Impact of CD14 Polymorphisms on Anti-Apolipoprotein A-1 IgG-Related Coronary Artery Disease Prediction in the General Population
We aimed to determine whether autoantibodies against apoA-1 (apolipoprotein A-1; anti-apoA-1 IgG) predict incident coronary artery disease (CAD), defined as adjudicated incident myocardial infarction, angina, percutaneous coronary revascularization, or bypass grafting, in the general population. We...
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| Published in | Arteriosclerosis, thrombosis, and vascular biology Vol. 37; no. 12; pp. 2342 - 2349 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.12.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1079-5642 1524-4636 1524-4636 |
| DOI | 10.1161/ATVBAHA.117.309602 |
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| Abstract | We aimed to determine whether autoantibodies against apoA-1 (apolipoprotein A-1; anti-apoA-1 IgG) predict incident coronary artery disease (CAD), defined as adjudicated incident myocardial infarction, angina, percutaneous coronary revascularization, or bypass grafting, in the general population. We further investigated whether this association is modulated by a functional CD14 receptor single nucleotide polymorphism.
In a prospectively studied, population-based cohort of 5220 subjects (mean age 52.6±10.7 years, 47.4% males), followed over a median period of 5.6 years, subjects positive versus negative for anti-apoA-1 IgG presented a total CAD rate of 3.9% versus 2.8% (
=0.077) and a nonfatal CAD rate of 3.6% versus 2.3% (
=0.018), respectively. After multivariate adjustment for established cardiovascular risk factors, the hazard ratios of anti-apoA-1 IgG for total and nonfatal CAD were: hazard ratio=1.36 (95% confidence interval, 0.94-1.97;
=0.105) and hazard ratio=1.53 (95% confidence interval, 1.03-2.26;
=0.034), respectively. In subjects with available genetic data for the C260T
single nucleotide polymorphism in the CD14 receptor gene (n=4247), we observed a significant interaction between anti-apoA-1 IgG and
allele status with regards to CAD risk, with anti-apoA-1 IgG conferring the highest risk for total and nonfatal CAD in non-TT carriers, whereas being associated with the lowest risk for total and nonfatal CAD in TT homozygotes (
for interaction =0.011 and
for interaction =0.033, respectively).
Anti-apoA-1 IgG are independent predictors of nonfatal incident CAD in the general population. The strength of this association is dependent on a functional polymorphism of the CD14 receptor gene, a finding suggesting a gene-autoantibody interaction for the development of CAD. |
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| AbstractList | We aimed to determine whether autoantibodies against apoA-1 (apolipoprotein A-1; anti-apoA-1 IgG) predict incident coronary artery disease (CAD), defined as adjudicated incident myocardial infarction, angina, percutaneous coronary revascularization, or bypass grafting, in the general population. We further investigated whether this association is modulated by a functional CD14 receptor single nucleotide polymorphism.
In a prospectively studied, population-based cohort of 5220 subjects (mean age 52.6±10.7 years, 47.4% males), followed over a median period of 5.6 years, subjects positive versus negative for anti-apoA-1 IgG presented a total CAD rate of 3.9% versus 2.8% (
=0.077) and a nonfatal CAD rate of 3.6% versus 2.3% (
=0.018), respectively. After multivariate adjustment for established cardiovascular risk factors, the hazard ratios of anti-apoA-1 IgG for total and nonfatal CAD were: hazard ratio=1.36 (95% confidence interval, 0.94-1.97;
=0.105) and hazard ratio=1.53 (95% confidence interval, 1.03-2.26;
=0.034), respectively. In subjects with available genetic data for the C260T
single nucleotide polymorphism in the CD14 receptor gene (n=4247), we observed a significant interaction between anti-apoA-1 IgG and
allele status with regards to CAD risk, with anti-apoA-1 IgG conferring the highest risk for total and nonfatal CAD in non-TT carriers, whereas being associated with the lowest risk for total and nonfatal CAD in TT homozygotes (
for interaction =0.011 and
for interaction =0.033, respectively).
