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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The relative rarity of stroke in oral contraceptive (OC) users, estimated at 14/100,000 women per year, does not mean that the risk is not significant; it is 4 to 9 times as high for OC users as for controls. 86 well-documented cases of stroke in OC users treated at a neurologic clinic in Paris between 1974 and 1984 are analyzed. There were 5 groups of patients: 1) 66 cases of cerebrovascular accidents, 64 of which were ischemic 2) 6 cases of intracranial venous thrombosis 3) 6 cases of benign and reversible intracranial hypertension or cerebral pseudotumor without demonstrated venous thrombosis 4) 5 cases of vascular complications in the retina or optic nerve, and 5) a miscellaneous group of 5 cases. The patients were aged from 16-49 years and the mean age was 30.5 years. The duration of use of OCs varied from a few days to 15 years, with an average of 39 months. 42 to 56% had family histories of cerebrovascular problems and 40 to 50% had personal or familial histories of migraine. Among 79 OC users with strokes, 41% used moderate dosed and 59% used microdose pills. No patients used microdose progestin only pills. There were 2 peak age groups of patients, those 25-29 and 38-42 years old. Young women aged 25-29 had intracranial venous thrombosis, intracranial hypertension or pseudotumor, and acute ischemia of the optic nerve. The average age of the 64 patients with ischemic cerebral vascular accidents was 31 years. Of the 30 infarcts, 1/3 left significant sequelae and 3 were fatal. There were 21 transitory ischemic accidents and 13 prolonged reversible ischemic accidents usually without sequelae. There were warning signals in 52% of infarct cases. 45% of patients with cerebrovascular accidents had family histories of cerebrovascular accidents or cardiac infarct and 40 to 50% had personal or family histories of migraine. Fewer than 25% had hyperlipidemia, 20% smoked, and 8% had diabetes or a problem of glycoregulation. Coagulation changes were found in 6 of 64 patients, but 22 of 26 had immune complexes and anti-ethinyl estradiol or antiprogesterone antibodies. Among the 6 cases of intracranial venous thrombolic accidents there were 2 deaths and 2 cases of very serious sequelae. The average age of these patients was about 27. The role of OCs is difficult to confirm because there are too few cases for statistical analysis. Antihormone antibodies were found in 3 such cases studied, but coagulation problems were not observed. Patients in the study who had laboratoratory or angiographic evidence of atheromatous disorders mostly were in the older peak age groups. The younger patients with cerebral ischemic accidents were largely without atheromatous lesions, but were very likely to have antiestrogen or antiprogesterone antibodies.
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PMID:[Stroke and combined oral contraceptives]. 1228 Feb

The main concern of physicians prescribing oral contraceptives (OCs) is the possibility of cardiovascular accidents, not because of their number but of their seriousness. Cardiovascular risk affects primarily women over 35. A 1986 survey of 600 physicians indicated that avoiding cardiovascular risk was their main objective when prescribing pills, with avoidance of modifications in lipid and glucose metabolism virtually as great a concern. Less than 50% were concerned with functional symptoms such as spotting which can be managed by therapeutic adjustments. Numerous cofactors participate in cardiovascular risk, including family history, life style, and intercurrent illness. The frequency of vascular accidents is only slightly higher among OC users than in the control population. Numerous Anglo-Saxon studies have found the risk of deep venous thrombosis to be multiplied by 4 or 5 for OC users and of superficial thrombosis to be multiplied by 2 or 3. Age and obesity play no role in the increased risk for OC users, smoking has a minor role, and family history and bed rest are the only major cofactors. Risk of venous thrombosis under OC use does not depend on duration of use and disappears the month after termination of use. The synthetic estrogen is primarily responsible because of the modifications it produces on coagulation factors. OC use increases the risk of coronary accidents by 3 or 4. 3 hypotheses have been advanced to explain the pathogenic mechanism: classic atherogenesis, alteration of the intima, or immunological factors. Atheromatous arterial accidents are related to age, smoking, problems of glucose or lipid metabolism, and blood pressure. The factors have a synergistic effect on each other. Risks increase with duration of use and dose level, and depend also on the biochemical properties of the estrogen and progestin. Some accidents in young women about 30 years old show no relation to duration of use or dose. The only elements differentiating the women involved are smoking, family histories of vascular accidents, and intense headaches in the days before a cerebrovascular accident. They seem to be associated not with atherogenesis but with thickening of the intima secondary to a proliferation of smooth muscle cells with subendothelial fibrosis. 90% of OC users experiencing vascular accidents have been found to have anti-ethinyl estradiol antibodies, compared to 30% of users never having vascular accidents and no nonusers. The practical import of this finding remains undetermined. Under some circumstances the causes of headaches should be investigated and OC use should be terminated. Careful attention to patient selection and development of new progestins with fewer androgenic and metabolic effects should reduce cardiovascular risks from OCs to a minimum. The new synthetic progestin gestodene has given very satisfactory results in a triphasic formulation and should be on the market soon.
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PMID:[Combined contraceptives and cardiovascular risk]. 1231 99

