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

Carotid endarterectomy (CE), when performed in patients with previous stable stroke followed by complete or almost complete recovery, seems to be affected by a higher peroperative risk. From January 1982 to March 1988, we performed 230 CE in 207 patients, 188 (81.8%, Group 1) in patients with TIA or an asymptomatic plaque and 42 (18.2%, Group 2) in patients with previous strokes. The need for a temporary indwelling shunt has been evaluated with the measurement of carotid back pressure and, in the last 100 CEE, with the monitoring of somatosensory evoked responses (the shunt has however been used routinely anyway in the very first part of our experience). The incidence of carotid back-pressure values and of positive somatosensory evoked responses were similar in the two groups of C.E., even if the differences in the prealable evaluation were not statistically significant. The shunt has been nevertheless used more frequently in Group 2 (40.5 vs 28.2%). Statistical analysis has been performed with the chi 2 method. The incidence of permanent and transient neurologic deficits and of the peroperative mortality due to neurological and non-neurological causes was, respectively, 0.5, 2.6, 1.6, 0% (Group 1) and 2.4, 7.3, 2.4, 2.4% (Group 2) (non-significant). If we exclude the first 50 operations (in which technical and/or anaesthesiological problems may have influenced the neurological outcome of the patients operated upon), the previous values become, respectively, 0,07*, 0,7, 0% (Group 1) and 0, 5,5*, 0, 2,7% (Group 2) (*p less than 0,01, the only significant difference).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Peroperative morbidity and mortality in thromboendarterectomy of the carotid bifurcation in patients with a previous stabilized stroke. Our results and review of the literature]. 268 26

The bulk of the experimental data suggest beneficial effects of estrogen (both premenopausal use of OCs and postmenopausal use of ERT-HRT). An intriguing finding from the monkey studies is that social subordination, which induces estrogen deficiency in female monkeys, accelerates atherosclerosis premenopausally and predicts extent of postmenopausal atherosclerosis. This effect can be inhibited by exogenous estrogen, premenopausally. The results suggest that more effort on detecting and regulating premenopausal ovarian dysfunction may be justified. A complication in understanding estrogen action may be the result of varying extents of arterial damage. For example, primary prevention studies in both postmenopausal animals and women have provided strong evidence of atheroprotection with a variety of estrogens. In contrast, the results of secondary prevention studies [10,12] have in general suggested little cardioprotection with either ERT or HRT. Studies in rabbits suggest the antiatherogenic effect of estrogen may not be present when the endothelium is damaged [64]. The state of the endothelium may be critical for some estrogen actions. For those effects of estrogen that require the ER, be it ERalpha or ERbeta, the presence of the receptor may vary with age, disease state, or type of hormone therapy. If continuous combined HRT therapy decreases ER in the artery as it does in the uterus, this may eliminate those estrogen actions requiring the ER, but not others. Older women who have not been exposed to estrogens for many years may be more sensitive to some estrogen effects, and may need lower doses of ERT-HRT. Recent reports suggest that lower doses of estrogens maintain beneficial effects on lipoproteins and coagulation factors [95], while also requiring lower doses of progestogens to protect the uterus [96]. These beneficial findings are very promising in light of the improvements in CHD risk and decreased stroke risk reported with low-dose estrogens [5]. It ill be interesting to see if CRP is increased with lower doses of estrogens and whether these changes are associated with increased early risk of CHD. Perhaps older women with CHD are also more obese, may have diabetes, and may be more susceptible to inflammatory and thrombotic effects of higher doses of estrogens. There are many questions left unanswered. It is hoped that some of the answers may come from the WHI, which is a large prospective trial assessing ERT and HRT. The age range is also relatively large and may be able to determine if older women respond differently than younger women. Some initial data from the WHI have been made available suggesting a small increased risk in the first 2 years and a trend for decreasing risk in the last months of the first 2 years [34]. Just recently, the CEE + MPA arm of the study was stopped early by the data and-safety monitoring board as the overall health risks exceeded benefits with increases in both breast cancer and CVD [97]. The remainder of the study groups including an estrogen-only arm, are expected to continue until 2005.
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PMID:Reproductive hormones and cardiovascular disease mechanism of action and clinical implications. 1235 69

