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In a follow-up of a trial comparing endovascular thrombectomy with conventional therapy for acute ischemic stroke, the beneficial effect on functional recovery that was observed at 90 days was maintained at 2 years. Quality of life was better at 2 years with endovascular treatment. We reported previously the 90-day outcomes of a trial (Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands [MR CLEAN]) in which standard treatment was compared with endovascular treatment, administered within 6 hours after the onset of acute ischemic stroke caused by an intracranial arterial occlusion of the anterior circulation. 1 Most patients in the intervention group were treated by mechanical thrombectomy with the use of retrievable stents. The trial showed that functional recovery at 90 days was better with the intervention than with standard treatment. Subsequently, the beneficial effect of mechanical thrombectomy on 90-day outcomes . . .

Feature extraction based on EEG signals and construction of classification models using machine learning methods are key to intelligent assisted diagnosis of brain diseases (such as stroke classification). However, the quality of the extracted features directly affects the classification performance. This study proposes a multi-dimensional feature extraction method based on autocorrelation and complexity theory. It introduces an improved multifractal detrended fluctuation analysis (MFDFA) algorithm based on optimized empirical mode decomposition to extract high-quality autocorrelation features. In addition, we find that the ratio of fuzzy entropy between high-frequency band and low-frequency band of cerebral infarction signals is significantly lower than that of cerebral hemorrhage signals. On this basis, we propose a new complexity feature - fuzzy asymmetric index (FAI) based on constant Gaussian membership function. The study then integrates hierarchical fuzzy entropy, asymmetric entropy, and FAI to obtain complex fusion features. These extracted and fused features demonstrate excellent classification performance for differentiating cerebral hemorrhage and cerebral infarction. Using the random forest algorithm with a constant Gaussian membership function, the classification achieves an accuracy of 99.33%, precision of 100%, sensitivity of 98.57%, specificity of 100%, F1-score of 99.23%, and MCC of 98.73%. The proposed multi-dimensional features, combining autocorrelation and complexity characteristics, perform remarkably well in the classification of stroke EEG signals.

Anticoagulants are more effective than antiplatelet agents at reducing stroke risk in patients with atrial fibrillation, but whether this benefit outweighs the increased risk of bleeding in elderly patients is unknown. We assessed whether warfarin reduced risk of major stroke, arterial embolism, or other intracranial haemorrhage compared with aspirin in elderly patients. 973 patients aged 75 years or over (mean age 81·5 years, SD 4·2) with atrial fibrillation were recruited from primary care and randomly assigned to warfarin (target international normalised ratio 2–3) or aspirin (75 mg per day). Follow-up was for a mean of 2·7 years (SD 1·2). The primary endpoint was fatal or disabling stroke (ischaemic or haemorrhagic), intracranial haemorrhage, or clinically significant arterial embolism. Analysis was by intention to treat. This study is registered as an International Standard Randomised Controlled Trial, number ISRCTN89345269. There were 24 primary events (21 strokes, two other intracranial haemorrhages, and one systemic embolus) in people assigned to warfarin and 48 primary events (44 strokes, one other intracranial haemorrhage, and three systemic emboli) in people assigned to aspirin (yearly risk 1·8% vs 3·8%, relative risk 0·48, 95% CI 0·28–0·80, p=0·003; absolute yearly risk reduction 2%, 95% CI 0·7–3·2). Yearly risk of extracranial haemorrhage was 1·4% (warfarin) versus 1·6% (aspirin) (relative risk 0·87, 0·43–1·73; absolute risk reduction 0·2%, −0·7 to 1·2). These data support the use of anticoagulation therapy for people aged over 75 who have atrial fibrillation, unless there are contraindications or the patient decides that the benefits are not worth the inconvenience.

