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Meta-analysis identifies six new susceptibility loci for atrial fibrillation
Open accessAbstract
Atrial fibrillation is a highly prevalent arrhythmia and a major risk factor for stroke, heart failure and death. We conducted a genome-wide association study (GWAS) in individuals of European ancestry, including 6,707 with and 52,426 without atrial fibrillation. Six new atrial fibrillation susceptibility loci were identified and replicated in an additional sample of individuals of European ancestry, including 5,381 subjects with and 10,030 subjects without atrial fibrillation (P < 5 × 10(-8)). Four of the loci identified in Europeans were further replicated in silico in a GWAS of Japanese individuals, including 843 individuals with and 3,350 individuals without atrial fibrillation. The identified loci implicate candidate genes that encode transcription factors related to cardiopulmonary development, cardiac-expressed ion channels and cell signaling molecules.
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“The AF-GRS comprised 12 SNPs that had been previously shown to be associated with AF at genome-wide significance.”
From Twelve-single nucleotide polymorphism genetic risk score identifies individuals at increased risk for future atrial fibrillation and stroke (2014) · cites this paper as [23]
In the citing paper
“These are all the SNPs that have been reported to be associated with AF at a genome-wide significance level (P<5×10−8), including 4 SNPs at PITX2 locus.18-23”
From Twelve-single nucleotide polymorphism genetic risk score identifies individuals at increased risk for future atrial fibrillation and stroke (2014) · cites this paper as [23]
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“At the two AF loci previously annotated as SYNPO2L and NEURL (MIM: 603804), both located on chromosome 10, we identified missense variants situated in the genes previously highlighted as putative functional genes for AF (SYNPO2L and NEURL).(11,12) We identified three AF-associated missense SYNPO2L variants (rs34163229…”
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Modeling Human TBX5 Haploinsufficiency Predicts Regulatory Networks for Congenital Heart Disease
Kathiriya, I. S., Rao, K. S., Iacono, G., Devine, W. P., Blair, A. P., Hota, S. K., Lai, M. H., Garay, B. I., Thomas, R., Gong, H. Z., et al. (2021) · Developmental Cell · doi:10.1016/j.devcel.2020.11.020 · Cited by 116
“In addition, an enrichment of chromatin occupancy of TBX5 and cardiac transcription factors is observed near genes associated with EP-GWAS (Table S5) (Pfeufer et al., 2010; Smith et al., 2011; Ellinor et al., 2012; Cordell et al., 2013a; 2013b; Hoed et al., 2013; Hu et al., 2013).”
BackgroundInfluentialAtrial fibrillation from the pathologist’s perspective
Corradi, D. (2013) · Cardiovascular Pathology · doi:10.1016/j.carpath.2013.12.001 · Cited by 119
Tada, H., Shiffman, D., Smith, J. G., Sjögren, M., Lubitz, S. A., Ellinor, P. T., Louie, J. Z., Catanese, J. J., Engström, G., Devlin, J. J., et al. (2014) · Stroke · doi:10.1161/strokeaha.114.006072 · Cited by 110
Self-citationHeritability of Atrial Fibrillation
Weng, L.-C. C., Choi, S. H., Klarin, D. M., Smith, J. G., Loh, P., Chaffin, M. D., Roselli, C., Hulme, O. L., Lunetta, K. L., Dupuis, J., et al. (2017) · Circulation Cardiovascular Genetics · doi:10.1161/circgenetics.117.001838 · Cited by 112
Self-citationVerkerk, A. O., & Wilders, R. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms16023071 · Cited by 107
“It is, therefore, not surprising that the HCN4 locus has been identified as a modulator of heart rate in a genome-wide association study (GWAS) [12] and that reduced HCN4 expression due to endurance exercise is associated with a lower resting heart rate [13].”
