METHODS: This is a cross-sectional study of adults aged 18 and above attending a blood pressure screening program in community in conjunction with May Measurement Month 2017 in Malaysia. A structured self-administered questionnaire was given to the participants who gave verbal consent. Data analysis was done using SPSS v. 23 and multiple logistic regression was used to identify the determinants of knowledge on actions to be taken during stroke and recognition of stroke symptoms.
RESULTS: Out of 4096 respondents, 82.9-92.1% of them able to recognise the common stroke symptoms. and 74.2% of the study respondents will go to hospital within 4.5 h of stroke onset. According to binomial logistic regression analyses, adults aged 45 years old and above (OR 1.39 95%CI 1.01-1.92), being Malay (OR 1.74, 95% CI 1.27-2.40), being non-smokers (OR = 2.491, 95% CI: 1.64-3.78), hypertensives (OR: 1.57, 95% CI: 1.02-2.42)and diabetics (OR: 2.54, 95% CI:1.38-4.69) are determinants of right actions to be taken during stroke. Meanwhile, respondents aged 45 years old and older (OR = 1.68, 95% CI: 1.39-2.03), being Malay (OR = 1.49, 95% CI: 1.24-1.79), hypertensive (OR = 1.32, 95% CI: 1.04-1.66) and those who had a previous history of stroke (OR = 2.25, 95% CI: 1.01-5.00) are determinants of good recognition of stroke symptoms.
CONCLUSIONS: The overall knowledge of stroke in our study population was good. Older age, being Malay, non-smokers, hypertensives and diabetics are determinants of right actions to be taken during stroke. Meanwhile, older age, being Malay, hypertensive and those who had a previous history of stroke are determinants of good recognition of stroke symptoms.
METHODS: We did an international, randomised placebo-controlled trial in adults with intracerebral haemorrhage from acute stroke units at 124 hospital sites in 12 countries. Participants were randomly assigned (1:1) to receive 1 g intravenous tranexamic acid bolus followed by an 8 h infusion of 1 g tranexamic acid or a matching placebo, within 8 h of symptom onset. Randomisation was done centrally in real time via a secure website, with stratification by country and minimisation on key prognostic factors. Treatment allocation was concealed from patients, outcome assessors, and all other health-care workers involved in the trial. The primary outcome was functional status at day 90, measured by shift in the modified Rankin Scale, using ordinal logistic regression with adjustment for stratification and minimisation criteria. All analyses were done on an intention-to-treat basis. This trial is registered with the ISRCTN registry, number ISRCTN93732214.
FINDINGS: We recruited 2325 participants between March 1, 2013, and Sept 30, 2017. 1161 patients received tranexamic acid and 1164 received placebo; the treatment groups were well balanced at baseline. The primary outcome was assessed for 2307 (99%) participants. The primary outcome, functional status at day 90, did not differ significantly between the groups (adjusted odds ratio [aOR] 0·88, 95% CI 0·76-1·03, p=0·11). Although there were fewer deaths by day 7 in the tranexamic acid group (101 [9%] deaths in the tranexamic acid group vs 123 [11%] deaths in the placebo group; aOR 0·73, 0·53-0·99, p=0·0406), there was no difference in case fatality at 90 days (250 [22%] vs 249 [21%]; adjusted hazard ratio 0·92, 95% CI 0·77-1·10, p=0·37). Fewer patients had serious adverse events after tranexamic acid than after placebo by days 2 (379 [33%] patients vs 417 [36%] patients), 7 (456 [39%] vs 497 [43%]), and 90 (521 [45%] vs 556 [48%]).
INTERPRETATION: Functional status 90 days after intracerebral haemorrhage did not differ significantly between patients who received tranexamic acid and those who received placebo, despite a reduction in early deaths and serious adverse events. Larger randomised trials are needed to confirm or refute a clinically significant treatment effect.
FUNDING: National Institute of Health Research Health Technology Assessment Programme and Swiss Heart Foundation.
METHODS: The discovery stage of our genome-wide association studies included 4505 cases and 21 968 controls of European, South-Asian, and African ancestry, drawn from 6 studies. In Stage 2, we selected the lead genetic variants at loci with association P<5×10(-6) and performed in silico association analyses in an independent sample of ≤1003 cases and 7745 controls.
RESULTS: One stroke susceptibility locus at 10q25 reached genome-wide significance in the combined analysis of all samples from the discovery and follow-up stages (rs11196288; odds ratio =1.41; P=9.5×10(-9)). The associated locus is in an intergenic region between TCF7L2 and HABP2. In a further analysis in an independent sample, we found that 2 single nucleotide polymorphisms in high linkage disequilibrium with rs11196288 were significantly associated with total plasma factor VII-activating protease levels, a product of HABP2.
CONCLUSIONS: HABP2, which encodes an extracellular serine protease involved in coagulation, fibrinolysis, and inflammatory pathways, may be a genetic susceptibility locus for early-onset stroke.