determined by screening Medicaid claims files for related diagnoses, procedures, or prescription claims. Multiple logistic regression was used to model ERT use, and proportional hazards regression was used to model duration of use. Fourteen percent of these women filled an ERT prescription, with use varying by age, race, and place of residence. Oral dosage forms were the most popular (80.8%), followed by vaginal cream or ring (22.2%), and transdermal patch (7.3%). In adjusted models, osteoporosis, heart disease, hypertension, hyperlipidemia, diabetes, ovarian cancer, and thromboembolic disease were positively associated and dementia and breast cancer were negatively associated with ERT use. None of these medical conditions predicted the duration of estrogen therapy. Use of ERT was very low among these women despite coverage of prescription medications, and the presence of clinical indications had no influence on the length of therapy among these women despite known benefits for long-term preventive therapy.
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PMID:Clinical correlates of estrogen replacement therapy use and duration of use among medicaid recipients. 1170 94

Progesterone receptors are present in the arterial wall and it is, therefore, likely that the arterial effects of progestins are mediated through progesterone receptors as well as through down-regulation of the estradiol receptor. Progestin therapy affects arterial function, as it can stabilize arteries in a state of vasomotor instability, but may also induce vasoconstriction of estrogenized vessels. Thus, the cardiovascular effects of progestins may influence the cardioprotective effect of estrogens. There has been some concern that a combined estrogen-progestogen therapy may attenuate some of estrogen's beneficial effects on cardiovascular health. This is a reflection of the past epidemiologic studies which have used primarily unopposed estrogen. The PEPI trial is the only large-scale, long-term study to compare directly the effects of different combined hormone replacement therapy regimens upon plasma lipids in healthy women. This study has shown that the adjunctive clinical impact of different progestogens on the beneficial effect of estrogen replacement therapy is trivial. It has never been proved that in normocholesterolemic women, e.g., those included in the PEPI trial, the increase in HDL reduces cardiovascular mortality or morbidity. Based on the results of PEPI, hormone replacement therapy has positive effects on key heart disease risk factors and endometrial tissue, and the magnitude of those effects does not differ significantly across the hormone replacement therapy regimens used. At present there are only few and inconclusive data available on the vascular effect of progestins in menopausal women. Some studies found that progestins reduced the beneficial effect of estrogens, while others did not. Our group has recently shown that different estrogen-progestin treatments have different effects upon vascular reactivity and that a careful selection of the progestin to be added to estrogen is of capital importance to preserve, or even enhance the positive vascular effects of estrogens. Few epidemiological studies have investigated the effect of adding a progestin to estrogen therapy upon cardiovascular mortality and morbidity, and all have suggested that hormone replacement therapy may be more effective than estrogen replacement alone in reducing cardiovascular events in primary prevention. The results of the recently published Heart and Estrogen/progestin Replacement Study (HERS) have added some critical data on the effect of hormone replacement therapy for secondary prevention in women with coronary artery disease. The study, however, is affected by several important methodological and statistical problems, which make its interpretation difficult and its conclusions useless for clinical practice. The results of the study should be evaluated with caution by physicians who give advice on hormone replacement therapy, and no woman should be taken off hormone replacement therapy because of HERS. Of importance, the results of HERS should not be used to suggest alternative forms of treatment, especially the selective estrogen receptor modulators (SERMs), for cardiovascular protection in postmenopausal women.
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PMID:Comparative cardiovascular effects of different progestins in menopause. 1172 Jan 97

This is a brief review of the rationale for estrogen replacement as prevention of coronary artery disease. Epidemiological data suggest that Premarin (0.625 mg) together with medroxyprogesterone acetate (2.5 mg) can prevent or delay the onset of coronary artery disease in postmenopausal women. The major effects of estrogens are: improving the lipid profile by lowering low-density lipoprotein and raising high-density lipoprotein; acting on vessel walls to reduce intimal damage and plaque formation; dilating vessels by both an endothelial dependent and an independent pathway; and acting as an antioxidant, thereby reducing the oxidation of low density lipoprotein and increasing the production of nitric oxide locally in the blood vessel. Oral estrogens and transdermal estrogens may act differently on coagulation factors and lipids. The role of specific estrogen receptor modulators as possible treatment for postmenopausal women in part will depend on the effect of these drugs in preventing coronary artery disease. The specific estrogen receptor modulators decrease low-density lipoprotein and prevent triglyceride increases but it is unknown if they have estrogenic effects on blood vessel walls. Better compliance with estrogen replacement therapy will depend on educating women about their risk of getting coronary artery disease, and assisting them in decision making, as well as reducing side effects. The Heart and Estrogen/Progestin Replacement Study provides evidence that Prempro (Premarin/ medroxyprogesterone acetate) should not be given to someone who already has heart disease without careful monitoring. (c) 2000 by CHF, Inc.
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PMID:Hormone replacement therapy (estrogen and progesterone): is it necessary for heart disease prevention? 1183 12

