http://researchonline.federation.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10162 Wed 07 Apr 2021 13:55:29 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5099 Wed 07 Apr 2021 13:44:43 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:4526 Wed 07 Apr 2021 13:43:59 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:2136 = 0.1) single nucleotide polymorphisms in LRP6 were genotyped in 703 individuals from 213 Polish pedigrees (Silesian Cardiovascular Study families). The family-based analysis revealed that the minor allele of rs10845493 clustered with elevated LDL-C in offspring more frequently than expected by chance (P=0.0053). The quantitative analysis restricted to subjects free of lipid-lowering treatment confirmed the association between rs10845493 and age-, sex-, and BMI-adjusted circulating levels of LDL-C in families as well as 2 additional populations - 218 unrelated subjects from Silesian Cardiovascular Study replication panel and 1138 individuals from Young Men Cardiovascular Association cohort (P=0.0268, P=0.0476, and P=0.0472, respectively). In the inverse variance weighted meta-analysis of the 3 populations each extra minor allele copy of rs10845493 was associated with 0.14 mmol/L increase in age-, sex-, and BMI-adjusted LDL-C (SE=0.05, P=0.0038). Conclusions-Common polymorphism in the gene underlying monogenic form of coronary artery disease impacts on risk of LDL-C elevation. (Arterioscler Thromb Vasc Biol. 2009;29:1316-1321.)]]> Wed 07 Apr 2021 13:33:12 AEST ]]>