Genome-wide analysis identifies novel susceptibility loci for myocardial infarction

While most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI. We sought to address the hypothesis that some of the genetic factors which establish atherosclerosis may be distinct from those that predispos...

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Published inEuropean heart journal Vol. 42; no. 9; pp. 919 - 933
Main Authors Hartiala, Jaana A, Han, Yi, Jia, Qiong, Hilser, James R, Huang, Pin, Gukasyan, Janet, Schwartzman, William S, Cai, Zhiheng, Biswas, Subarna, Trégouët, David-Alexandre, Smith, Nicholas L, Seldin, Marcus, Pan, Calvin, Mehrabian, Margarete, Lusis, Aldons J, Bazeley, Peter, Sun, Yan V, Liu, Chang, Quyyumi, Arshed A, Scholz, Markus, Thiery, Joachim, Delgado, Graciela E, Kleber, Marcus E, März, Winfried, Howe, Laurence J, Asselbergs, Folkert W, van Vugt, Marion, Vlachojannis, Georgios J, Patel, Riyaz S, Lyytikäinen, Leo-Pekka, Kähönen, Mika, Lehtimäki, Terho, Nieminen, Tuomo V M, Kuukasjärvi, Pekka, Laurikka, Jari O, Chang, Xuling, Heng, Chew-Kiat, Jiang, Rong, Kraus, William E, Hauser, Elizabeth R, Ferguson, Jane F, Reilly, Muredach P, Ito, Kaoru, Koyama, Satoshi, Kamatani, Yoichiro, Komuro, Issei, Stolze, Lindsey K, Romanoski, Casey E, Khan, Mohammad Daud, Turner, Adam W, Miller, Clint L, Aherrahrou, Redouane, Civelek, Mete, Ma, Lijiang, Björkegren, Johan L M, Kumar, S Ram, Tang, W H Wilson, Hazen, Stanley L, Allayee, Hooman
Format Journal Article
LanguageEnglish
Published England Oxford University Press 01.03.2021
Subjects
Clnical Research
Coronary Artery Disease - genetics
Editor's Choice
Endothelial Cells
Genetic Predisposition to Disease - genetics
Genome-Wide Association Study
Humans
Japan
Myocardial Infarction - genetics
Polymorphism, Single Nucleotide - genetics
Risk Factors
Japan
Myocardial infarction
SLC44A3
Genetic factors
Genome-wide association study
Meta-analysis
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Abstract While most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI. We sought to address the hypothesis that some of the genetic factors which establish atherosclerosis may be distinct from those that predispose to vulnerable plaques and thrombus formation. We carried out a genome-wide association study for MI in the UK Biobank (n∼472 000), followed by a meta-analysis with summary statistics from the CARDIoGRAMplusC4D Consortium (n∼167 000). Multiple independent replication analyses and functional approaches were used to prioritize loci and evaluate positional candidate genes. Eight novel regions were identified for MI at the genome wide significance level, of which effect sizes at six loci were more robust for MI than for CAD without the presence of MI. Confirmatory evidence for association of a locus on chromosome 1p21.3 harbouring choline-like transporter 3 (SLC44A3) with MI in the context of CAD, but not with coronary atherosclerosis itself, was obtained in Biobank Japan (n∼165 000) and 16 independent angiography-based cohorts (n∼27 000). Follow-up analyses did not reveal association of the SLC44A3 locus with CAD risk factors, biomarkers of coagulation, other thrombotic diseases, or plasma levels of a broad array of metabolites, including choline, trimethylamine N-oxide, and betaine. However, aortic expression of SLC44A3 was increased in carriers of the MI risk allele at chromosome 1p21.3, increased in ischaemic (vs. non-diseased) coronary arteries, up-regulated in human aortic endothelial cells treated with interleukin-1β (vs. vehicle), and associated with smooth muscle cell migration in vitro. A large-scale analysis comprising ∼831 000 subjects revealed novel genetic determinants of MI and implicated SLC44A3 in the pathophysiology of vulnerable plaques.