Cardiovascular diseases are the leading cause of death in the industrialised countries and display significant gender-based differences. Estrogen plays an important role in the pathogenesis of heart disease and is able to modulate the progression of cardiovascular disease. The focus on the beneficial influence of estrogen is gradually shifting from the vascular system to the myocardium. The presence of functional estrogen receptors in the myocardium has been demonstrated. Estrogen is important for cardiovascular baseline physiology and modulates the myocardial response under pathological conditions. Here we summarise the current knowledge of the regulatory network of estrogenic action in the myocardium and its effects on cardiovascular function.
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PMID:Estrogenic hormone action in the heart: regulatory network and function. 1186 Oct 41

Coronary artery disease (CAD) is the number 1 cause of death and disability in the Western world. The incidence of CAD increases with age, although, on average, women present with symptomatic CAD about 10 years later than men. The belief that hormone replacement therapy (HRT) may reduce the incidence of CAD is based on its favorable effects on (1) vasoreactivity, (2) progression of atherosclerosis, (3) lipids and lipoproteins, (4) hemostasis, and (5) impaired glucose tolerance. However, unopposed estrogen may be related to an increased risk of endometrial cancer. The belief that HRT has an overall beneficial effect on cardiovascular disease comes from the results of prospective cohort studies. The Heart and Estrogen/progestin Replacement Study (HERS), however, showed no beneficial effect of HRT on cardiovascular morbidity and mortality. Uncertainty exists about the duration and optimal type of HRT regimen to use, because different estrogens and progestins have yielded different results. Results of ongoing trials addressing similar questions will be published in future years. The Women's Hormone Intervention Secondary Prevention (WHISP) pilot study, using a different HRT regimen from that used in HERS, will assess the effect of HRT on lipid and hemostatic risk markers of heart disease, and it may provide the rationale for a large trial evaluating the effect of HRT on morbidity and mortality.
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PMID:Clinical cardiovascular studies of hormone replacement therapy. 1210 38

This is a review and presentation of recent clinical trials designed to ascertain the effects of estrogen or estrogen plus progesterone on the risks of heart disease. The framework of the epidemiologic evidence that estrogen is cardioprotective is reviewed and the impact of these data on apparent findings from clinical trials discussed. The Heart and Estrogen/Progestin Replacement Study is examined in detail, and the most frequent criticisms of its findings are presented. Findings from other clinical trials are presented and the clinical implications from the data discussed in relation to the larger body of literature pertaining to hormone replacement therapy and heart disease.
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PMID:The controversy over estrogen replacement therapy: an update on clinical trials. 1211 7

Several biases in studies of estrogen replacement therapy suggest that claims that estrogen replacement therapy reduces the risk of heart disease are exaggerated. Women who have taken part in these studies are usually healthier than the average woman. In fact, for many years, physicians had not prescribed hormones to women whom they considered to be in less than excellent health. Thus, women on estrogen replacement therapy would tend not to suffer heart disease. Even though hormonal therapy does protect against osteoporosis in postmenopausal women, physicians should not prescribe hormonal therapy just to protect women from heart disease. The American Heart Association reported in the autumn of 1993 that estrogen use has been linked to a 50% reduction in the risk of coronary heart disease and stroke, but it also warns that one must be cautious when interpreting these studies, since physicians may prescribe hormones to primarily healthier women to relieve symptoms of menopause. Women must visit a physician before beginning hormone replacement, and they are more likely to enter heart disease prevention programs than women not on estrogen. Women on hormone replacement therapy have higher incomes and more education than women who are not on this therapy. In fact, higher income and education make women more healthy than poor, less educated women. Since 10 times more women die of heart disease in the US than of osteoporosis, we need to know whether hormone replacement therapy really prevents heart disease. The Heart Estrogen Replacement Study and the Women's Health Initiative have recently begun carefully controlled studies examining whether hormone replacement therapy protects against heart disease. They should produce results in 5-6 years.
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PMID:Estrogen's protection against heart disease may be overstated. 1217 78

