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

Albert Henry, Xiaodong Mo, Chris Finan, Mark D. Chaffin, Doug Speed, Hanane Issa, Spiros Denaxas, James S. Ware, Sean L. Zheng, Anders Malarstig, Jasmine Gratton, Isabelle Bond, Carolina Roselli, David Miller, Sandesh Chopade, A. Floriaan Schmidt, Erik Abner, Lance Adams, Charlotte Andersson, Krishna G. AragamJohan Ärnlöv, Geraldine Asselin, Anna Axelsson Raja, Joshua D. Backman, Traci M. Bartz, Kiran J. Biddinger, Mary L. Biggs, Heather L. Bloom, Eric Boersma, Jeffrey Brandimarto, Michael R. Brown, Søren Brunak, Mie Topholm Bruun, Leonard Buckbinder, Henning Bundgaard, David J. Carey, Daniel I. Chasman, Xing Chen, James P. Cook, Tomasz Czuba, Simon de Denus, Abbas Dehghan, Graciela E. Delgado, Alexander S. Doney, Marcus Dörr, Vinicius Tragante, Pim van der Harst, Jessica van Setten, Marion van Vugt, Folkert W. Asselbergs, , , ,

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

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.

Original languageEnglish
Article number163
Pages (from-to)815-828
Number of pages14
JournalNature genetics
Volume57
Issue number4
DOIs
Publication statusPublished - Apr 2025

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