Anti-apoA-1 IgG are independent predictors of nonfatal incident CAD in the general population. The strength of this association is dependent on a functional polymorphism of the CD14 receptor gene, a finding suggesting a gene-autoantibody interaction for the development of CAD. We aimed to determine whether autoantibodies against apoA-1 (apolipoprotein A-1; anti-apoA-1 IgG) predict incident coronary artery disease (CAD), defined as adjudicated incident myocardial infarction, angina, percutaneous coronary revascularization, or bypass grafting, in the general population. We further investigated whether this association is modulated by a functional CD14 receptor single nucleotide polymorphism.OBJECTIVEWe aimed to determine whether autoantibodies against apoA-1 (apolipoprotein A-1; anti-apoA-1 IgG) predict incident coronary artery disease (CAD), defined as adjudicated incident myocardial infarction, angina, percutaneous coronary revascularization, or bypass grafting, in the general population. We further investigated whether this association is modulated by a functional CD14 receptor single nucleotide polymorphism.In a prospectively studied, population-based cohort of 5220 subjects (mean age 52.6±10.7 years, 47.4% males), followed over a median period of 5.6 years, subjects positive versus negative for anti-apoA-1 IgG presented a total CAD rate of 3.9% versus 2.8% (P=0.077) and a nonfatal CAD rate of 3.6% versus 2.3% (P=0.018), respectively. After multivariate adjustment for established cardiovascular risk factors, the hazard ratios of anti-apoA-1 IgG for total and nonfatal CAD were: hazard ratio=1.36 (95% confidence interval, 0.94-1.97; P=0.105) and hazard ratio=1.53 (95% confidence interval, 1.03-2.26; P=0.034), respectively. In subjects with available genetic data for the C260T rs2569190 single nucleotide polymorphism in the CD14 receptor gene (n=4247), we observed a significant interaction between anti-apoA-1 IgG and rs2569190 allele status with regards to CAD risk, with anti-apoA-1 IgG conferring the highest risk for total and nonfatal CAD in non-TT carriers, whereas being associated with the lowest risk for total and nonfatal CAD in TT homozygotes (P for interaction =0.011 and P for interaction =0.033, respectively).APPROACH AND RESULTSIn a prospectively studied, population-based cohort of 5220 subjects (mean age 52.6±10.7 years, 47.4% males), followed over a median period of 5.6 years, subjects positive versus negative for anti-apoA-1 IgG presented a total CAD rate of 3.9% versus 2.8% (P=0.077) and a nonfatal CAD rate of 3.6% versus 2.3% (P=0.018), respectively. After multivariate adjustment for established cardiovascular risk factors, the hazard ratios of anti-apoA-1 IgG for total and nonfatal CAD were: hazard ratio=1.36 (95% confidence interval, 0.94-1.97; P=0.105) and hazard ratio=1.53 (95% confidence interval, 1.03-2.26; P=0.034), respectively. In subjects with available genetic data for the C260T rs2569190 single nucleotide polymorphism in the CD14 receptor gene (n=4247), we observed a significant interaction between anti-apoA-1 IgG and rs2569190 allele status with regards to CAD risk, with anti-apoA-1 IgG conferring the highest risk for total and nonfatal CAD in non-TT carriers, whereas being associated with the lowest risk for total and nonfatal CAD in TT homozygotes (P for interaction =0.011 and P for interaction =0.033, respectively).Anti-apoA-1 IgG are independent predictors of nonfatal incident CAD in the general population. The strength of this association is dependent on a functional polymorphism of the CD14 receptor gene, a finding suggesting a gene-autoantibody interaction for the development of CAD.CONCLUSIONSAnti-apoA-1 IgG are independent predictors of nonfatal incident CAD in the general population. The strength of this association is dependent on a functional polymorphism of the CD14 receptor gene, a finding suggesting a gene-autoantibody interaction for the development of CAD. |
| Author | Hartley, Oliver Kutalik, Zoltan Pagano, Sabrina Mach, François Satta, Nathalie Vollenweider, Peter Waeber, Gerard Marques-Vidal, Pedro Montecucco, Fabrizio Virzi, Julien Vuilleumier, Nicolas Antiochos, Panagiotis |
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Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 3 givenname: Julien surname: Virzi fullname: Virzi, Julien organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. 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Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 5 givenname: Nathalie surname: Satta fullname: Satta, Nathalie organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 6 givenname: Oliver surname: Hartley fullname: Hartley, Oliver organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 7 givenname: Fabrizio surname: Montecucco fullname: Montecucco, Fabrizio organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 8 givenname: François surname: Mach fullname: Mach, François organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 9 givenname: Zoltan surname: Kutalik fullname: Kutalik, Zoltan organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 10 givenname: Gerard surname: Waeber fullname: Waeber, Gerard organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 11 givenname: Peter surname: Vollenweider fullname: Vollenweider, Peter organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches – sequence: 12 givenname: Nicolas surname: Vuilleumier fullname: Vuilleumier, Nicolas organization: From the Department of Internal Medicine, University Hospital of Lausanne, Switzerland (P.A., P.M.-V., G.W., P.V.); Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, Switzerland (J.V., S.P., N.S., F. Montecucco, N.V.); Department of Human Protein Sciences, Faculty of Medicine, (J.V., S.P., N.S., N.V.), Department of Pathology and Immunology, Faculty of Medicine (O.H.), and Division of Cardiology, Foundation for Medical Researches |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29074586$$D View this record in MEDLINE/PubMed |
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| Keywords | coronary artery disease apolipoprotein A-1 risk stratification autoimmunity CD14 polymorphism autoantibodies HDL cholesterol |
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| SubjectTerms | Adult Apolipoprotein A-I - immunology Autoantibodies - blood Biomarkers - blood Chi-Square Distribution Coronary Artery Disease - blood Coronary Artery Disease - epidemiology Coronary Artery Disease - genetics Coronary Artery Disease - immunology Female Gene Frequency Genetic Association Studies Genetic Predisposition to Disease Heterozygote Homozygote Humans Immunoglobulin G - blood Incidence Kaplan-Meier Estimate Lipopolysaccharide Receptors - genetics Lipopolysaccharide Receptors - immunology Male Middle Aged Multivariate Analysis Phenotype Polymorphism, Single Nucleotide Proportional Hazards Models Prospective Studies Risk Assessment Risk Factors Switzerland - epidemiology Time Factors |
| Title | Impact of CD14 Polymorphisms on Anti-Apolipoprotein A-1 IgG-Related Coronary Artery Disease Prediction in the General Population |
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