An integrated polygenic tool substantially enhances coronary artery disease prediction

Summary-level CAD GWAS data generated by Genomics plc as presented in:

Riveros-Mckay F. et al. An integrated polygenic tool substantially enhances coronary artery disease prediction. Circulation: Genomics and Precision Medicine (in press). 

If you have any questions or comments regarding these files, please contact Genomics plc at [e-mail]

NOTES
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These analyses were carried out using the full UK Biobank imputation data release (v3b). Analyses were restricted to a subset of UK Biobank, described as “Group I” in the published paper.  Group I, “no PCE/QRISK3 available”, included 114,196 European-ancestry individuals with missing data that prevented PCE or QRISK3 calculation.

CAD case phenotypes were defined as described in the “Phenotype definitions” section of the paper’s Supplementary Materials, using both prevalent (pre-baseline) and incident (post-baseline) events.

All analyses included Age at assessment, sex, genotyping chip, and 10 principal components as covariates. 

We used plink2.0 logistic regression. For chromosome X variants males were treated as having 0 or 2 alternative alleles. 

The results are not adjusted for genomic control.

DATA FILE CONTENT DESCRIPTION
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cpra Variant ID in ‘CPRA’ format. Position reflects position in b37. 
chrom Chromosome
pos Position in base pairs (b37, 1-based)
alt Alternative allele (effect allele)
beta Effect size (log odds ratio)
standard_error Standard error of beta 
minus_log10_p Minus log(base 10) of P-value
ref Reference allele (non-effect allele)
ncase Number of cases
ncontrol Number of controls