BackgroundThe small-molecule BGP-15 protects against heart failure and atrial fibrillation in mice
Sapra, G., Tham, Y. K., Cemerlang, N., Matsumoto, A., Kiriazis, H., Bernardo, B. C., Henstridge, D. C., Ooi, J. Y. Y., Pretorius, L., Boey, E. J. H., et al. (2014) · Nature Communications · doi:10.1038/ncomms6705 · Cited by 107
PITX2 Modulates Atrial Membrane Potential and the Antiarrhythmic Effects of Sodium-Channel Blockers
Syeda, F., Holmes, A. P., Yu, T. Y., Tull, S. P., Kuhlmann, S., Pavlović, D., Betney, D., Riley, G., Kučera, J., Jousset, F., et al. (2016) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2016.07.766 · Cited by 109
Duhme, N., Schweizer, P. A., Thomas, D., Becker, R., Schröter, J., Barends, T. R. M., Schlichting, I., Draguhn, A., Bruehl, C., Katus, H. A., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs391 · Cited by 104
“–8 Moreover, recent studies suggested a contribution of HCN4 dysfunction to atrial and ventricular arrhythmogenesis.(6,8,25,26) Interestingly, in a canine model, atrial tachypacing leads to significant down-regulation of If -current and caused SND, indicating an association between atrial tachyarrhythmia and SAN disea…”
BackgroundNielsen, J. C., Lin, Y., Figueiredo, M. J. D. O., Shamloo, A. S., Alfie, A., Bovéda, S., Dagres, N., Toro, D. D., Eckhardt, L. L., Ellenbogen, K. A., et al. (2020) · Journal of Arrhythmia · doi:10.1002/joa3.12338 · Cited by 106
Nielsen, J. C., Lin, Y.-J., de Oliveira Figueiredo, M. J., Sepehri Shamloo, A., Alfie, A., Boveda, S., Dagres, N., Di Toro, D., Eckhardt, L. L., Ellenbogen, K., et al. (2020) · EP Europace · doi:10.1093/europace/euaa065 · Cited by 98
Atrial fibrillation—a complex polygenetic disease
Andersen, J. H., Andreasen, L., & OLESEN, M. S. (2020) · European Journal of Human Genetics · doi:10.1038/s41431-020-00784-8 · Cited by 100
“The structural proteins encoded by these genes are both expressed in skeletal and cardiac muscle, however it is unknown which of these genes are driving the association [24].”
BackgroundStroke Genetics: A Review and Update
Lindgren, A. G. (2014) · Journal of Stroke · doi:10.5853/jos.2014.16.3.114 · Cited by 93
Genome-wide compendium and functional assessment of in vivo heart enhancers
Dickel, D. E., Barozzi, I., Zhu, Y., Fukuda-Yuzawa, Y., Osterwalder, M., Mannion, B. J., May, D., Spurrell, C. H., Plajzer-Frick, I., Pickle, C. S., et al. (2016) · Nature Communications · doi:10.1038/ncomms12923 · Cited by 93
Identification of atrial fibrillation associated genes and functional non-coding variants
van Ouwerkerk, A. F., Bosada, F. M., van Duijvenboden, K., Hill, M. C., Montefiori, L. E., Scholman, K. T., Liu, J., de Vries, A. A. F., Boukens, B. J., Ellinor, P. T., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-12721-5 · Cited by 94
Self-citationPinho-Gomes, A. C., Reilly, S., Brandes, R. P., & Casadei, B. (2014) · Antioxidants & Redox Signaling · doi:10.1089/ars.2013.5542 · Cited by 94
Genetics of Atrial Fibrillation
Feghaly, J., Zakka, P., London, B., MacRae, C. A., & Refaat, M. M. (2018) · Journal of the American Heart Association · doi:10.1161/jaha.118.009884 · Cited by 96
“Ellinor et al conducted a meta-analysis of SNPs and their association with the development of AF.(105) Although”
MethodGenetics of atrial fibrillation: from families to genomes
