Diabetes mellitus and obesity among South Asians with ischemic stroke across three countries.

BACKGROUND: Diabetes mellitus and central obesity are more common among South Asian populations than among White British people. This study explores the differences in diabetes and obesity in South Asians with stroke living in the United Kingdom, India, and Qatar compared with White British stroke patients. METHODS: The study included the UK, Indian, and Qatari arms of the ongoing large Bio-Repository of DNA in Stroke (BRAINS) international prospective hospital-based study for South Asian stroke. BRAINS includes 4580 South Asian and White British recruits from UK, Indian, and Qatar sites with first-ever ischemic stroke. RESULTS: The study population comprises 1751 White British (WB) UK residents, 1165 British South Asians (BSA), 1096 South Asians in India (ISA), and 568 South Asians in Qatar (QSA). ISA, BSA, and QSA South Asians suffered from higher prevalence of diabetes compared with WB by 14.5% (ISA: 95% confidence interval (CI) = 18.6-33.0, p < 0.001), 31.7% (BSA: 95% CI = 35.1-50.2, p < 0.001), and 32.7% (QSA: 95% CI = 28.1-37.3, p < 0.001), respectively. Although WB had the highest prevalence of body mass index (BMI) above 27 kg/m2 compared with South Asian patients (37% vs 21%, p < 0.001), South Asian patients had a higher waist circumference than WB (94.8 cm vs 90.8 cm, p < 0.001). Adjusting for traditional stroke risk factors, ISA, BSA, and QSA continued to display an increased risk of diabetes compared with WB by 3.28 (95% CI: 2.53-4.25, p < 0.001), 3.61 (95% CI: 2.90-4.51, p < 0.001), and 5.24 (95% CI: 3.93-7.00, p < 0.001), respectively. CONCLUSION: South Asian ischemic stroke patients living in Britain and Qatar have a near 3.5-fold risk of diabetes compared with White British stroke patients. Their body composition may partly help explain that increased risk. These findings have important implications for public health policymakers in nations with large South Asian populations.

Atrial fibrillation in UK South Asian hospitalized ischemic stroke patients: The BRAINS study.

INTRODUCTION: South Asian diaspora comprise one of the largest ethnic minority groups in the world yet data about atrial fibrillation (AF) in this demographic is understudied. Our aim is to identify differences in AF prevalence and treatment between South Asians and white British stroke patients. METHOD: The UK arm of a prospective ongoing large international repository on stroke was analysed. Ethnic differences in AF prevalence and management in those with ischemic stroke were analysed. RESULTS: Of the 3515 individuals recruited with ischemic stroke, 1482 (men: 972, women: 510) were South Asian and 2033 (men:1141, women:892) of white British ethnicity. AF was present in 462 white British and 193 South Asians stroke patients, with South Asians displaying a lower prevalence of AF (South Asians: 13.0% vs white British 22.7%, P<0.001). Despite adjustment for traditional AF risk factors, South Asians had a significantly lower OR of AF compared to white British stroke patients (OR: 0.40, 95%CI: 0.33:0.49, P<0.001). Among confirmed AF cases, 31.8% of South Asians and 41.4% of white British were untreated at admission (P = 0.02). Antiplatelet treatment was significantly higher among South Asians at both admission (South Asian: 47.4% vs. white British: 29.9%, P<0.001) and discharge (South Asian: 49.5% vs. white British: 34.7%, P = 0.001), although anticoagulation treatment was similar across both ethnic groups at admission (South Asian: 28.5% vs white British: 28.1%, P = 0.93), and discharge (South Asian: 45.1% vs white British: 43.1%, P = 0.64). CONCLUSION: Stroke patients of South Asian descent are at significantly lower risk of AF but more likely to be on antiplatelet treatment compared to their white British counterparts.

Ischaemic stroke in South Asians: The BRAINS study.