Oral anticoagulation therapy reduces risk of vascular events in patients with atrial fibrillation. However, long-term monitoring is necessary and many patients cannot achieve optimum anticoagulation. We assessed whether clopidogrel plus aspirin was non-inferior to oral anticoagulation therapy for prevention of vascular events. Patients were enrolled if they had atrial fibrillation plus one or more risk factor for stroke, and were randomly allocated to receive oral anticoagulation therapy (target international normalised ratio of 2·0–3·0; n=3371) or clopidogrel (75 mg per day) plus aspirin (75–100 mg per day recommended; n=3335). Outcome events were adjudicated by a blinded committee. Primary outcome was first occurrence of stroke, non-CNS systemic embolus, myocardial infarction, or vascular death. Analyses were by intention-to-treat. This study is registered with ClinicalTrials.gov, number NCT00243178. The study was stopped early because of clear evidence of superiority of oral anticoagulation therapy. There were 165 primary events in patients on oral anticoagulation therapy (annual risk 3·93%) and 234 in those on clopidogrel plus aspirin (annual risk 5·60%; relative risk 1·44 (1·18–1.76; p=0.0003). Patients on oral anticoagulation therapy who were already receiving this treatment at study entry had a trend towards a greater reduction in vascular events (relative risk 1·50, 95% CI 1·19–1·89) and a significantly (p=0·03 for interaction) lower risk of major bleeding with oral anticoagulation therapy (1.30; 0.94–1.79) than patients not on this treatment at study entry (1·27, 0·85–1·89 and 0·59, 0·32–1·08, respectively). Oral anticoagulation therapy is superior to clopidogrel plus aspirin for prevention of vascular events in patients with atrial fibrillation at high risk of stroke, especially in those already taking oral anticoagulation therapy.

Stroke is the third leading cause of disability and mortality worldwide. Accurate identification of stroke-type—ischemic or hemorrhagic—is critical for guiding treatment; however, it typically requires costly neuroimaging, which is often inaccessible in rural areas of developing countries. This study employs machine learning (ML) to identify stroke-type using only clinical data, aiming to develop a cost-effective method, particularly for resource-limited settings lacking neuroimaging facilities. A dataset from 2,190 stroke patients with 79 clinical attributes has been collected in-house and used for the development of the proposed ML-framework. The framework robustly addresses missing data through Multiple Imputation by Chained Equation (MICE), ensuring it to function robustly even when some laboratory test results are unavailable. Further, the research addresses target leakage through statistical tests and utilizes SHAP-analysis to identify the most important attributes for classification. The proposed framework achieves 82.42% weighted accuracy, 82.33% accuracy, 82.19% sensitivity, 82.65% specificity, and an 86.68% F1-score. Notably, with only the 19 most significant attributes identified via SHAP, the framework maintains a weighted accuracy of 82.20%. Prospective validation on an independent dataset demonstrates a 16.42% improvement over the best-performing clinical score, Siriraj. The proposed ML-framework may help reduce the time to treatment for patients in resource-limited settings by enabling prompt primary care and timely referral to stroke-ready facilities.

Throughout the usual LDL cholesterol range in Western populations, lower blood concentrations are associated with lower cardiovascular disease risk. In such populations, therefore, reducing LDL cholesterol may reduce the development of vascular disease, largely irrespective of initial cholesterol concentrations. 20,536 UK adults (aged 40-80 years) with coronary disease, other occlusive arterial disease, or diabetes were randomly allocated to receive 40 mg simvastatin daily (average compliance: 85%) or matching placebo (average non-study statin use: 17%). Analyses are of the first occurrence of particular events, and compare all simvastatin-allocated versus all placebo-allocated participants. These \"intention-to-treat\" comparisons assess the effects of about two-thirds (85% minus 17%) taking a statin during the scheduled 5-year treatment period, which yielded an average difference in LDL cholesterol of 1.0 mmol/L (about two-thirds of the effect of actual use of 40 mg simvastatin daily). Primary outcomes were mortality (for overall analyses) and fatal or non-fatal vascular events (for subcategory analyses), with subsidiary assessments of cancer and of other major morbidity. All-cause mortality was significantly reduced (1328 [12.9%] deaths among 10,269 allocated simvastatin versus 1507 [14.7%] among 10,267 allocated placebo; p=0.0003), due to a highly significant 18% (SE 5) proportional reduction in the coronary death rate (587 [5.7%] vs 707 [6.9%]; p=0.0005), a marginally significant reduction in other vascular deaths (194 [1.9%] vs 230 [2.2%]; p=0.07), and a non-significant reduction in non-vascular deaths (547 [5.3%] vs 570 [5.6%]; p=0.4). There were highly significant reductions of about one-quarter in the first event rate for non-fatal myocardial infarction or coronary death (898 [8.7%] vs 1212 [11.8%]; p<0.0001), for non-fatal or fatal stroke (444 [4.3%] vs 585 [5.7%]; p<0.0001), and for coronary or non-coronary revascularisation (939 [9.1%] vs 1205 [11.7%]; p<0.0001). For the first occurrence of any of these major vascular events, there was a definite 24% (SE 3; 95% CI 19-28) reduction in the event rate (2033 [19.8%] vs 2585 [25.2%] affected individuals; p<0.0001). During the first year the reduction in major vascular events was not significant, but subsequently it was highly significant during each separate year. The proportional reduction in the event rate was similar (and significant) in each subcategory of participant studied, including: those without diagnosed coronary disease who had cerebrovascular disease, or had peripheral artery disease, or had diabetes; men and, separately, women; those aged either under or over 70 years at entry; and--most notably--even those who presented with LDL cholesterol below 3.0 mmol/L (116 mg/dL), or total cholesterol below 5.0 mmol/L (193 mg/dL). The benefits of simvastatin were additional to those of other cardioprotective treatments. The annual excess risk of myopathy with this regimen was about 0.01%. There were no significant adverse effects on cancer incidence or on hospitalisation for any other non-vascular cause. Adding simvastatin to existing treatments safely produces substantial additional benefits for a wide range of high-risk patients, irrespective of their initial cholesterol concentrations. Allocation to 40 mg simvastatin daily reduced the rates of myocardial infarction, of stroke, and of revascularisation by about one-quarter. After making allowance for non-compliance, actual use of this regimen would probably reduce these rates by about one-third. Hence, among the many types of high-risk individual studied, 5 years of simvastatin would prevent about 70-100 people per 1000 from suffering at least one of these major vascular events (and longer treatment should produce further benefit). The size of the 5-year benefit depends chiefly on such individuals' overall risk of major vascular events, rather than on their blood lipid concentrations alone.