Christophersen, I. E., & Ellinor, P. T. (2016) · Journal of Human Genetics · doi:10.1038/jhg.2015.44 · Cited by 92
Self-citationGenetic mechanisms of atrial fibrillation: impact on response to treatment
Darbar, D., & Roden, D. M. (2013) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2013.53 · Cited by 93
Self-citationvon der Heyde, B., Emmanouilidou, A., Mazzaferro, E., Vicenzi, S., Höijer, I., Klingström, T., Jumaa, S., Dethlefsen, O., Snieder, H., de Geus, E. J. C., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-68567-1 · Cited by 92
Parvez, B., Shoemaker, M. B., Muhammad, R., Richardson, R., Jiang, L., Blair, M. A., Roden, D. M., & Darbar, D. (2013) · Heart Rhythm · doi:10.1016/j.hrthm.2013.02.018 · Cited by 94
“Recent genome-wide association studies have identified numerous common polymorphisms associated with both lone and typical AF.8 The 3 loci most strongly associated with AF occur on chromosomes 4q25 (near PITX2),9 16q22 (in ZFHX3),10 and 1q21 (in KCNN3).11 These findings indicate that variable mechanisms contribute to…”
InfluentialSelf-citationKirchhof, P. F., Medicine, E. C. R. A. E. A. W. S. O. P., Sipido, K. R., Medicine, E. C. R. A. E. A. W. S. O. P., Cowie, M., Medicine, E. C. R. A. E. A. W. S. O. P., Eschenhagen, T., Medicine, E. C. R. A. E. A. W. S. O. P., Fox, K. A. A., Medicine, E. C. R. A. E. A. W. S. O. P., et al. (2014) · European Heart Journal · doi:10.1093/eurheartj/ehu312 · Cited by 93
van Setten, J., Brody, J. A., Jamshidi, Y., Swenson, B. R., Butler, A. M., Campbell, H., Fabiola Del Greco, M., Evans, D. S., Gibson, Q., Gudbjartsson, D. F., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-04766-9 · Cited by 87
Self-citationMcManus, D. D., Lin, H., Tanrıverdi, K., Quercio, M., Yin, X., Larson, M. G., Ellinor, P. T., Levy, D. A., Freedman, J. E., & Benjamin, E. J. (2014) · Heart Rhythm · doi:10.1016/j.hrthm.2014.01.018 · Cited by 91
Self-citationZhang, X.-D., Timofeyev, V., Li, N., Myers, R. E., Zhang, D., Singapuri, A., Lau, V. C., Bond, C. T., Adelman, J. P., Lieu, D. K., et al. (2013) · Cardiovascular Research · doi:10.1093/cvr/cvt262 · Cited by 86
Atrial Fibrillation Mechanisms and Implications for Catheter Ablation
Cheniti, G., Vlachos, K. G., Pambrun, T., Hooks, D. A., Frontera, A., Takigawa, M., Bourier, F. J., Kitamura, Τ., Lam, A., Martin, C., et al. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.01458 · Cited by 87
“The majority of mutations underlying AF affect genes that encode transcription factors related to cardiopulmonary development, cardiac-expressed ion channels and cell signaling molecules (Roberts and Gollob, 2010, 2014; Ellinor et al., 2012).”
BackgroundAtrial Fibrillation and Endothelial Dysfunction
Corban, M., Toya, T., Ahmad, A., Lerman, L. O., Lee, H.-C., & Lerman, A. (2021) · Mayo Clinic Proceedings · doi:10.1016/j.mayocp.2020.11.005 · Cited by 87
Aberrant sodium influx causes cardiomyopathy and atrial fibrillation in mice
Wan, E. Y., Abrams, J., Weinberg, R. L., Katchman, A. N., Bayne, J., Zakharov, S. I., Yang, L., Morrow, J., Garan, H., & Marx, S. O. (2015) · Journal of Clinical Investigation · doi:10.1172/jci84669 · Cited by 84
“There is also an important component of genetic susceptibility, shown by recent genome-wide association studies and identification of relatively rare mutants in K + and Na + channels and ryanodine receptors (3–5).”