BACKGROUND AND PURPOSE: Studies on stroke in South Asian populations are sparse. The aim of this study was to compare differences in age of onset of ischaemic stroke in South Asian patients living in the United Kingdom and South Asian patients living in India versus White British stroke patients. METHODS: We studied the UK and Indian arms of the ongoing BRAINS study, an international prospective hospital-based study of South Asian stroke patients. The BRAINS study includes 4038 South Asian and White British patients with first-ever ischaemic stroke, recruited from sites in the United Kingdom and India. RESULTS: Of the included patients, 1126 were South Asians living in India (ISA), while 1176 were British South Asian (BSA) and 1736 were White British (WB) UK residents. Patients in the ISA and BSA groups experienced stroke 19.5 years and 7.2 years earlier than their WB counterparts, respectively (mean [interquartile range] age: BSA 64.3 [22] years vs. ISA 52.0 [18] years vs. WB 71.5 [19] years; p < 0.001). Patients in the BSA group had higher rates of hypertension, diabetes mellitus and hypercholesterolaemia than those in the ISA and WB groups. After adjustment for traditional stroke risk factors, an earlier age of stroke onset of 18.9 years (p < 0.001) and 8.9 years (p < 0.001) was still observed in the ISA and BSA groups, respectively. In multivariable stepwise linear regression analysis, ethnicity accounted for 24.7% of the variance in early age onset. CONCLUSION: Patients in the BSA and ISA groups experienced ischaemic stroke approximately 9 and 19 years earlier, respectively, than their WB counterparts. Ethnicity is an independent predictor of early age of stroke onset. Our study has considerable implications for public health policymakers in countries with sizable South Asian populations.

Hypertensive encephalopathy mimicking cerebral vasculitis with pontine oedema, cerebellar white matter lesions and multiple cerebral infarctions.

A 47-year-old man with poorly controlled hypertension presented with headaches, right-sided weakness and dysarthria. CT and MRI scans of the brain showed widespread abnormalities including significant pontine oedema, basal ganglia and corona radiata infarctions and cerebellar white matter high signal. Imaging of the intracerebral vasculature also demonstrated wall irregularities. Initially a central nervous system inflammatory disorder was thought to be the most likely diagnosis, possibly acute demyelinating encephalomyelitis or cerebral vasculitis, and the patient was treated with high-dose intravenous steroids. The diagnosis of hypertensive encephalopathy was made because (1) the patient was hypertensive and (2) the patients MRI findings resolved with antihypertensive treatment.Blood pressure treatment was instigated from admission, and the patients symptoms improved with resolution of the radiological abnormalities.

A Stroke Registry Data on the Use of Intravenous Recombinant Tissue Plasminogen Activator in Stroke of Unknown Time of Onset.

BACKGROUND: Stroke of unknown time of onset (SUTO) constitutes one fifth of all ischemic stroke admissions, and routine use of intravenous recombinant tissue plasminogen activator (IV rtPA) is recommended only in patients with a symptom onset time of less than 4.5 hours. There are limited data on clinical outcome in patients with SUTO versus patients with symptoms onset less than 4.5 hours from onset time. We hypothesized that efficacy and safety outcomes of IV rtPA therapy in selected SUTO patients are comparable to those with known onset time. METHODS: We compared 90 days' modified Rankin Scale (mRS), rates of symptomatic intracerebral hemorrhage (sICH), in-hospital mortality, and death due to sICH between 3 groups treated with IV rtPA: SUTO, 3 hours or less, and 3.0-4.5 hours from prospective patient admissions between April 1, 2012, and July 31, 2013. RESULTS: There were 65 participants in the SUTO group, 186 in the 3 hours or less group, and 51 in the 3.0-4.5 hours group. In-hospital mortality rates were 14.5%, 13.5%, and 11.8%, respectively. sICH risks were 1.5%, 1.6%, and 5.8%, and death rates due to sICH were 0%, 1.1%, and 1.9%, respectively. Ninety days' odds of excellent clinical outcome (mRS score 0-1) were not different between the SUTO group (odds ratio [OR] 1.14, 95% confidence interval [CI]: .63-2.10), the 3 hours or less group (OR .87, 95% CI: .48-1.60), and the 3.0-4.5 hours group (OR .79, 95% CI: .48-1.60) (P = .82). CONCLUSION: Thrombolytic therapy outcome in SUTO is not different from in-license use in our patient population. There is an urgent need to include this patient group in ongoing randomized multicenter trials.

