https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Genetic risk factors for ischaemic stroke and its subtypes (the METASTROKE Collaboration): a meta-analysis of genome-wide association studies https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:18827 Wed 11 Apr 2018 13:01:16 AEST ]]> 17q25 Locus is associated with white matter hyperintensity volume in ischemic stroke, but not with lacunar stroke status https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:13946 Wed 11 Apr 2018 09:27:26 AEST ]]> Genome-wide association study identifies a variant in HDAC9 associated with large vessel ischemic stroke https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25277 −11; odds ratio (OR) = 1.42, 95% confidence interval (CI) = 1.28–1.57). All four loci exhibited evidence for heterogeneity of effect across the stroke subtypes, with some and possibly all affecting risk for only one subtype. This suggests distinct genetic architectures for different stroke subtypes.]]> Sat 24 Mar 2018 07:38:17 AEDT ]]> Relative effects of LDL-C on ischemic stroke and coronary disease: a Mendelian randomization study https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42483 p = 1.1 x 10−8). By contrast, the causal effect of LDL-C was much weaker for IS (OR 1.12, 95% CI 0.96−1.30, p = 0.14; p for heterogeneity = 2.6 x 10−3) and, in particular, for cardioembolic stroke (OR 1.06, 95% CI 0.84−1.33, p = 0.64; p for heterogeneity = 8.6 x 10−3) when compared with that for CHD. Conclusions: In contrast with the consistent effects of LDL-C-lowering therapies on IS and CHD, genetic variants that confer lifelong LDL-C differences show a weaker effect on IS than on CHD. The relevance of etiologically distinct IS subtypes may contribute to the differences observed.]]> Fri 26 Aug 2022 13:56:54 AEST ]]>