Pitx2 impairs calcium handling in a dose-dependent manner by modulating Wnt signalling
Lozano-Velasco, E., Hernández‐Torres, F., Daimi, H., Serra, S. A., Herraiz, A., Hove‐Madsen, L., Aránega, A. E., & Franco, D. (2015) · Cardiovascular Research · doi:10.1093/cvr/cvv207 · Cited by 83
A Missense Variant in PLEC Increases Risk of Atrial Fibrillation
Þórólfsdóttir, R. B., Sveinbjörnsson, G., Sulem, P., Helgadóttir, A., Grétarsdóttir, S., Benónísdóttir, S., Magnusdottir, A., Davidsson, O. B., Rajamani, S., Roden, D. M., et al. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.09.005 · Cited by 77
“Variant rs72700114 is located 400 kb from a previously reported AF locus, represented by rs651386, close to PRRX1 (Figure 1B) (9).”
InfluentialSelf-citationEpigenetic and Transcriptional Networks Underlying Atrial Fibrillation
van Ouwerkerk, A. F., Hall, A. W., Kadow, Z. A., Lazarevic, S., Reyat, J. S., Tucker, N. R., Nadadur, R. D., Bosada, F. M., Bianchi, V., Ellinor, P. T., et al. (2020) · Circulation Research · doi:10.1161/circresaha.120.316574 · Cited by 79
Self-citationGenetics of Atrial Fibrillation: State of the Art in 2017
Fatkin, D., Santiago, C. F., Huttner, I. G., Lubitz, S. A., & Ellinor, P. T. (2017) · Heart Lung and Circulation · doi:10.1016/j.hlc.2017.04.008 · Cited by 74
Self-citationDiness, J. G., Skibsbye, L., Simó‐Vicens, R., Santos, J. L., Lundegaard, P. R., Citerni, C., Sauter, D. R. P., Bomholtz, S. H., Svendsen, J. H., Olesen, S., et al. (2017) · Circulation Arrhythmia and Electrophysiology · doi:10.1161/circep.117.005125 · Cited by 74
A Functional Variant Associated with Atrial Fibrillation Regulates PITX2c Expression through TFAP2a
Ye, J., Tucker, N. R., Weng, L.-C. C., Clauß, S., Lubitz, S. A., & Ellinor, P. T. (2016) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2016.10.001 · Cited by 77
“To date, at least four independent AF-associated regions at the 4q25 locus are adjacent to the transcription-factorencoding gene PITX2 (MIM: 601542).8,9 Three isoforms of PITX2 (PITX2a, PITX2b, and PITX2c) have been identified in mammals,11 and PITX2c is the dominant isoform in the developing and adult left atrium.12…”
BackgroundInfluentialSelf-citationLee, J.-Y., Kim, T., Yang, P., Lim, H. E., Choi, E., Shim, J., Shin, E., Uhm, J., Kim, J. S., Joung, B., et al. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx213 · Cited by 75
“Although several studies have replicated these identified loci in Asian populations, some studies showed weak or no association with AF due to different allele frequencies and linkage disequilibrium (LD) patterns compared with European ancestry.(10,15,16) The purposes of this study were to: (1) examine previously iden…”
ResultAtrial fibrillation: pathophysiology, genetic and epigenetic mechanisms
Vinciguerra, M., Dobrev, D., & Nattel, S. (2024) · The Lancet Regional Health - Europe · doi:10.1016/j.lanepe.2023.100785 · Cited by 81
A novel trafficking-defective HCN4 mutation is associated with early-onset atrial fibrillation
Macri, V., Mahida, S., Zhang, M. L., Sinner, M. F., Dolmatova, E. V., Tucker, N. R., McLellan, M. A., Shea, M. A., Milan, D. J., Lunetta, K. L., et al. (2014) · Heart Rhythm · doi:10.1016/j.hrthm.2014.03.002 · Cited by 73
Self-citationBiological significance of miR-126 expression in atrial fibrillation and heart failure
Wei, X. J., Han, M., Yang, F. Y., Wei, G., Liang, Z. G., Yao, H., Ji, C., Xie, R. S., Gong, C., & Tian, Y. (2015) · Brazilian Journal of Medical and Biological Research · doi:10.1590/1414-431x20154590 · Cited by 72
“In addition, abundant epidemiological data have indicated endogenous causes in the development of AF/HF, indicating that genetics may contribute to the onset of these diseases (9,10).”
