TY - JOUR
T1 - Common-variant and rare-variant genetic architecture of heart failure across the allele-frequency spectrum
AU - Penn Medicine BioBank
AU - Lee, David S.M.
AU - Cardone, Kathleen M.
AU - Zhang, David Y.
AU - Tsao, Noah L.
AU - Abramowitz, Sarah
AU - Sharma, Pranav
AU - DePaolo, John S.
AU - Conery, Mitchell
AU - Aragam, Krishna G.
AU - Biddinger, Kiran
AU - Dilitikas, Ozan
AU - Hoffman-Andrews, Lily
AU - Judy, Renae L.
AU - Khan, Atlas
AU - Kullo, Iftikhar J.
AU - Puckelwartz, Megan J.
AU - Reza, Nosheen
AU - Satterfield, Benjamin A.
AU - Singhal, Pankhuri
AU - Drivas, Theodore
AU - Verma, Shefali S.
AU - Verma, Anurag
AU - Sirugo, Giorgio
AU - Arany, Zoltan
AU - Cappola, Thomas P.
AU - Carruth, Eric D.
AU - Day, Sharlene M.
AU - Do, Ron
AU - Haggerty, Christopher M.
AU - Joseph, Jacob
AU - McNally, Elizabeth M.
AU - Nadkarni, Girish
AU - Owens, Anjali T.
AU - Rader, Daniel J.
AU - Ritchie, Marylyn D.
AU - Sun, Yan V.
AU - Voight, Benjamin F.
AU - Levin, Michael G.
AU - Damrauer, Scott M.
N1 - Publisher Copyright:
© This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2025.
PY - 2025/4
Y1 - 2025/4
N2 - Heart failure is a complex trait, influenced by environmental and genetic factors, affecting over 30 million individuals worldwide. Here we report common-variant and rare-variant association studies of all-cause heart failure and examine how different classes of genetic variation impact its heritability. We identify 176 common-variant risk loci at genome-wide significance in 2,358,556 individuals and cluster these signals into five broad modules based on pleiotropic associations with anthropomorphic traits/obesity, blood pressure/renal function, atherosclerosis/lipids, immune activity and arrhythmias. In parallel, we uncover exome-wide significant associations for heart failure and rare predicted loss-of-function variants in TTN, MYBPC3, FLNC and BAG3 using exome sequencing of 376,334 individuals. We find that total burden heritability of rare coding variants is highly concentrated in a small set of Mendelian cardiomyopathy genes, while common-variant heritability is diffusely spread throughout the genome. Finally, we show that common-variant background modifies heart failure risk among carriers of rare pathogenic truncating variants in TTN. Together, these findings discern genetic links between dysregulated metabolism and heart failure and highlight a polygenic component to heart failure not captured by current clinical genetic testing.
AB - Heart failure is a complex trait, influenced by environmental and genetic factors, affecting over 30 million individuals worldwide. Here we report common-variant and rare-variant association studies of all-cause heart failure and examine how different classes of genetic variation impact its heritability. We identify 176 common-variant risk loci at genome-wide significance in 2,358,556 individuals and cluster these signals into five broad modules based on pleiotropic associations with anthropomorphic traits/obesity, blood pressure/renal function, atherosclerosis/lipids, immune activity and arrhythmias. In parallel, we uncover exome-wide significant associations for heart failure and rare predicted loss-of-function variants in TTN, MYBPC3, FLNC and BAG3 using exome sequencing of 376,334 individuals. We find that total burden heritability of rare coding variants is highly concentrated in a small set of Mendelian cardiomyopathy genes, while common-variant heritability is diffusely spread throughout the genome. Finally, we show that common-variant background modifies heart failure risk among carriers of rare pathogenic truncating variants in TTN. Together, these findings discern genetic links between dysregulated metabolism and heart failure and highlight a polygenic component to heart failure not captured by current clinical genetic testing.
UR - https://www.scopus.com/pages/publications/105002472482
U2 - 10.1038/s41588-025-02140-2
DO - 10.1038/s41588-025-02140-2
M3 - Article
AN - SCOPUS:105002472482
SN - 1061-4036
VL - 57
SP - 829
EP - 838
JO - Nature Genetics
JF - Nature Genetics
IS - 4
M1 - 163
ER -