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

The Heart and Estrogen/Progestin Replacement Study (HERS) was the first randomised, double-blind, placebo-controlled study to evaluate the outcome of hormone replacement therapy (HRT) on subsequent cardiac events in postmenopausal women with established coronary heart disease (CHD). Of the 2763 women enrolled, 1380 were randomised to receive 0.625mg of conjugated equine estrogens plus 2.5mg of medroxyprogesterone daily (Prempro) and 1383 were randomised to receive a placebo. The results were surprising: 179 women in the hormone group and 182 women in the placebo group experienced either a nonfatal myocardial infarction or CHD death (relative hazard 0.99, 95% confidence interval 0.81 to 1.22). This occurred despite a net 11% reduction in low density lipoprotein (LDL) and a net 10% increase in high density lipoprotein (HDL) after 1 year of follow-up (p < 0.001 for LDL and HDL). Also, there were no differences between the 2 treatment groups in any secondary cardiovascular outcomes. The overall null effect may have been the result of an unexpected early adverse effect of the HRT regimen that offset a later reduction in risk. Clearly, the use of HRT for secondary prevention of heart disease is more complex than was initially believed. More data are needed from other clinical trials concerning the risks and benefits of HRT to confirm or refute the puzzling HERS results. HERS also underscores the need for trials with clinical end-points to evaluate both the safety and efficacy of drug therapy. Although observational studies are useful, they cannot provide definitive answers regarding treatment recommendations. Until further data are available, clinicians should not use estrogen plus medroxyprogesterone for the sole purpose of secondary prevention of CHD.
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PMID:The Heart and Estrogen/Progestin Replacement Study: what have we learned and what questions remain? 1064 52

In the premenopausal period, the risk of heart disease is considerably lower in women than in men; however, in the postmenopausal period, when estrogen levels are considerably lower, women's risk of heart disease increases dramatically and approaches that of men. Numerous animal studies, using a variety of models, also confirm estrogen's cardioprotective effect. Although the results of numerous population-based, observational studies have demonstrated a lower risk of heart disease in women who receive estrogen replacement therapy, evidence from prospective, randomized clinical trials is scant. The Postmenopausal Estrogen/Progestin Intervention (PEPI) trial evaluated cardiovascular risk factors, not events, in a large, prospective, randomized trial and found that estrogen improved lipid profiles and other known risk factors. In addition, the PEPI trial compared several estrogen/progestogen treatment regimens, including both medroxyprogesterone acetate (MPA) and micronized progesterone (MP), and found that combined hormone replacement therapy regimens including MP attenuated the beneficial effects of estrogen less than those containing MPA. In the Heart and Estrogen/Progestin Replacement Study (HERS), however, which prospectively evaluated whether estrogen and MPA use reduced the number of nonfatal myocardial infarctions and cardiovascular events, no effect was seen. Although HERS was a null trial, the vast literature base showing a cardioprotective effect should not be discounted. Further research will be required before blanket recommendations on the cardioprotective effects of hormone therapy can be made.
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PMID:Preserving cardiovascular benefits of hormone replacement therapy. 1075 7

