Stroke In Postmenopausal Women Research Articles

Oestrogen did not prevent death or non-fatal stroke in postmenopausal women with ischaemic stroke or transient ischaemic attack

(2001) N Engl J Med 345, 1243. Viscoli CM, Brass LM, Kernan WN, et al. . A clinical trial of estrogen-replacement therapy after ischemic stroke. . Oct 25; . :...

Intake of antioxidant vitamins and risk of death from stroke in postmenopausal women

Antioxidant vitamins may play a role in the prevention of stroke because they scavenge free radicals and prevent LDL oxidation. Epidemiologic studies that have examined this relation produced conflicting results. We examined the association between antioxidant vitamin intakes and death from stroke. This was a prospective cohort study of 34492 postmenopausal women. During follow-up, 215 deaths from stroke were documented. Total vitamin A, carotenoid, and vitamin E intakes were not associated with death from stroke after multivariate adjustment. Relative risks (RRs) and 95% CIs of the highest compared with the lowest category were 0.79 (0.45, 1.38; P for trend = 0.33) for vitamin A, 0.80 (0.45, 1.40; P for trend = 0.40) for carotenoids, and 0.91 (0.55, 1.52; P for trend = 0.86) for vitamin E. The test for trend for total vitamin C intake was significant, although the association appeared somewhat U-shaped, not monotonic. An inverse association was seen between death from stroke and vitamin E intake from food. RRs (and 95% CIs) of death from stroke from the lowest to highest intake categories were 1.0, 0.80 (0.51, 1.26), 0.93 (0.58, 1. 49), 0.67 (0.39, 1.14), 0.40 (0.20, 0.80); P for trend = 0.008. The results suggest inverse associations between death from stroke and intakes of the most concentrated vitamin E food sources consumed by this cohort: mayonnaise, nuts, and margarine. Our results suggest a protective effect of vitamin E from foods on death from stroke but do not support a protective role for supplemental vitamin E or other antioxidant vitamins. However, given the number of deaths from stroke in the present cohort, a small-to-moderate association could not be ruled out.

Hormone replacement therapy and stroke risk in older women.

Studies of the effect of hormone replacement therapy (HRT) on the risk of stroke in postmenopausal women have yielded divergent results. Many of the studies had small numbers of estrogen-using women and relatively young women. All were confounded because women who use estrogen are healthier than the general population. Case-control studies, which included a larger number of cases, usually were limited to stroke survivors and had problems of recall bias regarding exposure. We describe the independent risk of fatal and nonfatal stroke in a socioeconomically homogeneous cohort of older, postmenopausal, community-dwelling women in Rancho Bernardo, California, who had a high rate of past or current HRT use. During 1984-1987, estrogen use and stroke risk factors were ascertained for 1031 women over age 60 without a history of stroke in the Rancho Bernardo cohort. Stroke deaths were monitored by obtaining 100% of death certificates, and nonfatal strokes were determined through questionnaires. At baseline, the average age was 73.1 years, 27% were current estrogen users, and 45% were past estrogen users. Over 8.8 follow-up years, 263 deaths occurred, and 37 of the death certificates listed stroke as an underlying or contributing cause of death. Only 7 of current HRT users had a stroke compared with 16 former users and 14 never users. The age-adjusted odds ratio (OR) was 0.92 (95% CI = 0.56-1.50) in HRT users versus never users. Results were not materially changed in multiply adjusted analyses. Similar analyses of nonfatal strokes and transient ischemic attacks (n = 20) showed an increased risk (OR = 3.02, 95% CI = 0.70-13.08). This study provides no evidence that HRT prevents stroke in older women, but the confidence intervals are wide, suggesting that more studies are needed.

Will the Route of Administration Influence the Potential Cardiovascular Benefits of Postmenopausal HRT?

A widely held, though as yet unproven, belief is that HRT will reduce the incidence of myocardial infarction and stroke in postmenopausal women, in contrast to the slight increase in risk of venous thrombotic events. As oral HRT induces an unphysiological peak in the concentrations of oestrogen in the liver, hepatic protein synthesis is over-stimulated, leading to increased plasma levels of many of the proteins involved in vascular disease, such as apolipoproteins, coagulation factors and components of the renin-angiotensin system. Non-oral HRT minimises hepatic first-pass and so avoids these effects. This has led to a belief that the excess risk of venous thrombo-embolism seen in users of oral HRT will be negated. Non-oral HRT may also have less impact on aspects of the renin-angiotensin system; it may also reduce insulin responses to glucose and improve insulin sensitivity. However, plasma levels of PAI-1, are lowered by oral but not transdermal oestradiol. It is even more difficult to predict whether non-oral HRT will be better or worse in terms of the effect on lipoprotein risk markers for CHD. Non-oral oestrogens are less able to reduce plasma levels of LDL and Lp(a), but may protect these lipoproteins from oxidation. The increased HDL levels typical of oral therapy are not seen, but neither are the elevated triglycerides. Experimental studies, especially those using animal models of atherosclerosis, indicate that non-oral therapies will reduce the risk of arterial disease. It would seem unlikely that there will be any substantial differences between the effects of oral and non-oral HRT on CHD risk.

Estrogen attenuates over-expression of β-amyloid precursor protein messager RNA in an animal model of focal ischemia

Cerebral ischemia is a risk factor for late onset Alzheimer's disease. Since estrogen replacement therapy benefits the outcome of cerebral stroke in post-menopausal women, we designed the present study to investigate the effects of estrogen on the expression of β-amyloid precursor protein (APP) mRNA following focal ischemia in female rats. Female rats were ovariectomized (OVX) for two weeks. A single dose of 17 β-estradiol (E 2) (100 μg/kg) was injected s.c. two hours before a unilateral middle cerebral artery (MCA) occlusion. Brain samples were harvested from ischemic core and penumbra of cortices at one hour and twenty-four hours following MCA occlusion. The expression of APP mRNA was assessed by RT-PCR. At one hour after MCA occlusion, OVX rats had a 67.9% ( p<0.05) increase in APP mRNA in the penumbra. E 2 treatment reduced this APP mRNA over-expression by 26.3% at that region. At twenty four hours following MCA occlusion, OVX rats had increases in APP mRNA of 52.9% and 57.0% ( p<0.05) in the core and penumbra, respectively. E 2 treatment reduced the APP mRNA over-expression by 61.0% and 48.6% ( p<0.05) in these two regions, respectively. These effects appeared to reflect an interaction between hormonal environment and ischemia, since in the absence of MCA occlusion, there were no significant differences in APP mRNA expression among OVX, OVX-E 2 treated and intact female rats. The present study demonstrates that estrogen may have an important role in reducing the over-expression of APP mRNA following focal ischemia.

Estrogen use, hypertension and stroke in postmenopausal women

Among nondiabetic women aged 58–79 years in a stable retirement community, use of oral estrogens was significantly associated with hypertension. Estrogen use was not significantly associated with stroke when the data were adjusted for the association of estrogen use with hypertension.