Soybeans are a natural dietary source of isoflavones, which have estrogen-like properties. Therefore, it is worthwhile to consider the implications for soy of the recently published findings of the Heart and Estrogen/Progestin Replacement Study (HERS) I/II and the Women's Health Initiative (WHI). The WHI found coronary heart disease (CHD) risk to be increased in women receiving hormone replacement therapy, and both studies found increases in venous thromboembolic disease in such women. Additionally, stroke and breast cancer risk were increased in the WHI, although risk of colorectal cancer and fracture was decreased. Because research suggests that it is the combination of estrogen plus progestin, and not estrogen alone, that increases breast cancer risk, soy seems unlikely to increase risk because it has no progestin activity. Similarly, there is no evidence to suggest that soy will increase venous thromboembolic disease or stroke; however, only limited data are available in this area. There are promising data suggesting that soy may decrease CHD risk, although studies conducted thus far have examined only markers of risk and not actual CHD events. Similarly, short-term studies generally suggest that soy reduces bone loss in postmenopausal women; however, such effects have been noted primarily only at the spine, and longer-term studies are needed. Finally, very limited human research suggests that soy may decrease colon cancer risk, but this is highly speculative. The results of HERS I/II and WHI suggest that soy may have some of the advantages, but not the disadvantages, of combined hormone replacement therapy (at least with respect to the specific hormones and doses used in the HERS I/II and WHI), but that large, long-term intervention studies examining disease outcome are needed before definitive conclusions can be drawn. Nevertheless, the evidence warrants recommendations that menopausal women include soy in their diets.
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PMID:Soy foods and soybean isoflavones and menopausal health. 1255 10

Estrogen produces both beneficial and adverse effects on cardiovascular health via mechanisms that remain unclear. Stroke-prone spontaneously hypertensive rats (SHRSP) maintained on Stroke-Prone Rodent Diet and 1% NaCl drinking water (starting at 8 wk of age) rapidly develop stroke and malignant nephrosclerosis that can be prevented, despite continued hypertension, by drugs targeting angiotensin II and aldosterone actions. This study evaluated estrogen's effects in the SHRSP model. Female SHRSP that were sham operated (SHAM), ovariectomized (OVX) at 4 wk of age, or OVX and treated with estradiol benzoate (E2,30 microg x kg-1 x wk-1) were studied. In a survival protocol, OVX rats lived significantly longer (15.1 +/- 0.3 wk) compared with SHAM (13.6 +/- 0.2 wk) or OVX+E2 rats (12.4 +/- 0.2 wk). In a protocol in which animals were matched for age, at 11.5 wk, terminal systolic blood pressure and urine protein excretion were elevated in SHAM and OVX+E2 rats compared with OVX rats; blood urea nitrogen, renal microvascular and glomerular lesions, and plasma renin concentration were elevated in OVX+E2 relative to SHAM or OVX rats. In a survival protocol using intact female SHRSP, treatment with an antiestrogen (tamoxifen, 7 mg.kg-1.wk-1) prolonged survival by >2 wk compared with controls (P < 0.01). The data indicate that estrogen promotes microangiopathy in the kidney and stroke in saline-drinking SHRSP.
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PMID:Estrogen promotes microvascular pathology in female stroke-prone spontaneously hypertensive rats. 1267 Aug 33

