A comprehensive 1,000 Genomes-based genome-wide association meta-analysis of coronary artery disease
- Nikpay M
- Goel A
- Won HH
- Hall LM
- Willenborg C
- Kanoni S
- Saleheen D
- Kyriakou T
- Nelson CP
- Hopewell JC
- Webb TR
- Zeng L
- Dehghan A
- Alver M
- Armasu SM
- Auro K
- Bjonnes A
- Chasman DI
- Chen S
- Ford I
- Franceschini N
- Gieger C
- Grace C
- Gustafsson S
- Huang J
- Hwang SJ
- Kim YK
- Kleber ME
- Lau KW
- Lu X
- Lu Y
- Lyytikäinen LP
- Mihailov E
- Morrison AC
- Pervjakova N
- Qu L
- Rose LM
- Salfati E
- Saxena R
- Scholz M
- Smith AV
- Tikkanen E
- Uitterlinden A
- Yang X
- Zhang W
- Zhao W
- de Andrade M
- de Vries PS
- van Zuydam NR
- Anand SS
- Bertram L
- Beutner F
- Dedoussis G
- Frossard P
- Gauguier D
- Goodall AH
- Gottesman O
- Haber M
- Han BG
- Huang J
- Jalilzadeh S
- Kessler T
- König IR
- Lannfelt L
- Lieb W
- Lind L
- Lindgren CM
- Lokki ML
- Magnusson PK
- Mallick NH
- Mehra N
- Meitinger T
- Memon FU
- Morris AP
- Nieminen MS
- Pedersen NL
- Peters A
- Rallidis LS
- Rasheed A
- Samuel M
- Shah SH
- Sinisalo J
- Stirrups KE
- Trompet S
- Wang L
- Zaman KS
- Ardissino D
- Boerwinkle E
- Borecki IB
- Bottinger EP
- Buring JE
- Chambers JC
- Collins R
- Cupples LA
- Danesh J
- Demuth I
- Elosua R
- Epstein SE
- Esko T
- Feitosa MF
- Franco OH
- Franzosi MG
- Granger CB
- Gu D
- Gudnason V
- Hall AS
- Hamsten A
- Harris TB
- Hazen SL
- Hengstenberg C
- Hofman A
- Ingelsson E
- Iribarren C
- Jukema JW
- Karhunen PJ
- Kim BJ
- Kooner JS
- Kullo IJ
- Lehtimäki T
- Loos RJ
- Melander O
- Metspalu A
- März W
- Palmer CN
- Perola M
- Quertermous T
- Rader DJ
- Ridker PM
- Ripatti S
- Roberts R
- Salomaa V
- Sanghera DK
- Schwartz SM
- Seedorf U
- Stewart AF
- Stott DJ
- Thiery J
- Zalloua PA
- O'Donnell CJ
- Reilly MP
- Assimes TL
- Thompson JR
- Erdmann J
- ClarkeR
- Watkins H
- Kathiresan S
- McPherson R
- Deloukas P
- Schunkert H
- Samani NJ
- Farrall M
- CARDIoGRAMplusC4D Consortium
DOIAbstract
Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association study (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of similar to 185,000 CAD cases and controls, interrogating 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants. In addition to confirming most known CAD-associated loci, we identified ten new loci (eight additive and two recessive) that contain candidate causal genes newly implicating biological processes in vessel walls. We observed intralocus allelic heterogeneity but little evidence of low-frequency variants with larg...
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