Findings from randomised trials have shown a higher early risk of stroke after carotid artery stenting than after carotid endarterectomy. We assessed whether white-matter lesions affect the perioperative risk of stroke in patients treated with carotid artery stenting versus carotid endarterectomy. Patients with symptomatic carotid artery stenosis included in the International Carotid Stenting Study (ICSS) were randomly allocated to receive carotid artery stenting or carotid endarterectomy. Copies of baseline brain imaging were analysed by two investigators, who were masked to treatment, for the severity of white-matter lesions using the age-related white-matter changes (ARWMC) score. Randomisation was done with a computer-generated sequence (1:1). Patients were divided into two groups using the median ARWMC. We analysed the risk of stroke within 30 days of revascularisation using a per-protocol analysis. ICSS is registered with controlled-trials.com, number ISRCTN 25337470. 1036 patients (536 randomly allocated to carotid artery stenting, 500 to carotid endarterectomy) had baseline imaging available. Median ARWMC score was 7, and patients were dichotomised into those with a score of 7 or more and those with a score of less than 7. In patients treated with carotid artery stenting, those with an ARWMC score of 7 or more had an increased risk of stroke compared with those with a score of less than 7 (HR for any stroke 2·76, 95% CI 1·17–6·51; p=0·021; HR for non-disabling stroke 3·00, 1·10–8·36; p=0·031), but we did not see a similar association in patients treated with carotid endarterectomy (HR for any stroke 1·18, 0·40–3·55; p=0·76; HR for disabling or fatal stroke 1·41, 0·38–5·26; p=0·607). Carotid artery stenting was associated with a higher risk of stroke compared with carotid endarterectomy in patients with an ARWMC score of 7 or more (HR for any stroke 2·98, 1·29–6·93; p=0·011; HR for non-disabling stroke 6·34, 1·45–27·71; p=0·014), but there was no risk difference in patients with an ARWMC score of less than 7. The presence of white-matter lesions on brain imaging should be taken into account when selecting patients for carotid revascularisation. Carotid artery stenting should be avoided in patients with more extensive white-matter lesions, but might be an acceptable alternative to carotid endarterectomy in patients with less extensive lesions. Medical Research Council, the Stroke Association, Sanofi-Synthélabo, the European Union Research Framework Programme 5.