AbstractList While most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI. We sought to address the hypothesis that some of the genetic factors which establish atherosclerosis may be distinct from those that predispose to vulnerable plaques and thrombus formation. We carried out a genome-wide association study for MI in the UK Biobank (n∼472 000), followed by a meta-analysis with summary statistics from the CARDIoGRAMplusC4D Consortium (n∼167 000). Multiple independent replication analyses and functional approaches were used to prioritize loci and evaluate positional candidate genes. Eight novel regions were identified for MI at the genome wide significance level, of which effect sizes at six loci were more robust for MI than for CAD without the presence of MI. Confirmatory evidence for association of a locus on chromosome 1p21.3 harbouring choline-like transporter 3 (SLC44A3) with MI in the context of CAD, but not with coronary atherosclerosis itself, was obtained in Biobank Japan (n∼165 000) and 16 independent angiography-based cohorts (n∼27 000). Follow-up analyses did not reveal association of the SLC44A3 locus with CAD risk factors, biomarkers of coagulation, other thrombotic diseases, or plasma levels of a broad array of metabolites, including choline, trimethylamine N-oxide, and betaine. However, aortic expression of SLC44A3 was increased in carriers of the MI risk allele at chromosome 1p21.3, increased in ischaemic (vs. non-diseased) coronary arteries, up-regulated in human aortic endothelial cells treated with interleukin-1β (vs. vehicle), and associated with smooth muscle cell migration in vitro. A large-scale analysis comprising ∼831 000 subjects revealed novel genetic determinants of MI and implicated SLC44A3 in the pathophysiology of vulnerable plaques.
While most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI. We sought to address the hypothesis that some of the genetic factors which establish atherosclerosis may be distinct from those that predispose to vulnerable plaques and thrombus formation.AIMSWhile most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI. We sought to address the hypothesis that some of the genetic factors which establish atherosclerosis may be distinct from those that predispose to vulnerable plaques and thrombus formation.We carried out a genome-wide association study for MI in the UK Biobank (n∼472 000), followed by a meta-analysis with summary statistics from the CARDIoGRAMplusC4D Consortium (n∼167 000). Multiple independent replication analyses and functional approaches were used to prioritize loci and evaluate positional candidate genes. Eight novel regions were identified for MI at the genome wide significance level, of which effect sizes at six loci were more robust for MI than for CAD without the presence of MI. Confirmatory evidence for association of a locus on chromosome 1p21.3 harbouring choline-like transporter 3 (SLC44A3) with MI in the context of CAD, but not with coronary atherosclerosis itself, was obtained in Biobank Japan (n∼165 000) and 16 independent angiography-based cohorts (n∼27 000). Follow-up analyses did not reveal association of the SLC44A3 locus with CAD risk factors, biomarkers of coagulation, other thrombotic diseases, or plasma levels of a broad array of metabolites, including choline, trimethylamine N-oxide, and betaine. However, aortic expression of SLC44A3 was increased in carriers of the MI risk allele at chromosome 1p21.3, increased in ischaemic (vs. non-diseased) coronary arteries, up-regulated in human aortic endothelial cells treated with interleukin-1β (vs. vehicle), and associated with smooth muscle cell migration in vitro.METHODS AND RESULTSWe carried out a genome-wide association study for MI in the UK Biobank (n∼472 000), followed by a meta-analysis with summary statistics from the CARDIoGRAMplusC4D Consortium (n∼167 000). Multiple independent replication analyses and functional approaches were used to prioritize loci and evaluate positional candidate genes. Eight novel regions were identified for MI at the genome wide significance level, of which effect sizes at six loci were more robust for MI than for CAD without the presence of MI. Confirmatory evidence for association of a locus on chromosome 1p21.3 harbouring choline-like transporter 3 (SLC44A3) with MI in the context of CAD, but not with coronary atherosclerosis itself, was obtained in Biobank Japan (n∼165 000) and 16 independent angiography-based cohorts (n∼27 000). Follow-up analyses did not reveal association of the SLC44A3 locus with CAD risk factors, biomarkers of coagulation, other thrombotic diseases, or plasma levels of a broad array of metabolites, including choline, trimethylamine N-oxide, and betaine. However, aortic expression of SLC44A3 was increased in carriers of the MI risk allele at chromosome 1p21.3, increased in ischaemic (vs. non-diseased) coronary arteries, up-regulated in human aortic endothelial cells treated with interleukin-1β (vs. vehicle), and associated with smooth muscle cell migration in vitro.A large-scale analysis comprising ∼831 000 subjects revealed novel genetic determinants of MI and implicated SLC44A3 in the pathophysiology of vulnerable plaques.CONCLUSIONSA large-scale analysis comprising ∼831 000 subjects revealed novel genetic determinants of MI and implicated SLC44A3 in the pathophysiology of vulnerable plaques.