BackgroundPITX2‐dependent gene regulation in atrial fibrillation and rhythm control
Syeda, F., Kirchhof, P. F., & Fabritz, L. (2017) · The Journal of Physiology · doi:10.1113/jp273123 · Cited by 74
Liang, B., Soka, M. J., Christensen, A. H., OLESEN, M. S., Larsen, A. P., Knop, F. K., Wang, F., Nielsen, J. B., Andersen, M. N., Humphreys, D. T., et al. (2014) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2013.12.014 · Cited by 71
Genome-Wide Association Studies of Hypertension and Several Other Cardiovascular Diseases
Wang, Y., & Wang, J. (2018) · Pulse · doi:10.1159/000496150 · Cited by 71
Aging and cardiovascular diseases: the role of gene-diet interactions
Corella, D., & Ordovás, J. M. (2014) · Ageing Research Reviews · doi:10.1016/j.arr.2014.08.002 · Cited by 83
Long-range Pitx2c enhancer–promoter interactions prevent predisposition to atrial fibrillation
Zhang, M., Hill, M. C., Kadow, Z. A., Suh, J. H., Tucker, N. R., Hall, A. W., Tran, T. T., Swinton, P. S., Leach, J. P., Margulies, K. B., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1907418116 · Cited by 72
Self-citation
Metadata
- Authors
- Ellinor, P. T., Lunetta, K. L., Albert, C. M., Glazer, N. L., Ritchie, M. D., Smith, A. V., Arking, D. E., Müller-Nurasyid, M., Krijthe, B. P., Lubitz, S. A., Bis, J. C., Chung, M. K., Dörr, M., Ozaki, K., Roberts, J. D., Smith, J. G., Pfeufer, A., Sinner, M. F., Lohman, K., Ding, J., Smith, N. L., Smith, J. D., Rienstra, M., Rice, K. M., Van Wagoner, D. R., Magnani, J. W., Wakili, R., Clauss, S., Rotter, J. I., Steinbeck, G., Launer, L. J., Davies, R. W., Borkovich, M., Harris, T. B., Lin, H., Völker, U., Völzke, H., Milan, D. J., Hofman, A., Boerwinkle, E., Chen, L. Y., Soliman, E. Z., Voight, B. F., Li, G., Chakravarti, A., Kubo, M., Tedrow, U. B., Rose, L. M., Ridker, P. M., Conen, D., Tsunoda, T., Furukawa, T., Sotoodehnia, N., Xu, S., Kamatani, N., Levy, D., Nakamura, Y., Parvez, B., Mahida, S., Furie, K. L., Rosand, J., Muhammad, R., Psaty, B. M., Meitinger, T., Perz, S., Wichmann, H.-E., Witteman, J. C. M., Kao, W. H. L., Kathiresan, S., Roden, D. M., Uitterlinden, A. G., Rivadeneira, F., McKnight, B., Sjögren, M., Newman, A. B., Liu, Y., Gollob, M. H., Melander, O., Tanaka, T., Stricker, B. H. C., Felix, S. B., Alonso, A., Darbar, D., Barnard, J., Chasman, D. I., Heckbert, S. R., Benjamin, E. J., Gudnason, V., & Kääb, S.