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

Estrogen and progesterone are often thought of as steroid hormones that strongly influence reproductive and maternal behaviours. However, the steroids are now showing considerable promise as neuroprotective and neuroregenerative agents in stroke and traumatic brain injuries. Collectively, these two hormones have been reported to reduce the consequences of the injury cascade by enhancing anti-oxidant mechanisms, reducing excitotoxicity: altering glutamate receptor activity, reducing immune inflammation, providing neurotrophic support, stimulating axonal remyelinization and enhancing synaptogenesis and dendritic arborization. Estrogen has often been tried as a prophylactic treatment in females for ischemic brain injury, while progesterone has, thus far, been given as a post-injury treatment for both male and female subjects with acute, ischemic and traumatic injuries of the brain and spinal cord. This review compares and evaluates estrogen and progesterone as neuroactive agents in the acute treatment of brain damage caused by stroke and trauma.
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PMID:Estrogen and progesterone as neuroprotective agents in the treatment of acute brain injuries. 1274 91

We assessed whether sociodemographic and clinical characteristics were determinants of clinical trial participation in the Women's Estrogen for Stroke Trial (WEST) by examining data collected on women with a WEST consent visit completed after June 1996. We found no differences in consent rates by education or ethnic group (32% of white women compared with 34% of black women). Conditions associated with the intervention, such as a history of hysterectomy or previous estrogen replacement use, were strongly associated with a woman's decision to participate in this clinical trial. In multivariate models, features independently associated with consent to participate were age (odds ratio [OR] 0.96, 95% confidence interval [CI] 0.94-0.97), hysterectomy (OR 1.78, 95% CI 1.27-2.50), no cognitive impairment (OR 1.70, 95% CI 1.10-2.63), history of volunteerism (OR 1.62, 95% CI 1.02-2.63), and previous estrogen use (RR 1.58, 95% CI 1.08-2.30).
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PMID:Influence of race, clinical, and other socio-demographic features on trial participation. 1276 6

Estrogen has been comprehensively studied as a neuroprotective agent in women, animals, and a variety of in vitro models of neural injury and degeneration. Most data suggest that estrogen can benefit the ischemic brain and reduce cell death. However, recent data from the Women's Health Initiative have raised concerns about the utility and safety of chronic estrogen use in women. While estrogen is a potent and reproducible neuroprotectant in animals and in vitro, its current administration in women has had unanticipated and paradoxical effects. Nonetheless, estrogen's diverse actions make it an ideal prototype for developing new neuroprotectants such as selective estrogen receptor modulators (SERMs). SERMs represent a class of drugs with mixed estrogen agonistic and antagonistic activity. Experimental and clinical data suggest a neuroprotective role for SERMs in normal and injured brain. The discrepancy among observational studies, preclinical data, and clinical trials emphasizes the need for further study of the mechanisms leading to the increased incidence of stroke observed in postmenopausal women. Research is still needed to optimize combined or estrogen alone hormone replacement therapy options as well as the prevention/management of cerebrovascular/ central nervous system disorders. This review critiques estrogen and SERMs' neuroprotective potential in experimental and clinical studies of stroke and cerebrovascular disease.
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PMID:Estrogen and selective estrogen receptor modulators: neuroprotection in the Women's Health Initiative era. 1277 99

Stroke morbidity increases with age. That is the reason why it affects especially the middle aged and elderly. Life expectancy is longer for females than males by 10 years, that is why stroke is a major problem in women. Women die twice more frequently from stroke than men (16% vs. 8%). Stroke risk factors are basically the same in spite of gender. The most important are hypertension, diabetes, dyslipidaemia, atrial fibrillation, coronary heart disease, previous stroke, smoking, alcohol abuse, obesity and lack of physical activity. Their impact, however, is different in males and females. Women with diabetes, atrial fibrillation, myocardial infarction, obese, drinking excessive amounts of alcohol and smoking are more likely to suffer of stroke than males with the same burden. A less favourable outcome after stroke has been observed in female patients--higher mortality rates and disability. It is possible that poor prognosis is related to a drop in blood estrogen concentration after menopause. Estrogen replacement therapy has not proved to be beneficial in preventing stroke and improving outcome. There are several specific conditions: pregnancy, migraine in women associated with the occurrence of stroke.
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PMID:[Does gender exert influence on stroke?]. 1456 Jul


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