Journal
NATURE GENETICS
Volume 45, Issue 1, Pages 25-U52Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.2480
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Funding
- Merck
- British Heart Foundation (BHF) Centre of Research Excellence
- British Heart Foundation [RG/08/014/24067, RG/09/012/28096, PG/08/094/26019] Funding Source: researchfish
- Medical Research Council [G0700931, MC_CF023241, MC_U137686857, G0801566, G0601261, MC_UU_12015/1, G0601966] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0611-10099, NF-SI-0611-10170, RP-PG-0310-1002] Funding Source: researchfish
- MRC [G0601966, G0601261, G0801566, G0700931, MC_U137686857] Funding Source: UKRI
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Coronary artery disease (CAD) is the commonest cause of death. Here, we report an association analysis in 63,746 CAD cases and 130,681 controls identifying 15 loci reaching genome-wide significance, taking the number of susceptibility loci for CAD to 46, and a further 104 independent variants (r(2) < 0.2) strongly associated with CAD at a 5% false discovery rate (FDR). Together, these variants explain approximately 10.6% of CAD heritability. Of the 46 genome-wide significant lead SNPs, 12 show a significant association with a lipid trait, and 5 show a significant association with blood pressure, but none is significantly associated with diabetes. Network analysis with 233 candidate genes (loci at 10% FDR) generated 5 interaction networks comprising 85% of these putative genes involved in CAD. The four most significant pathways mapping to these networks are linked to lipid metabolism and inflammation, underscoring the causal role of these activities in the genetic etiology of CAD. Our study provides insights into the genetic basis of CAD and identifies key biological pathways.
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