Background: There is paucity of data on the long-term outcomes after acute ischemic posterior circulation stroke (PCS). Additionally, the long-term prognostic value of the New England Medical Center-Posterior Circulation Registry (NEMC-PCR) classification of PCS has not been studied. Patients and methods: All consecutive patients with PCS registered in the Athens Stroke Registry between 01/1993 and 12/2012 were prospectively followed for up to 10 years and included in the analysis. The NEMC-PCR criteria were applied to classify them in relation to topography. The main studied outcomes were all cause mortality, stroke recurrence and major adverse cardiovascular events (MACEs). Results: A total of 653 patients with PCS (455 men, mean age 68.06 years) were followed up for 52.8 ± 44.0 months. Seventy-four (11.3%), 219 (33.5%), 335 (51.3%), and 25 (3.8%) patients had proximal, middle, distal, and multiple territories PCS, respectively. During the 10-year follow-up period, 217 patients died (7.6 per 100 patient years), 127 developed recurrent stroke (4.2 per 100 patient years), and 209 had a MACE (7.3 per 100 patient years). The cumulative 10-year mortality was higher in distal and multiple territories PCS compared to middle and proximal PCS (55.6%, 58.8%, 40.0%, 35.5%, respectively, p < 0.001 by log-rank test). Patients with distal location PCS had almost twofold increased 10-year risk of mortality compared to proximal location patients after adjusting for all confounding variables (HR 1.99, 95% CI 1.05–3.77). Per TOAST classification, large artery atherosclerosis was associated with almost two-fold increase in risk of mortality, stroke recurrence and MACEs. Discussion and conclusion: A large proportion of PCS patients experienced 10-year death, stroke and MACE occurrence after PCS. NEMC-PCR topographic classification was found to have significant prognostic value, with distal and middle PCS having worse long-term outcomes than proximal PCS. Graphical abstract

It has been suggested that increased intake of various antioxidant vitamins reduces the incidence rates of vascular disease, cancer, and other adverse outcomes. 20 536 UK adults (aged 40–80) with coronary disease, other occlusive arterial disease, or diabetes were randomly allocated to receive antioxidant vitamin supplementation (600 mg vitamin E, 250 mg vitamin C, and 20 mg β-carotene daily) or matching placebo. Intention-to-treat comparisons of outcome were conducted between all vitamin-allocated and all placebo-allocated participants. An average of 83% of participants in each treatment group remained compliant during the scheduled 5-year treatment period. Allocation to this vitamin regimen approximately doubled the plasma concentration of α-tocopherol, increased that of vitamin C by one-third, and quadrupled that of β-carotene. Primary outcomes were major coronary events (for overall analyses) and fatal or non-fatal vascular events (for subcategory analyses), with subsidiary assessments of cancer and of other major morbidity. There were no significant differences in all-cause mortality (1446 [14·1%] vitamin-allocated vs 1389 [13·5%] placebo-allocated), or in deaths due to vascular (878 [8·6%] vs 840 [8·2%]) or non-vascular (568 [5·5%] vs 549 [5·3%]) causes. Nor were there any significant differences in the numbers of participants having non-fatal myocardial infarction or coronary death (1063 [10·4%] vs 1047 [10·2%]), non-fatal or fatal stroke (511 [5·0%] vs 518 [5·0%]), or coronary or non-coronary revascularisation (1058 [10·3%] vs 1086 [10·6%]). For the first occurrence of any of these “major vascular events”, there were no material differences either overall (2306 [22·5%] vs 2312 [22·5%]; event rate ratio 1·00 [95% CI 0·94–1·06]) or in any of the various subcategories considered. There were no significant effects on cancer incidence or on hospitalisation for any other non-vascular cause. Among the high-risk individuals that were studied, these antioxidant vitamins appeared to be safe. But, although this regimen increased blood vitamin concentrations substantially, it did not produce any significant reductions in the 5-year mortality from, or incidence of, any type of vascular disease, cancer, or other major outcome.

Some observational studies have suggested that women who are receiving estrogen-replacement therapy have a lower risk of stroke and death than others. The Women's Estrogen for Stroke Trial was a double-blind, placebo-controlled trial of estradiol-17β in 664 women with a recent cerebrovascular event. Estrogen therapy did not reduce the risk of stroke or death in these women and was associated with a borderline increase in the risk of fatal stroke; this therapy was also associated with adverse effects on the endometrium. In this double-blind, placebo-controlled trial, in 664 women, estrogen therapy did not reduce the risk of stroke or death. This therapy was also associated with adverse effects on the endometrium. Although many observational studies have linked postmenopausal estrogen therapy with a reduced risk of vascular disease, especially morbidity and mortality from cardiovascular causes, 1 concern has persisted that these findings may be attributable not to estrogen therapy but to other differences between users and nonusers of such therapy. 2 Although estrogen therapy may have favorable effects on lipid metabolism, 3 coagulation, 4 , 5 and vascular tone, 6 , 7 it may also have adverse prothrombotic and proinflammatory effects. 8 , 9 In 1998, the findings of the first placebo-controlled, randomized clinical trial of hormone-replacement therapy for the secondary prevention of cardiac disease in postmenopausal women, the Heart and . . .