Library research reports from Sweden, England, and other countries have been studied in an effort to determine the effect of oral contraceptives (OCs) on lipoprotein metabolism. The results are conflicting, possibly due to the fact that there are different amounts of estrogen and progesterone in the various kinds of pills. Estrogen is known to cause increased glycerides in the blood, but progesterone can reduce the concentration of the glycerides. Blood lipids and glycerides increase after taking OCs, and high density lipoproteins decrease. Cholesterol and phospholipids usually decrease, but reports on this are also conflicting. It has been widely reported that OCs increase the risk of heart disease, but data from Great Britian indicate that the pills may actually protect the user from heart disease. Because the results of the aforementioned research are not conclusive, in depth research should be carried out to determine the relationship between OCs and lipoprotein metabolism. All clinical tests regarding OCs should take this relationship into consideration, in order to gather large amounts of reliable data.
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PMID:[[Effect of oral contraceptives on lipid and lipoprotein metabolism]]. 1233 79

Cardiovascular disease is the leading cause of death in women. In pooled analysis, observational studies have shown a 50% reduction in death and myocardial infarction among users of hormone replacement therapy (HRT) for the primary and secondary prevention of cardiovascular disease. The first randomized trial of HRT for secondary prevention of heart disease found no benefit to therapy (Heart and Estrogen/progestin Replacement Study ). Even after 6.8 years of follow-up, there was still no cardiovascular benefit from the use of HRT (HERS II). HRT was associated with a 50% increased risk of heart attacks within the first year as well as an increased risk of deep venous thrombosis (DVT) and pulmonary embolism (PE) (relative risk 2.89) and gallbladder disease (RR 1.38). The Estrogen Replacement and Atherosclerosis trial found no evidence that HRT slowed the progression of subclinical angiographic disease either. This was despite a favorable effect on high-density lipoprotein and low-density lipoprotein. The first randomized trial of HRT for the primary prevention of heart disease found no overall benefit (Women's Health Initiative). The combination of estrogen and progestin resulted in a 29% increase in heart attacks, 41% increase in stroke, a doubling of thrombotic events (DVT and PE), as well as a 26% increase in breast cancer. The risk for thrombotic events was greatest in the first year whereas the risk of breast cancer increased progressively with duration of therapy. HRT is no longer recommended for the primary or secondary prevention of cardiovascular disease or stroke. It may still be considered for short-term relief of menopausal symptoms in women without high-risk conditions, but alternatives exist.
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PMID:Hormone Replacement Therapy for Primary and Secondary Prevention of Heart Disease. 1268 16

We evaluated the association of hemostatic factors with insulin resistance in relation to reproductive hormones including FSH, estradiol, testosterone, and SHBG. SHBG was used to calculate the free estradiol index and free androgen index. We studied 3,200 women, aged 42-52 yr, in the Study of Women's Health Across the Nation, a prospective multiethnic study of the menopausal transition. We measured the hemostatic factors, fibrinogen, factor VIIc, tissue plasminogen activator (t-PA), and plasminogen activator inhibitor type 1 (PAI-1), as well as glucose and insulin to calculate insulin resistance. After adjustment for body mass index, site, and ethnicity, SHBG was correlated with PAI-1 (partial r = -0.30) and t-PA (partial r = -0.12). Although testosterone was associated with t-PA (partial r = 0.13) and PAI-1 (partial r = 0.07), free androgen index was strongly correlated with t-PA (partial r = 0.18) and PAI-1 (partial r = 0.26). SHBG modified the association of hemostatic factors with insulin resistance. Women with greater insulin resistance had lower SHBG and higher PAI-1. Estrogen measures were not associated with insulin resistance. The influence of sex hormones on hemostatic factors and insulin resistance is poorly understood. SHBG, which influences the amount of bioavailable hormone, significantly modified the association of PAI-1 and t-PA with insulin resistance. The longitudinal Study of Women's Health Across the Nation will help us discern whether this interaction contributes to heart disease and diabetes among postmenopausal women.
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PMID:Insulin resistance, hemostatic factors, and hormone interactions in pre- and perimenopausal women: SWAN. 1455 72


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