- Affiliations
- Massachusetts General Hospital (US)
- Boston University (US)
- Brigham and Women's Hospital (US)
- University of Washington (US)
- Pennsylvania State University (US)
- University of Iceland (IS)
- Johns Hopkins University (US)
- Erasmus MC (NL)
- Cleveland Clinic (US)
- Universität Greifswald (DE)
- RIKEN (JP)
- Ottawa Heart Institute (CA)
- Broad Institute (US)
- TUM Klinikum (DE)
- Wake Forest University Health Sciences (US)
- Group Health Cooperative (US)
- University Medical Center Groningen (NL)
- Ludwig-Maximilians-Universität München (DE)
- Cedars-Sinai Medical Center (US)
- National Institutes of Health (US)
- The University of Texas Health Science Center at Houston (US)
- University of Minnesota (US)
- University Hospital of Basel (CH)
- Tokyo Medical and Dental University (JP)
- Institute of Medical Science, The University of Tokyo (JP)
- Vanderbilt University (US)
- Harvard University (US)
- Helmholtz Munich (DE)
- München Klinik (DE)
- Lund University (SE)
- University of Pittsburgh (US)
- Corresponding author
- Ellinor, Patrick T
- Kääb, Stefan
- ORCID
- Ellinor, Patrick T
- Lunetta, Kathryn L
- Albert, Christine M
- Glazer, Nicole L
- Ritchie, Marylyn D
- Smith, Albert V
- Arking, Dan E
- Lubitz, Steven A
- Bis, Joshua C
- Chung, Mina K
- Dörr, Marcus
- Ozaki, Kouichi
- Roberts, Jason D
- Sinner, Moritz F
- Ding, Jingzhong
- Smith, Nicholas L
- Smith, Jonathan D
- Rienstra, Michiel
- Rice, Kenneth M
- Magnani, Jared W
- Wakili, Reza
- Clauss, Sebastian
- Rotter, Jerome I
- Steinbeck, Gerhard
- Launer, Lenore J
- Harris, Tamara B
- Lin, Honghuang
- Völker, Uwe
- Völzke, Henry
- Milan, David J
- Boerwinkle, Eric
- Chen, Lin Y
- Soliman, Elsayed Z
- Voight, Benjamin F
- Chakravarti, Aravinda
- Kubo, Michiaki
- Tedrow, Usha B
- Rose, Lynda M
- Ridker, Paul M
- Conen, David
- Tsunoda, Tatsuhiko
- Furukawa, Tetsushi
- Kamatani, Naoyuki
- Levy, Daniel
- Nakamura, Yusuke
- Mahida, Saagar
- Furie, Karen L
- Rosand, Jonathan
- Psaty, Bruce M
- Meitinger, Thomas
- Wichmann, H-Erich
- Kao, W H Linda
- Kathiresan, Sekar
- Roden, Dan M
- Rivadeneira, Fernando
- Newman, Anne B
- Liu, Yongmei
- Gollob, Michael H
- Melander, Olle
- Tanaka, Toshihiro
- Stricker, Bruno H Ch
- Felix, Stephan B
- Darbar, Dawood
- Barnard, John
- Chasman, Daniel I
- Heckbert, Susan R
- Benjamin, Emelia J
- Gudnason, Vilmundur
- Kääb, Stefan
- Venue
- Nature Genetics
- Published
- 2012-04-29
- Volume
- 44
- Issue
- 6
- Pages
- 670-675
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- PMC
- PMC3366038
- OpenAlex
- W2149665587
- Cited by
- 601
- References
- 32
- Citations by year
- 2026: 17 · 2025: 20 · 2024: 28 · 2023: 25 · 2022: 19 · 2021: 33 · 2020: 53 · 2019: 35 · 2018: 41 · 2017: 64 · 2016: 62 · 2015: 56 · 2014: 61 · 2013: 64 · 2012: 22
- FWCI
- 41.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Site cant be reached (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000124)
- Japan Society for the Promotion of Science (23390205, 23659413)
- National Heart, Lung, and Blood Institute (U19HL065962, L30 HL097675, R01HL104156, R01HL092217, R01HL105756, R01HL090620, K24HL105780, R21HL106092)
- National Institute on Drug Abuse (R21DA027021)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Atrial Fibrillation Management and Outcomes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- atrial fibrillation, genetic susceptibility loci, genome-wide association study, European ancestry, transcription factors, cardiac ion channels, signaling molecules, cardiac arrhythmias
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Atrial Fibrillation, Child, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Male, Middle Aged, Risk Factors, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, White People, Asian People, Genome-Wide Association Study, Young Adult, Genetic Loci
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