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<jats:p> <jats:bold>Background</jats:bold> - Coronary artery disease (CAD) is accelerated in subjects with type 2 diabetes (T2D). </jats:p> <jats:p> <jats:bold>Methods</jats:bold> - To test whether this reflects differential genetic influences on CAD-risk in subjects with T2D, we performed a systematic assessment of genetic overlap between CAD and T2D in 66,643 subjects (27,708 with CAD and 24,259 with T2D). Variants showing apparent association with CAD in stratified analyses and/or evidence of interaction were evaluated in a further 117,787 subjects (16,694 with CAD and 11,537 with T2D). </jats:p> <jats:p> <jats:bold>Results</jats:bold> - None of the previously characterised CAD loci was found to have specific effects on CAD in T2D individuals and a genome-wide interaction analysis found no new variants for CAD that could be considered T2D specific. When we considered the overall genetic correlations between CAD and its risk factors, we found no substantial differences in these relationships by T2D background. </jats:p> <jats:p> <jats:bold>Conclusions</jats:bold> - This study found no evidence that the genetic architecture of CAD differs in those with T2D compared to those without T2D. </jats:p>

Original publication

DOI

10.1161/circgen.119.002769

Type

Journal article

Journal

Circulation: Genomic and Precision Medicine

Publisher

Ovid Technologies (Wolters Kluwer Health)

Publication Date

13/08/2020