The polygenic architecture of left ventricular mass mirrors the clinical epidemiology
Left ventricular (LV) mass is a prognostic biomarker for incident heart disease and all-cause mortality. Large-scale genome-wide association studies have identified few SNPs associated with LV mass. We hypothesized that a polygenic discovery approach using LV mass measurements made in a clinical pop...
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| Veröffentlicht in: | Scientific reports 2020-05, Vol.10 (1), p.7561-7561, Article 7561 |
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| creator | Mosley, Jonathan D. Levinson, Rebecca T. Farber-Eger, Eric Edwards, Todd L. Hellwege, Jacklyn N. Hung, Adriana M. Giri, Ayush Shuey, Megan M. Shaffer, Christian M. Shi, Mingjian Brittain, Evan L. Chung, Wendy K. Kullo, Iftikhar J. Arruda-Olson, Adelaide M. Jarvik, Gail P. Larson, Eric B. Crosslin, David R. Williams, Marc S. Borthwick, Ken M. Hakonarson, Hakon Denny, Joshua C. Wang, Thomas J. Stein, Charles M. Roden, Dan M. Wells, Quinn S. |
| description | Left ventricular (LV) mass is a prognostic biomarker for incident heart disease and all-cause mortality. Large-scale genome-wide association studies have identified few SNPs associated with LV mass. We hypothesized that a polygenic discovery approach using LV mass measurements made in a clinical population would identify risk factors and diseases associated with adverse LV remodeling. We developed a polygenic single nucleotide polymorphism-based predictor of LV mass in 7,601 individuals with LV mass measurements made during routine clinical care. We tested for associations between this predictor and 894 clinical diagnoses measured in 58,838 unrelated genotyped individuals. There were 29 clinical phenotypes associated with the LV mass genetic predictor at FDR q |
| doi_str_mv | 10.1038/s41598-020-64525-z |
| format | Article |
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Large-scale genome-wide association studies have identified few SNPs associated with LV mass. We hypothesized that a polygenic discovery approach using LV mass measurements made in a clinical population would identify risk factors and diseases associated with adverse LV remodeling. We developed a polygenic single nucleotide polymorphism-based predictor of LV mass in 7,601 individuals with LV mass measurements made during routine clinical care. We tested for associations between this predictor and 894 clinical diagnoses measured in 58,838 unrelated genotyped individuals. There were 29 clinical phenotypes associated with the LV mass genetic predictor at FDR q < 0.05. Genetically predicted higher LV mass was associated with modifiable cardiac risk factors, diagnoses related to organ dysfunction and conditions associated with abnormal cardiac structure including heart failure and atrial fibrillation. Secondary analyses using polygenic predictors confirmed a significant association between higher LV mass and body mass index and, in men, associations with coronary atherosclerosis and systolic blood pressure. In summary, these analyses show that LV mass-associated genetic variability associates with diagnoses of cardiac diseases and with modifiable risk factors which contribute to these diseases.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-64525-z</identifier><identifier>PMID: 32372017</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/208/205 ; 692/4019/592/1540 ; Arteriosclerosis ; Blood pressure ; Body mass index ; Cardiovascular diseases ; Congestive heart failure ; Coronary artery disease ; Echocardiography ; Epidemiology ; Female ; Fibrillation ; Genetic analysis ; Genetic Predisposition to Disease ; Genetic variability ; Genome-wide association studies ; Genome-Wide Association Study ; Genomes ; Genotype ; Health risk assessment ; Heart Diseases - diagnosis ; Heart Diseases - epidemiology ; Heart Diseases - etiology ; Heart Diseases - mortality ; Heart Ventricles - anatomy & histology ; Heart Ventricles - diagnostic imaging ; Heart Ventricles - pathology ; Humanities and Social Sciences ; Humans ; Male ; multidisciplinary ; Multifactorial Inheritance ; Odds Ratio ; Organ Size ; Phenotype ; Phenotypes ; Polymorphism, Single Nucleotide ; Risk Assessment ; Risk Factors ; Science ; Science (multidisciplinary) ; Single-nucleotide polymorphism ; Ventricle ; Ventricular Remodeling - genetics</subject><ispartof>Scientific reports, 2020-05, Vol.10 (1), p.7561-7561, Article 7561</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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Large-scale genome-wide association studies have identified few SNPs associated with LV mass. We hypothesized that a polygenic discovery approach using LV mass measurements made in a clinical population would identify risk factors and diseases associated with adverse LV remodeling. We developed a polygenic single nucleotide polymorphism-based predictor of LV mass in 7,601 individuals with LV mass measurements made during routine clinical care. We tested for associations between this predictor and 894 clinical diagnoses measured in 58,838 unrelated genotyped individuals. There were 29 clinical phenotypes associated with the LV mass genetic predictor at FDR q < 0.05. Genetically predicted higher LV mass was associated with modifiable cardiac risk factors, diagnoses related to organ dysfunction and conditions associated with abnormal cardiac structure including heart failure and atrial fibrillation. Secondary analyses using polygenic predictors confirmed a significant association between higher LV mass and body mass index and, in men, associations with coronary atherosclerosis and systolic blood pressure. In summary, these analyses show that LV mass-associated genetic variability associates with diagnoses of cardiac diseases and with modifiable risk factors which contribute to these diseases.