In every year since 1984, cardiovascular disease has claimed the lives of more females than males. More than 450,000 women succumb to heart disease annually, and 250,000 die of coronary artery disease. Despite the proportions, most women believe they will die of breast cancer. The perception that heart disease is a man's disease and that women are more likely to die of breast cancer is alarming. Although women develop heart disease about 10 years later than men, they are likely to fare worse after a heart attack. The poorer outcomes are due, in part, to the failure to identify heart attack symptoms. Approximately 35% of heart attacks in women are believed to go unnoticed or unreported. However, because of increased age, women are more likely to have co-morbid diseases such as diabetes and hypertension. In women, not only is "tightness" or discomfort in the chest a warning sign, but in addition, nausea and dizziness are common indicators of myocardial ischemia. Other symptoms include breathlessness, perspiration, a sensation of fluttering in the heart, and fullness in the chest. In comparison to men, women are less likely to undergo tertiary care interventions such as cardiac catheterization, angioplasty, thrombolytic therapy, and bypass surgery; to participate in cardiac rehabilitation; and to return to work full-time after myocardial infarction. In the past, most research about treatments for heart disease focused on men, and gender differences have been ignored. Recent studies are enrolling enough women to test if there are differences between men and women in outcomes. One of the major areas of research relates to estrogen and hormonal replacement therapy to reduce the relative risk of heart attack and stroke. The Women's Health Initiative is a major NIH-sponsored trial that addresses the issue of primary prevention of cardiac disease by hormonal replacement therapy. The results will be available in 2004. The Heart Estrogen/Progestin Replacement Study (HERS), disappointingly, did not show a significant reduction of coronary events in women taking hormonal replacement therapy, nor did the Estrogen Replacement and Atherosclerosis (ERA) trial of 309 postmenopausal women who underwent coronary angiography. New insight into the role of vitamins, phytoestrogens and other natural sources, and selective estrogen receptor modulators may provide other options for management. Until then, modification of risk factors and healthy life style choices are recommended for reducing the risk of cardiac disease. In fact, the key to a healthy heart in the year 2000 appears closely tied to life style choices. Prevention of disease is the key, and current recommendations are simply to stop smoking, or do not start; treat and control blood pressure >140/90 mm Hg; manage elevated lipids by diet, exercise, and cholesterol-lowering medications (if necessary); treat diabetes; lose weight so that BMI is <25; walk for 20-30 minutes at least three times a week; and take an aspirin tablet daily.
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PMID:Heart disease in women. 1114 May 44

It is necessary to adopt a proactive, prevention-based strategy for addressing gynecologic and obstetric issues in the adolescent with heart disease. Pregnancy carries known cardiovascular alterations, manifestations and risks. The nature of the underlying cardiac disease needs to be considered in preconception counseling and in the prevention of pregnancy. Specific risks of oral contraceptive methods must be considered as well. Estrogen-based oral contraceptives may confer risks of thromboembolic phenomenon, whereas progesterone-based agents may be associated with increased risk of bleeding. Medical termination of pregnancy may pose risks to the young woman with cyanotic heart disease or pulmonary hypertension. Full prepregnancy evaluation helps to ensure a good outcome for both mother and baby. There are risks of continuing specific cardiovascular medications during pregnancy; however, certain medications are continued to safeguard maternal health. This is particularly problematic in the patient who must remain on anticoagulation.
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PMID:Gynecologic and obstetric issues in the adolescent with heart disease. 1122 29

Cardiovascular disease, primarily coronary heart disease (CHD), outnumbers the next 16 causes of death in women combined. However, the long-held belief that heart disease in women has a more benign prognosis than in men has resulted in less aggressive diagnosis and management patterns. Appreciation of the differences between men and women in CHD risk factors and presentation can assist in treatment decisions. Although estrogen replacement offers substantial beneficial effects on lipid levels in postmenopausal women, the first 2 randomized trials of estrogen alone and estrogen plus progestin, the Heart and Estrogen/Progestin Replacement Study and Estrogen Replacement and Atherosclerosis Study, observed no benefit in reducing risk of CHD death and nonfatal myocardial infarction and angiographic progression of CHD, respectively, in women with CHD. Available data show that lipid-lowering therapy reduces women's CHD risk and mortality but also indicate that a considerable proportion of women remains untreated or undertreated. Randomized trials of statins for primary and secondary prevention of coronary heart disease suggest that these agents are at least as effective for lowering coronary disease risk in women as in men. Therefore, statin drugs should be the drug of first choice for women with established CHD. Hypercholesterolemic postmenopausal women who require estrogen for menopausal symptoms may derive further reductions in low-density lipoprotein cholesterol and reductions in trigyceride levels with the addition of a statin drug.
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PMID:Cardiovascular disease and dyslipidemia in women. 1160 57

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


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