Clinical and laboratory predictors of deep vein thrombosis after acute stroke.

BACKGROUND: Deep vein thrombosis (DVT) is a common complication of acute stroke, but the new incidence in the era of improved specialist input in stroke care is yet unknown. The models for VTE diagnosis is well established, but prediction models to target at-risk patients for pharmacological prophylaxis is lacking and requires further research, particularly in the aftermath of acute stroke. OBJECTIVES: To predict DVT after acute stroke using markers of haemostatic activation and stroke severity scores. METHODS: We examined the clinical utility of laboratory factors such as thrombin generation, D-dimer, fibrinogen alongside clinical factors (National Institute of Health Stroke Scale and Barthel Index) in the prediction of asymptomatic DVT, among 92 consecutively admitted patients. RESULTS: One in five patients (19.6%) had objectively confirmed DVT (6 proximal, 12 distal). Thrombolytic therapy did not protect against DVT, with 21% (6/29) of patients treated with r-tPA went on to develop DVT. Thrombin generation and fibrinogen had no clinical utility, but D-dimer at baseline and week 2 had high clinical potential in the prediction of asymptomatic DVT (2425ng/mL versus 1010ng/mL; p=0.001) and (2240 Vs 970ng/mL; p<0.001) respectively. Patients with DVT had worse stroke severity, and are functionally less able, with lower Barthel index (p=0.05), and high National Institute of Health Stroke Score (p=0.07). CONCLUSION: Thrombolytic therapy and specialist stroke intervention does not protect against DVT risk. D-dimer concentration within 48h of acute stroke is independently associated with development of DVT. This observation would require confirmation in a large study.

Thrombin Generation in Acute Ischaemic Stroke.

Introduction. Stroke remains a global leading cause of death and disability. Traditional description of plasma biology in the aftermath of acute ischaemic stroke favours development of hypercoagulability, resulting from complex interplay between plasma and endothelial factors. However, no single assay measures the overall global coagulation process. We postulate that thrombin generation would assist in identifying coagulation abnormalities after acute stroke. Aim. To investigate the coagulation abnormalities after acute ischaemic stroke using thrombin generation. Methods. We evaluated thrombin generation, measured with calibrated automated thrombography in stroke of different aetiological types (n = 170) within 48 hours of symptoms onset (baseline) and in the second week (time 2) and in normal healthy volunteers (n = 71). Results. Two-point thrombin generation assays showed prolonged lag time and time to peak at baseline (3.3 (2.9, 4.0) versus 3.6 (3.2, 4.7); p = 0.005) and (3.3 (2.9, 4.0) versus 3.6 (3.2, 4.7); p = 0.002), respectively, and at time 2 (3.5 (2.9, 4.2) versus 4.0 (3.1, 4.9); p = 0.004) and (5.9 (5.3, 6.6) versus 6.8 (5.8, 7.7) p = 0.05), respectively, in cardioembolic stroke (n = 39), when compared to noncardioembolic stroke (n = 117). The result was reproduced in multiple comparisons between acute ischaemic stroke subgroups and normal healthy volunteers. Endogenous thrombin potential and peak thrombin did not indicate hypercoagulability after acute ischaemic stroke, and thrombolytic therapy did not affect thrombin generation assays. Conclusion. Our findings suggest that thrombin generation in platelet poor plasma is not useful in defining hypercoagulability in acute ischaemic stroke. This is similar to observed trend in coronary artery disease and contrary to other hypercoagulable states.