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GWAS Study

Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes.

Henry A, Mo X, Finan C et al.

40038546 PubMed ID
GWAS Study Type
1968806 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

HA
Henry A
MX
Mo X
FC
Finan C
CM
Chaffin MD
SD
Speed D
IH
Issa H
DS
Denaxas S
WJ
Ware JS
ZS
Zheng SL
MA
Malarstig A
GJ
Gratton J
BI
Bond I
RC
Roselli C
MD
Miller D
CS
Chopade S
SA
Schmidt AF
AE
Abner E
AL
Adams L
AC
Andersson C
AK
Aragam KG
ÄJ
Ärnlöv J
AG
Asselin G
RA
Raja AA
BJ
Backman JD
BT
Bartz TM
BK
Biddinger KJ
BM
Biggs ML
BH
Bloom HL
BE
Boersma E
BJ
Brandimarto J
BM
Brown MR
BS
Brunak S
BM
Bruun MT
BL
Buckbinder L
BH
Bundgaard H
CD
Carey DJ
CD
Chasman DI
CX
Chen X
CJ
Cook JP
CT
Czuba T
DD
de Denus S
DA
Dehghan A
DG
Delgado GE
DA
Doney AS
DM
Dörr M
DJ
Dowsett J
DS
Dudley SC
EG
Engström G
EC
Erikstrup C
ET
Esko T
FE
Farber-Eger EH
FS
Felix SB
FS
Finer S
FI
Ford I
GM
Ghanbari M
GS
Ghasemi S
GJ
Ghouse J
GV
Giedraitis V
GF
Giulianini F
GJ
Gottdiener JS
GS
Gross S
GD
Guðbjartsson DF
GH
Gui H
GR
Gutmann R
HS
Hägg S
HC
Haggerty CM
Hedman ÅK
HA
Helgadottir A
HH
Hemingway H
HH
Hillege H
HC
Hyde CL
AJ
Aagaard Jensen B
JJ
Jukema JW
KI
Kardys I
KR
Karra R
KM
Kavousi M
KJ
Kizer JR
KM
Kleber ME
KL
Køber L
KA
Koekemoer A
KK
Kuchenbaecker K
LY
Lai YP
LD
Lanfear D
LC
Langenberg C
LH
Lin H
LL
Lind L
LC
Lindgren CM
LP
Liu PP
LB
London B
LB
Lowery BD
LJ
Luan J
LS
Lubitz SA
MP
Magnusson P
MK
Margulies KB
MN
Marston NA
MH
Martin H
MW
März W
MO
Melander O
MI
Mordi IR
MM
Morley MP
MA
Morris AP
MA
Morrison AC
ML
Morton L
NM
Nagle MW
NC
Nelson CP
NA
Niessner A
NT
Niiranen T
NR
Noordam R
NC
Nowak C
OM
O'Donoghue ML
OS
Ostrowski SR
OA
Owens AT
PC
Palmer CNA
PG
Paré G
PO
Pedersen OB
PM
Perola M
PM
Pigeyre M
PB
Psaty BM
RK
Rice KM
RP
Ridker PM
RS
Romaine SPR
RJ
Rotter JI
RC
Ruff CT
SM
Sabatine MS
SN
Sallah N
SV
Salomaa V
SN
Sattar N
SA
Shalaby AA
SA
Shekhar A
SD
Smelser DT
SN
Smith NL
SE
Sørensen E
SS
Srinivasan S
SK
Stefansson K
SG
Sveinbjörnsson G
SP
Svensson P
TM
Tammesoo ML
TJ
Tardif JC
TM
Teder-Laving M
TA
Teumer A
TG
Thorgeirsson G
TU
Thorsteinsdottir U
TC
Torp-Pedersen C
TV
Tragante V
TS
Trompet S
UA
Uitterlinden AG
UH
Ullum H
VD
van der Harst P
VH
van Heel D
VS
van Setten J
VV
van Vugt M
VA
Veluchamy A
VM
Verschuuren M
VN
Verweij N
VC
Vissing CR
VU
Völker U
VA
Voors AA
WL
Wallentin L
WY
Wang Y
WP
Weeke PE
WK
Wiggins KL
WL
Williams LK
YY
Yang Y
YB
Yu B
ZF
Zannad F
ZC
Zheng C
AF
Asselbergs FW
CT
Cappola TP
DM
Dubé MP
DM
Dunn ME
LC
Lang CC
SN
Samani NJ
SS
Shah S
VR
Vasan RS
SJ
Smith JG
HH
Holm H
SS
Shah S
EP
Ellinor PT
HA
Hingorani AD
WQ
Wells Q
LR
Lumbers RT
Chapter II

Abstract

Summary of the research findings

Heart failure (HF) is a major contributor to global morbidity and mortality. While distinct clinical subtypes, defined by etiology and left ventricular ejection fraction, are well recognized, their genetic determinants remain inadequately understood. In this study, we report a genome-wide association study of HF and its subtypes in a sample of 1.9 million individuals. A total of 153,174 individuals had HF, of whom 44,012 had a nonischemic etiology (ni-HF). A subset of patients with ni-HF were stratified based on left ventricular systolic function, where data were available, identifying 5,406 individuals with reduced ejection fraction and 3,841 with preserved ejection fraction. We identify 66 genetic loci associated with HF and its subtypes, 37 of which have not previously been reported. Using functionally informed gene prioritization methods, we predict effector genes for each identified locus, and map these to etiologic disease clusters through phenome-wide association analysis, network analysis and colocalization. Through heritability enrichment analysis, we highlight the role of extracardiac tissues in disease etiology. We then examine the differential associations of upstream risk factors with HF subtypes using Mendelian randomization. These findings extend our understanding of the mechanisms underlying HF etiology and may inform future approaches to prevention and treatment.

139,533 European ancestry cases, 1,568,809 European ancestry controls, 9,413 East Asian ancestry cases, 203,040 East Asian ancestry controls, 3,292 African ancestry cases, 13,574 African ancestry controls, 779 South Asian ancestry cases, 28,150 South Asian ancestry controls, 157 Admixed American ancestry cases, 2,059 Admixed American ancestry controls

Chapter III

Study Statistics

Key metrics and study information

1968806
Total Participants
GWAS
Study Type
No
Replicated
European, East Asian, African unspecified, South Asian, Hispanic or Latin American
Ancestry
Canada, Netherlands, Sweden, U.S., Republic of Ireland, Denmark, U.K., Germany, Iceland, Estonia, Japan
Recruitment Country
Chapter IV

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