The Women's Health Initiative (WHI) a double-blind, placebo-controlled trial studying the effects of continuous combined estrogen-progestin regimen (CEE 0.625 mg plus 2.5 mg MPA daily), was stopped prematurely on the basis of a slight increase in the risk of invasive breast cancer, myocardial infarction and stroke. The study was not planned to examine other important aspects of HRT treatment, such as menopausal symptoms and quality of life, since the CEE only arm of the study was not terminated, it is possible that the specific drug tested in the study had different effects on outcome than other preparations available in the market. One should remember that many previous observational studies actually demonstrated cardiovascular benefits in women using other types or regimens of hormones. There seems to be a consensus on the interpretation of the WHI trial: 1) hormones are the best treatment for symptomatic women since there are no real alternatives; 2) women who use HRT for more than 5 years should discuss the latest data with their physician, in order to consider their individual risk-benefit equation; 3) it is logical to prefer hormones, which are different from CEE plus MPA daily.
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PMID:[Lessons from the Women's Health Initiative (WHI) using hormone replacement therapy with regard to heart disease--the dream that has been broken?]. 1269 64

Controversies about the safety of different postmenopausal hormone therapies (HTs) started 30 years ago and reached a peak in 2003 after the publication of the results from the Women Health Initiative (WHI) trial and the Million Women Study (MWS) [Writing group for the women's health initiative investigations. Risks and benefits of estrogen plus progestin in healthy postmenopausal women. JAMA 2002;288:321-33; Million women study collaborators. Breast cancer and hormone-replacement therapy in the million women study. Lancet 2003;362:419-27]. The single HT formulation used in the WHI trial for non hysterectomized women-an association of oral conjugated equine estrogens (CEE-0.625 mg/day) and a synthetic progestin, medroxyprogesterone acetate (MPA-2.5 mg/day)-increases the risks of venous thromboembolism, cardiovascular disease, stroke and breast cancer. The MWS, an observational study, showed an increased breast cancer risk in users of estrogens combined with either medroxyprogesterone acetate (MPA), norethisterone, or norgestrel. It is unclear and questionable to what extent these results might be extrapolated to other HRT regimens, that differ in their doses, compositions and administration routes, and that were not assessed in the WHI trial and the MWS. Significant results were achieved with the publication of the WHI estrogen-only arm study [Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women's Health Initiative randomized controlled trial. JAMA 2004;291:1701-1712] in which hormone therapy was reserved to women who had carried out hysterectomy. What emerged from this study will allow us to have some important argument to develop.
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PMID:New evidence regarding hormone replacement therapies is urgently required transdermal postmenopausal hormone therapy differs from oral hormone therapy in risks and benefits. 1596 66

The incidence of stroke increases substantially after menopause, and in the United States it is the third leading cause of death. Data exist suggesting that women have worse outcomes for stroke than do men. Trials of aspirin use further suggest that there is a gender difference regarding stroke. While men may have a coronary benefit from aspirin, postmenopausal women do not; yet ischemic stroke may be decreased in women but not in men. Among the traditional risk factors for stroke (such as smoking, hypertension, diabetes, obesity), hormonal therapy (HT) has been suggested to be a risk as well, although the data are not consistent. The previous Position Statement of the IMS published in 2004 was relatively silent on the issue of stroke. The annual rate of stroke in women increases rapidly with aging in postmenopausal women. While the rate is approximately 0.6-0.8/1000/year at age 50-59, it is over 2/1000 after age 60. In white women in the USA, it is 4.2/1000 at 65-74 years of age, and 11.3/1000 between ages 75 and 84 years. Thus, in trials such as the Women's Health Initiative (WHI), most of the strokes occurred in older women. Both the conjugated equine estrogen/medroxyprogesterone acetate (CEE/MPA) and CEE-alone trials in the WHI reported an increased risk of stroke in the entire population using nominal statistics: 1.41 (95% confidence interval (CI) 1.07-1.85) and 1.39 (95% CI 1.10-1.77), respectively. The increased risk was related to ischemic stroke and not hemorrhagic stroke. The absolute risk for the entire population was 0.8/1000 and 1.2/1000 woman-years (<1/1000 signifies a 'rare' event using the CIOMS classification). However, the risk was not increased in the 50-59-year-old age group, although the numbers are small. Here, the background prevalence of stroke is much lower as noted above. The results of the observational trial of the WHI were not consistent with the randomized clinical trial data and were more in keeping with older observational data showing no increased risk of stroke. The authors reconcile these differences by suggesting differences in the timing of initiation of hormones, which was at an earlier age in the observational cohort. Several recent observational studies, which will be presented, show no increased risk of ischemic stroke in younger cohorts, but possibly an increase in the risk of transient ischemic attack. These recent studies suggested the risk to be less with lower doses of estradiol < or =1 mg and to be consistent with older studies showing no risk with doses < 0.625 mg CEE. In addition, the risk was possibly lower with non-oral therapy, and was reduced if started prior to menopause. The existence of hypertension was shown to substantially increase the risk. However, data on progestogen use versus unopposed estrogen have not been consistent. At the same time, a recent body of evidence from basic science studies has reaffirmed the neuronal and stroke protective effects of estrogen. Thus, the discrepancy between these data and clinical data showing no benefit or increased risk of stroke remains to be explained. Recent trials in older women with osteoporosis have suggested an increased risk of stroke with tibolone and of stroke mortality with raloxifene. In conclusion, the current data suggest no increased risk of stroke with hormone therapy in younger (50-59 years) normotensive postmenopausal women, particularly when lower doses are prescribed soon after menopause.
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PMID:Menopause and stroke and the effects of hormonal therapy. 1788 69

