Genetic Predisposition to Coronary Artery Disease in Type 2 diabetes
van Zuydam NR., Ladenvall C., Voight BF., Strawbridge RJ., Fernandez Tajes J., Rayner NW., Robertson NR., Mahajan A., Vlachopoulou E., Goel A., Kleber ME., Nelson CP., Kwee LC., Esko T., Mihailov E., Mägi R., Milani L., Fischer K., Kanoni S., Kumar J., Song C., Hartiala JA., Pedersen NL., Perola M., Gieger C., Peters A., Qu L., Willems SM., Doney ASF., Morris AD., Zheng Y., Sesti G., Hu FB., Qi L., Laakso M., Thorsteinsdottir U., Grallert H., van Duijn C., Reilly MP., Ingelsson E., Deloukas P., Kathiresan S., Metspalu A., Shah SH., Sinisalo J., Salomaa V., Hamsten A., Samani NJ., März W., Hazen SL., Watkins H., Saleheen D., Morris AP., Colhoun HM., Groop L., McCarthy MI., Palmer CNA.
<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>