Association of Lipid-Related Genetic Variants with the Incidence of Atrial Fibrillation: The AFGen Consortium
Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF...
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| Vydáno v: | PloS one Ročník 11; číslo 3; s. e0151932 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Public Library of Science
21.03.2016
Public Library of Science (PLoS) |
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts.
We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score.
During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04).
In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. |
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| AbstractList | Background Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts. Methods We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score. Results During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98–1.03); 0.98 (0.96–1.01); 0.98 (0.95–1.02); 0.99 (0.97–1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97–1.03); 1.01 (0.99–1.04). Conclusions In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts. We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score. During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04). In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. BackgroundSeveral studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts.MethodsWe analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score.ResultsDuring a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04).ConclusionsIn this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts.BACKGROUNDSeveral studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts.We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score.METHODSWe analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score.During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04).RESULTSDuring a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04).In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF.CONCLUSIONSIn this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. BACKGROUND: Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts. METHODS: We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score. RESULTS: During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases wereidentified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04). CONCLUSIONS: In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. Background Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts. Methods We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score. Results During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98–1.03); 0.98 (0.96–1.01); 0.98 (0.95–1.02); 0.99 (0.97–1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97–1.03); 1.01 (0.99–1.04). Conclusions In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with AF risk, we assessed whether previously developed lipid gene scores, used as instrumental variables, are associated with the incidence of AF in 7 large cohorts. We analyzed 64,901 individuals of European ancestry without previous AF at baseline and with lipid gene scores. Lipid-specific gene scores, based on loci significantly associated with lipid levels, were calculated. Additionally, non-pleiotropic gene scores for high-density lipoprotein cholesterol (HDLc) and low-density lipoprotein cholesterol (LDLc) were calculated using SNPs that were only associated with the specific lipid fraction. Cox models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of AF per 1-standard deviation (SD) increase of each lipid gene score. During a mean follow-up of 12.0 years, 5434 (8.4%) incident AF cases were identified. After meta-analysis, the HDLc, LDLc, total cholesterol, and triglyceride gene scores were not associated with incidence of AF. Multivariable-adjusted HR (95% CI) were 1.01 (0.98-1.03); 0.98 (0.96-1.01); 0.98 (0.95-1.02); 0.99 (0.97-1.02), respectively. Similarly, non-pleiotropic HDLc and LDLc gene scores showed no association with incident AF: HR (95% CI) = 1.00 (0.97-1.03); 1.01 (0.99-1.04). In this large cohort study of individuals of European ancestry, gene scores for lipid fractions were not associated with incident AF. |
| Audience | Academic |
| Author | McManus, David D. Pankow, James S. Norby, Faye L. Hofman, Albert Niemeijer, Maartje N. Eijgelsheim, Mark Orho-Melander, Marju Chasman, Daniel L. Chen, Lin Y. Stricker, Bruno H. C. Gudnason, Vilmundur Heeringa, Jan Engström, Gunnar Schulz, Christina-Alexandra Benjamin, Emelia J. Hindy, George Smith, J. Gustav Eryd, Samuel Adamsson Albert, Christine M. Lutsey, Pamela L. Magnani, Jared W. Arking, Dan E. Rukh, Gull Agarwal, Sunil K. Uitterlinden, André G. Franco, Oscar H. Yin, Xiaoyan Alonso, Alvaro Rose, Lynda M. Smith, Albert V. |
| AuthorAffiliation | 7 Cardiology and Preventive Medicine Sections, Department of Biostatistics, Boston University School of Medicine, Boston, Massachusetts, United States of America 15 Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America 1 Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States of America 12 Cardiology and Preventive Medicine Sections, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America 16 Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts, United States of America 17 Department of Cardiology, Lund University, Lund, Sweden 2 Department of Clinical Sciences, Lund University, Malmö, Sweden 8 Icahn School of Medicine, Mount Sinai Heart Center, New York, New York, United States of America 18 Inspectorate of Health Ca |
| AuthorAffiliation_xml | – name: 5 Icelandic Heart Association, Research Institute, Kopavogur, Iceland – name: 10 Cardiac Arrhythmia Center, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America – name: 4 Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America – name: 7 Cardiology and Preventive Medicine Sections, Department of Biostatistics, Boston University School of Medicine, Boston, Massachusetts, United States of America – name: 18 Inspectorate of Health Care, Utrecht, the Netherlands – name: 1 Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States of America – name: 9 McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America – name: 12 Cardiology and Preventive Medicine Sections, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, United States of America – name: 6 The University of Iceland, Reykjavik, Iceland – name: 2 Department of Clinical Sciences, Lund University, Malmö, Sweden – name: 15 Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America – name: 16 Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts, United States of America – name: 17 Department of Cardiology, Lund University, Lund, Sweden – name: 3 Department of Epidemiology, Erasmus Medical Center—University Medical Center, Rotterdam, The Netherlands – name: University at Buffalo, UNITED STATES – name: 11 Department of Internal Medicine, Erasmus Medical Center—University Medical Center, Rotterdam, The Netherlands – name: 13 The National Heart, Lung and Blood Institute’s and Boston University’s Framingham Heart Study, Framingham, Massachusetts, United States of America – name: 14 Departments of Medicine and Quantitative Health Sciences, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America – name: 8 Icahn School of Medicine, Mount Sinai Heart Center, New York, New York, United States of America |