</description><subject>631/208/205</subject><subject>692/4019/592/1540</subject><subject>Arteriosclerosis</subject><subject>Blood pressure</subject><subject>Body mass index</subject><subject>Cardiovascular diseases</subject><subject>Congestive heart failure</subject><subject>Coronary artery disease</subject><subject>Echocardiography</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Fibrillation</subject><subject>Genetic analysis</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic variability</subject><subject>Genome-wide association studies</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Genotype</subject><subject>Health risk assessment</subject><subject>Heart Diseases - diagnosis</subject><subject>Heart Diseases - epidemiology</subject><subject>Heart Diseases - etiology</subject><subject>Heart Diseases - mortality</subject><subject>Heart Ventricles - anatomy & histology</subject><subject>Heart Ventricles - diagnostic imaging</subject><subject>Heart Ventricles - pathology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Male</subject><subject>multidisciplinary</subject><subject>Multifactorial Inheritance</subject><subject>Odds Ratio</subject><subject>Organ Size</subject><subject>Phenotype</subject><subject>Phenotypes</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Single-nucleotide polymorphism</subject><subject>Ventricle</subject><subject>Ventricular Remodeling - 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mirrors the clinical epidemiology</title><author>Mosley, Jonathan D. ; Levinson, Rebecca T. ; Farber-Eger, Eric ; Edwards, Todd L. ; Hellwege, Jacklyn N. ; Hung, Adriana M. ; Giri, Ayush ; Shuey, Megan M. ; Shaffer, Christian M. ; Shi, Mingjian ; Brittain, Evan L. ; Chung, Wendy K. ; Kullo, Iftikhar J. ; Arruda-Olson, Adelaide M. ; Jarvik, Gail P. ; Larson, Eric B. ; Crosslin, David R. ; Williams, Marc S. ; Borthwick, Ken M. ; Hakonarson, Hakon ; Denny, Joshua C. ; Wang, Thomas J. ; Stein, Charles M. ; Roden, Dan M. ; Wells, Quinn S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-c210ee8e98cbbd054819644739be2a5746e0aeeccd3c659432811d7e60bee2563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>631/208/205</topic><topic>692/4019/592/1540</topic><topic>Arteriosclerosis</topic><topic>Blood pressure</topic><topic>Body mass index</topic><topic>Cardiovascular 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ventricular mass mirrors the clinical epidemiology</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2020-05-05</date><risdate>2020</risdate><volume>10</volume><issue>1</issue><spage>7561</spage><epage>7561</epage><pages>7561-7561</pages><artnum>7561</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Left ventricular (LV) mass is a prognostic biomarker for incident heart disease and all-cause mortality. Large-scale genome-wide association studies have identified few SNPs associated with LV mass. We hypothesized that a polygenic discovery approach using LV mass measurements made in a clinical population would identify risk factors and diseases associated with adverse LV remodeling. We developed a polygenic single nucleotide polymorphism-based predictor of LV mass in 7,601 individuals with LV mass measurements made during routine clinical care. We tested for associations between this predictor and 894 clinical diagnoses measured in 58,838 unrelated genotyped individuals. There were 29 clinical phenotypes associated with the LV mass genetic predictor at FDR q < 0.05. Genetically predicted higher LV mass was associated with modifiable cardiac risk factors, diagnoses related to organ dysfunction and conditions associated with abnormal cardiac structure including heart failure and atrial fibrillation. Secondary analyses using polygenic predictors confirmed a significant association between higher LV mass and body mass index and, in men, associations with coronary atherosclerosis and systolic blood pressure. In summary, these analyses show that LV mass-associated genetic variability associates with diagnoses of cardiac diseases and with modifiable risk factors which contribute to these diseases.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32372017</pmid><doi>10.1038/s41598-020-64525-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Scientific reports, 2020-05, Vol.10 (1), p.7561-7561, Article 7561 |
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| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Springer Nature OA/Free Journals; Free Full-Text Journals in Chemistry |
| subjects | 631/208/205 692/4019/592/1540 Arteriosclerosis Blood pressure Body mass index Cardiovascular diseases Congestive heart failure Coronary artery disease Echocardiography Epidemiology Female Fibrillation Genetic analysis Genetic Predisposition to Disease Genetic variability Genome-wide association studies Genome-Wide Association Study Genomes Genotype Health risk assessment Heart Diseases - diagnosis Heart Diseases - epidemiology Heart Diseases - etiology Heart Diseases - mortality Heart Ventricles - anatomy & histology Heart Ventricles - diagnostic imaging Heart Ventricles - pathology Humanities and Social Sciences Humans Male multidisciplinary Multifactorial Inheritance Odds Ratio Organ Size Phenotype Phenotypes Polymorphism, Single Nucleotide Risk Assessment Risk Factors Science Science (multidisciplinary) Single-nucleotide polymorphism Ventricle Ventricular Remodeling - genetics |
| title | The polygenic architecture of left ventricular mass mirrors the clinical epidemiology |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T19%3A05%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20polygenic%20architecture%20of%20left%20ventricular%20mass%20mirrors%20the%20clinical%20epidemiology&rft.jtitle=Scientific%20reports&rft.au=Mosley,%20Jonathan%20D.&rft.date=2020-05-05&rft.volume=10&rft.issue=1&rft.spage=7561&rft.epage=7561&rft.pages=7561-7561&rft.artnum=7561&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/s41598-020-64525-z&rft_dat=%3Cproquest_pubme%3E2399239403%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2398570691&rft_id=info:pmid/32372017&rfr_iscdi=true |