Author Nieminen, Tuomo V M
Howe, Laurence J
Thiery, Joachim
Ma, Lijiang
Kamatani, Yoichiro
Komuro, Issei
Smith, Nicholas L
Schwartzman, William S
Seldin, Marcus
Pan, Calvin
Biswas, Subarna
Koyama, Satoshi
Kraus, William E
März, Winfried
Cai, Zhiheng
Heng, Chew-Kiat
Liu, Chang
Reilly, Muredach P
Tang, W H Wilson
Asselbergs, Folkert W
Lyytikäinen, Leo-Pekka
Lusis, Aldons J
Hazen, Stanley L
Mehrabian, Margarete
Khan, Mohammad Daud
Jiang, Rong
Romanoski, Casey E
Hilser, James R
Vlachojannis, Georgios J
Lehtimäki, Terho
Turner, Adam W
Björkegren, Johan L M
Miller, Clint L
Hartiala, Jaana A
Gukasyan, Janet
Chang, Xuling
Sun, Yan V
Patel, Riyaz S
Bazeley, Peter
Kähönen, Mika
Quyyumi, Arshed A
Laurikka, Jari O
Ito, Kaoru
van Vugt, Marion
Aherrahrou, Redouane
Kleber, Marcus E
Hauser, Elizabeth R
Kuukasjärvi, Pekka
Ferguson, Jane F
Civelek, Mete
Stolze, Lindsey K
Delgado, Graciela E
Jia, Qiong
Allayee, Hooman
Scholz, Markus
Han, Yi
Kumar, S Ram
Huang, Pin
Trégouët, David-Alexandre
AuthorAffiliation ehaa1040-aff24 Health Data Research UK and Institute of Health Informatics, University College London , London NW1 2DA, UK
ehaa1040-aff5 Department of Veterans Affairs, Seattle Epidemiologic Research and Information Center, Office of Research and Development , Seattle, WA 98108, USA
ehaa1040-aff13 Department of Cardiovascular & Metabolic Sciences, Cleveland Clinic , Cleveland, OH 44195, USA
ehaa1040-aff7 Department of Biological Chemistry and Center for Epigenetics and Metabolism, UC Irvine School of Medicine , Irvine, CA 92697, USA
ehaa1040-aff16 Division of Cardiology, Department of Medicine, Emory Clinical Cardiovascular Research Institute, Emory University School of Medicine , 1462 Clifton Rd NE, Suite # 507, Atlanta, GA 30322, USA
ehaa1040-aff18 LIFE Research Center for Civilization Diseases, University of Leipzig , 04103 Leipzig, Germany
ehaa1040-aff3 Institut National pour la Santé et la Recherche Médicale (INSERM) UMR_S 1219, Bordeaux Population Health Research Center, University of
AuthorAffiliation_xml – name: ehaa1040-aff49 Institute of Medical Science, The University of Tokyo , Tokyo, Japan
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– name: ehaa1040-aff8 Department of Human Genetics, David Geffen School of Medicine of UCLA , Los Angeles, CA 90095, USA
– name: ehaa1040-aff26 Bart's Heart Centre, St Bartholomew's Hospital , London EC1A 2DA, UK
– name: ehaa1040-aff9 Department of Medicine, David Geffen School of Medicine of UCLA , Los Angeles, CA 90095, USA
– name: ehaa1040-aff28 Department of Clinical Chemistry, Finnish Cardiovascular Research Center—Tampere, Faculty of Medicine and Health Technology, Tampere University , Tampere 33014, Finland
– name: ehaa1040-aff35 Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore , Singapore 119228, Singapore
– name: ehaa1040-aff18 LIFE Research Center for Civilization Diseases, University of Leipzig , 04103 Leipzig, Germany
– name: ehaa1040-aff52 Department of Biomedical Engineering, University of Virginia, Charlottesville University of Virginia , Charlottesville, VA 22904, USA
– name: ehaa1040-aff3 Institut National pour la Santé et la Recherche Médicale (INSERM) UMR_S 1219, Bordeaux Population Health Research Center, University of Bordeaux , 33076 Bordeaux, France
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– name: ehaa1040-aff36 Khoo Teck Puat—National University Children's Medical Institute, National University Health System , Singapore 119074, Singapore
– name: ehaa1040-aff29 Department of Cardiology, Heart Center, Tampere University Hospital , Tampere 33521, Finland
– name: ehaa1040-aff40 Department of Biostatistics & Bioinformatics, Duke University School of Medicine Durham , NC 27710, USA
– name: ehaa1040-aff5 Department of Veterans Affairs, Seattle Epidemiologic Research and Information Center, Office of Research and Development , Seattle, WA 98108, USA
– name: ehaa1040-aff51 Center for Public Health Genomics, University of Virginia, Charlottesville University of Virginia , Charlottesville, VA 22904, USA
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– name: ehaa1040-aff22 Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz , 8036 Graz, Austria
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– name: ehaa1040-aff46 Human Disease Genomics, Center for Genomic Medicine, Kyoto University Graduate School of Medicine , Kyoto 606-8501, Japan
