TY - JOUR
T1 - Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes
AU - Henry, Albert
AU - Mo, Xiaodong
AU - Finan, Chris
AU - Chaffin, Mark D.
AU - Speed, Doug
AU - Issa, Hanane
AU - Denaxas, Spiros
AU - Ware, James S.
AU - Zheng, Sean L.
AU - Malarstig, Anders
AU - Gratton, Jasmine
AU - Bond, Isabelle
AU - Roselli, Carolina
AU - Miller, David
AU - Chopade, Sandesh
AU - Schmidt, A. Floriaan
AU - Abner, Erik
AU - Adams, Lance
AU - Andersson, Charlotte
AU - Aragam, Krishna G.
AU - Ärnlöv, Johan
AU - Asselin, Geraldine
AU - Raja, Anna Axelsson
AU - Backman, Joshua D.
AU - Bartz, Traci M.
AU - Biddinger, Kiran J.
AU - Biggs, Mary L.
AU - Bloom, Heather L.
AU - Boersma, Eric
AU - Brandimarto, Jeffrey
AU - Brown, Michael R.
AU - Brunak, Søren
AU - Bruun, Mie Topholm
AU - Buckbinder, Leonard
AU - Bundgaard, Henning
AU - Carey, David J.
AU - Chasman, Daniel I.
AU - Chen, Xing
AU - Cook, James P.
AU - Dowsett, Joseph
AU - Ghouse, Jonas
AU - Køber, Lars
AU - Lind, Lars
AU - Ostrowski, Sisse Rye
AU - Pedersen, Ole Birger
AU - Sørensen, Erik
AU - Torp-Pedersen, Christian
AU - Ullum, Henrik
AU - Vissing, Christoffer Rasmus
AU - Zheng, Chaoqun
AU - Genes & Health Research Team
AU - Estonian Biobank Research Team
AU - DBDS Genomic Consortium
AU - HERMES Consortium
N1 - Publisher Copyright:
© The Author(s) 2025.
PY - 2025
Y1 - 2025
N2 - 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.
AB - 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.
U2 - 10.1038/s41588-024-02064-3
DO - 10.1038/s41588-024-02064-3
M3 - Journal article
C2 - 40038546
AN - SCOPUS:105003400740
SN - 1061-4036
VL - 57
SP - 815
EP - 828
JO - Nature Genetics
JF - Nature Genetics
IS - 4
ER -