| Author_xml | – sequence: 1 givenname: Faye L. surname: Norby fullname: Norby, Faye L. – sequence: 2 givenname: Samuel Adamsson surname: Eryd fullname: Eryd, Samuel Adamsson – sequence: 3 givenname: Maartje N. surname: Niemeijer fullname: Niemeijer, Maartje N. – sequence: 4 givenname: Lynda M. surname: Rose fullname: Rose, Lynda M. – sequence: 5 givenname: Albert V. surname: Smith fullname: Smith, Albert V. – sequence: 6 givenname: Xiaoyan surname: Yin fullname: Yin, Xiaoyan – sequence: 7 givenname: Sunil K. surname: Agarwal fullname: Agarwal, Sunil K. – sequence: 8 givenname: Dan E. surname: Arking fullname: Arking, Dan E. – sequence: 9 givenname: Daniel L. surname: Chasman fullname: Chasman, Daniel L. – sequence: 10 givenname: Lin Y. surname: Chen fullname: Chen, Lin Y. – sequence: 11 givenname: Mark surname: Eijgelsheim fullname: Eijgelsheim, Mark – sequence: 12 givenname: Gunnar surname: Engström fullname: Engström, Gunnar – sequence: 13 givenname: Oscar H. surname: Franco fullname: Franco, Oscar H. – sequence: 14 givenname: Jan surname: Heeringa fullname: Heeringa, Jan – sequence: 15 givenname: George surname: Hindy fullname: Hindy, George – sequence: 16 givenname: Albert surname: Hofman fullname: Hofman, Albert – sequence: 17 givenname: Pamela L. surname: Lutsey fullname: Lutsey, Pamela L. – sequence: 18 givenname: Jared W. surname: Magnani fullname: Magnani, Jared W. – sequence: 19 givenname: David D. surname: McManus fullname: McManus, David D. – sequence: 20 givenname: Marju surname: Orho-Melander fullname: Orho-Melander, Marju – sequence: 21 givenname: James S. surname: Pankow fullname: Pankow, James S. – sequence: 22 givenname: Gull surname: Rukh fullname: Rukh, Gull – sequence: 23 givenname: Christina-Alexandra surname: Schulz fullname: Schulz, Christina-Alexandra – sequence: 24 givenname: André G. surname: Uitterlinden fullname: Uitterlinden, André G. – sequence: 25 givenname: Christine M. surname: Albert fullname: Albert, Christine M. – sequence: 26 givenname: Emelia J. surname: Benjamin fullname: Benjamin, Emelia J. – sequence: 27 givenname: Vilmundur surname: Gudnason fullname: Gudnason, Vilmundur – sequence: 28 givenname: J. Gustav surname: Smith fullname: Smith, J. Gustav – sequence: 29 givenname: Bruno H. C. surname: Stricker fullname: Stricker, Bruno H. C. – sequence: 30 givenname: Alvaro surname: Alonso fullname: Alonso, Alvaro |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26999784$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2016 Public Library of Science 2016 Norby et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2016 Norby et al 2016 Norby et al |
| Copyright_xml | – notice: COPYRIGHT 2016 Public Library of Science – notice: 2016 Norby et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2016 Norby et al 2016 Norby et al |
| CorporateAuthor | Institutionen för kliniska vetenskaper, Lund Sektion II Lunds universitet Section II Profile areas and other strong research environments Department of Clinical Sciences, Malmö Lund University Kardiologi Department of Clinical Sciences, Lund Strategiska forskningsområden (SFO) EpiHealth: Epidemiology for Health EXODIAB: Excellence of Diabetes Research in Sweden Faculty of Medicine Strategic research areas (SRA) Medicinska fakulteten Cardiology Profilområden och andra starka forskningsmiljöer Institutionen för kliniska vetenskaper, Malmö |
| CorporateAuthor_xml | – name: Faculty of Medicine – name: Medicinska fakulteten – name: Sektion II – name: Strategiska forskningsområden (SFO) – name: Kardiologi – name: Section II – name: EpiHealth: Epidemiology for Health – name: Institutionen för kliniska vetenskaper, Malmö – name: Cardiology – name: Institutionen för kliniska vetenskaper, Lund – name: Strategic research areas (SRA) – name: Lunds universitet – name: Department of Clinical Sciences, Lund – name: Profilområden och andra starka forskningsmiljöer – name: Lund University – name: EXODIAB: Excellence of Diabetes Research in Sweden – name: Profile areas and other strong research environments – name: Department of Clinical Sciences, Malmö |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: FLN AA CMA EJB VG JGS BHCS. Analyzed the data: FLN SAE MNN LMR AVS XY. Wrote the paper: FLN AA SAE MNN LMR AVS XY SKA LYC PLL JSP JWM DEA. Analytical assistance: DLC ME GE OHF JH GH AH DDM MOM GR CAS AU. |
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| Snippet | Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood lipids with... Background Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood... BACKGROUND: Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood... BackgroundSeveral studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood... Background Several studies have shown associations between blood lipid levels and the risk of atrial fibrillation (AF). To test the potential effect of blood... |
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| SubjectTerms | Aged Analysis Atrial fibrillation Atrial Fibrillation - blood Atrial Fibrillation - genetics Biology and Life Sciences Blood Blood lipids Cardiac arrhythmia Cholesterol Cholesterol, HDL - blood Cholesterol, LDL - blood Clinical Medicine Cohort Studies Confidence Intervals Consortia Female Fibrillation Genetic Association Studies Genetic diversity Genetic Pleiotropy Genetic Predisposition to Disease Genetic variance Genetic Variation Health risk assessment Humans Incidence Klinisk medicin Lipids Lipids - blood Male Medical and Health Sciences Medicin och hälsovetenskap Medicine and Health Sciences Meta-Analysis as Topic Middle Aged Multivariate Analysis Pleiotropy Preventive medicine Risk factors Single-nucleotide polymorphism Womens health |
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| Title | Association of Lipid-Related Genetic Variants with the Incidence of Atrial Fibrillation: The AFGen Consortium |
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