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– name: ehaa1040-aff11 Center for Clinical Genomics, Cleveland Clinic , Cleveland, OH 44195, USA
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– name: ehaa1040-aff42 Cardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center , New York, NY 10032, USA
– name: ehaa1040-aff7 Department of Biological Chemistry and Center for Epigenetics and Metabolism, UC Irvine School of Medicine , Irvine, CA 92697, USA
– name: ehaa1040-aff33 Department of Cardio-Thoracic Surgery, Finnish Cardiovascular Research Center—Tampere, Faculty of Medicine and Health Technology, Tampere University , Tampere 33014, Finland
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– name: ehaa1040-aff1 Department of Preventive Medicine, Keck School of Medicine, University of Southern California , 2250 Alcazar Street, CSC202, Los Angeles, CA 90033, USA
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– name: ehaa1040-aff6 Kaiser Permanente Washington Health Research Institute, Kaiser Permanente Washington , Seattle, WA 98101, USA
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ContentType Journal Article
Copyright Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com. 2021
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CorporateAuthor The INVENT Consortium
The GENIUS-CHD Consortium
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Issue 9
Keywords Myocardial infarction
SLC44A3
Genetic factors
Genome-wide association study
Meta-analysis
Language English
License https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.
This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
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A full list of members in the INVENT Consortium, the CHARGE Consortium Hemostasis Working Group, and the GENIUS-CHD Consortium is provided in the Supplementary material online.
Jaana A. Hartiala and Yi Han contributed equally to this work.
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Nelson (2022102514262025600_ehaa1040-B10) 2017; 49
Erdmann (2022102514262025600_ehaa1040-B5) 2013; 504
Traiffort (2022102514262025600_ehaa1040-B22) 2013; 34
Shin (2022102514262025600_ehaa1040-B32) 2014; 46
(2022102514262025600_ehaa1040-B15) 2013; 45
Koeth (2022102514262025600_ehaa1040-B26) 2013; 19
Verweij (2022102514262025600_ehaa1040-B7) 2017; 7
Beutner (2022102514262025600_ehaa1040-B14) 2011; 6
Gimbrone (2022102514262025600_ehaa1040-B38) 2016; 118
Franzen (2022102514262025600_ehaa1040-B17) 2016; 353
van der Harst (2022102514262025600_ehaa1040-B11) 2018; 122
Koeth (2022102514262025600_ehaa1040-B27) 2014; 20
Klarin (2022102514262025600_ehaa1040-B9) 2017; 49
Cherepanova (2022102514262025600_ehaa1040-B39) 2016; 22
Malik (2022102514262025600_ehaa1040-B18) 2018; 50
Hansson (2022102514262025600_ehaa1040-B3) 2005; 352
2022102514262025600_ehaa1040-B29
Staley (2022102514262025600_ehaa1040-B16) 2016; 32
Reilly (2022102514262025600_ehaa1040-B13) 2011; 377
Ridker (2022102514262025600_ehaa1040-B2) 2008; 359
Schunkert (2022102514262025600_ehaa1040-B4) 2010; 31
Schlosser (2022102514262025600_ehaa1040-B34) 2020; 52
Go (2022102514262025600_ehaa1040-B1) 2014; 129
Howson (2022102514262025600_ehaa1040-B8) 2017; 49
Koyama (2022102514262025600_ehaa1040-B12) 2020; 52
Nikpay (2022102514262025600_ehaa1040-B6) 2015; 47
Li (2022102514262025600_ehaa1040-B30) 2018; 3
Sun (2022102514262025600_ehaa1040-B33) 2018; 558
33561196 - Eur Heart J. 2021 Mar 1;42(9):934-937. doi: 10.1093/eurheartj/ehaa1089
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Snippet While most patients with myocardial infarction (MI) have underlying coronary atherosclerosis, not all patients with coronary artery disease (CAD) develop MI....
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SubjectTerms Clnical Research
Coronary Artery Disease - genetics
Editor's Choice
Endothelial Cells
Genetic Predisposition to Disease - genetics
Genome-Wide Association Study
Humans
Japan
Myocardial Infarction - genetics
Polymorphism, Single Nucleotide - genetics
Risk Factors
Title Genome-wide analysis identifies novel susceptibility loci for myocardial infarction
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https://www.proquest.com/docview/2486155604
https://pubmed.ncbi.nlm.nih.gov/PMC7936531
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Volume 42
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