Carotid endarterectomy has a long history in stroke prevention, yet controversy remains concerning optimal techniques. Two methods frequently used are endarterectomy with patch angioplasty (CEAP) and eversion endarterectomy (CEE). The objective of this study was to compare hemodynamics-related stress and strain distributions between arteries repaired using CEAP and CEE. Mathematical models were based on in vivo three-dimensional arterial geometry, pulsatile velocity profiles, and intraluminal pressure inputs obtained from 16 patients with carotid artery disease. These data were combined with experimentally derived nonlinear, anisotropic carotid artery mechanical properties to create fluid-structure interaction models of CEAP and CEE. These models were then used to calculate hemodynamic parameters thought to promote recurrent disease and restenosis. Combining calculations of stress and strain into a composite risk index, called the integral abnormality factor, allowed for an overall comparison between CEAP and CEE. CEE demonstrated lower mechanical stresses in the arterial wall, whereas CEAP straightened the artery and caused high stress and strain concentrations at the suture-artery interface. CEAP produced a larger continuous region of oscillatory, low-shear, vortical flow in the carotid bulb. There was a more than two-fold difference in the integral abnormality factor, favoring CEE. In conclusion, in a realistically simulated carotid artery, fluid-structure interaction modeling demonstrated CEE to produce less mechanical wall stress and improved flow patterns compared with CEAP. Clinical validation with larger numbers of individual patients will ultimately be required to support modeling approaches to help predict arterial disease progression and comparative effectiveness of reconstruction methods and devices.
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PMID:A mathematical evaluation of hemodynamic parameters after carotid eversion and conventional patch angioplasty. 2381 86

Cardiovascular disease (CVD) remains the number one cause of death and morbidity worldwide, and while overall CVD incidence rates declined in both genders between 1999 and 2007, age-specific data suggest that coronary risk factors in women are on the rise. While early observational data favored menopausal hormone therapy's (MHT's) role in primary CVD prevention, the initial interventional study data from the WHI did not. Further detailed analyses of both observational and interventional data have pointed to the possibility that MHT may play a role in primary CVD prevention if initiated within 10 years of menopause and less than 60 years of age (the timing hypothesis). Unanswered questions remain regarding the optimal route and dosage of estrogen in MHT. Data so far, favor transdermal estradiol over conventional-dose CEE with respect to CVD risk and oral estradiol over conventional-dose CEE with respect to stroke risk. Low-dose oral CEE may similarly have benefit over conventional-dose oral CEE for some CVD events. In addition, the transdermal route of delivery may avoid the excess risk of certain CVD events associated with MHT and lower doses of estrogen may have fewer adverse effects than the doses previously tested in WHI. Because questions regarding benefits versus risks remain, MHT is yet to be recommended for CVD prevention. However, it is indicated for menopausal symptom management in women within 10 years of menopause and under the age of 60 years, in whom it does not appear to carry increased cardiovascular risk. Additional research is ongoing and needed to confirm or refute the comparative safety of the various MHT options.
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PMID:Hormone therapy in menopause: An update on cardiovascular disease considerations. 2627 Mar 18