Relation of Multiple Inflammatory Biomarkers to Incident Atrial Fibrillation
Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers (i.e., C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2...
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| Vydáno v: | The American journal of cardiology Ročník 104; číslo 1; s. 92 - 96 |
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| Hlavní autoři: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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New York, NY
Elsevier Inc
01.07.2009
Elsevier Elsevier Limited |
| Témata: | |
| ISSN: | 0002-9149, 1879-1913, 1879-1913 |
| On-line přístup: | Získat plný text |
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| Abstract | Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers (i.e., C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II) with incident AF in 2863 Framingham Offspring Study participants (mean age 60.7 years, SD = 9.4, 55% women). During follow-up (median 6 years), 148 participants (43% women) developed incident AF. In the multivariable proportional hazards models, the inflammatory biomarker panel was associated with incident AF (p = 0.03). With stepwise selection (p <0.01 for entry and retention), log-transformed osteoprotegerin was associated with incident AF (hazard ratio per SD 1.30, 95% confidence interval 1.08 to 1.56, p = 0.006). Adjusting for interim myocardial infarction or heart failure attenuated the association between osteoprotegerin and incident AF (hazard ratio 1.18, 95% confidence interval 0.98 to 1.43, p = 0.09). In conclusion, circulating osteoprotegerin concentration was significantly associated with incident AF in our community-based sample, possibly mediated by interim cardiovascular events. |
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| AbstractList | Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers (i.e., C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II) with incident AF in 2863 Framingham Offspring Study participants (mean age 60.7 years, SD = 9.4, 55% women). During follow-up (median 6 years), 148 participants (43% women) developed incident AF. In the multivariable proportional hazards models, the inflammatory biomarker panel was associated with incident AF (p = 0.03). With stepwise selection (p <0.01 for entry and retention), log-transformed osteoprotegerin was associated with incident AF (hazard ratio per SD 1.30, 95% confidence interval 1.08 to 1.56, p = 0.006). Adjusting for interim myocardial infarction or heart failure attenuated the association between osteoprotegerin and incident AF (hazard ratio 1.18, 95% confidence interval 0.98 to 1.43, p = 0.09). In conclusion, circulating osteoprotegerin concentration was significantly associated with incident AF in our community-based sample, possibly mediated by interim cardiovascular events. Basic and clinical studies suggest that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers [C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2 (mass and activity), monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, tumor necrosis factor receptor II] with incident AF in 2863 Framingham Offspring Study participants (mean age 60.7 years, SD=9.4, 55% women). During follow-up (median 6 years), 148 participants (43% women) developed incident AF. In multivariable proportional-hazards models, the inflammatory biomarker panel was associated with incident AF (p=0.03). With stepwise selection (p<0.01 for entry and retention), log-transformed osteoprotegerin was associated with incident AF (hazard ratio [HR] per standard deviation 1.30, 95% confidence interval [CI] 1.08–1.56, p=0.006). Adjusting for interim myocardial infarction or heart failure attenuated the association between osteoprotegerin and incident AF (HR 1.18, 95% CI 0.98–1.43, p=0.09). In conclusion, circulating osteoprotegerin concentration was significantly associated with incident AF in our community-based sample, possibly mediated by interim cardiovascular events. Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers (i.e., C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II) with incident AF in 2863 Framingham Offspring Study participants (mean age 60.7 years, SD = 9.4, 55% women). During follow-up (median 6 years), 148 participants (43% women) developed incident AF. In the multivariable proportional hazards models, the inflammatory biomarker panel was associated with incident AF (p = 0.03). With stepwise selection (p <0.01 for entry and retention), log-transformed osteoprotegerin was associated with incident AF (hazard ratio per SD 1.30, 95% confidence interval 1.08 to 1.56, p = 0.006). Adjusting for interim myocardial infarction or heart failure attenuated the association between osteoprotegerin and incident AF (hazard ratio 1.18, 95% confidence interval 0.98 to 1.43, p = 0.09). In conclusion, circulating osteoprotegerin concentration was significantly associated with incident AF in our community-based sample, possibly mediated by interim cardiovascular events. [PUBLICATION ABSTRACT] Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers (i.e., C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II) with incident AF in 2863 Framingham Offspring Study participants (mean age 60.7 years, SD = 9.4, 55% women). During follow-up (median 6 years), 148 participants (43% women) developed incident AF. In the multivariable proportional hazards models, the inflammatory biomarker panel was associated with incident AF (p = 0.03). With stepwise selection (p <0.01 for entry and retention), log-transformed osteoprotegerin was associated with incident AF (hazard ratio per SD 1.30, 95% confidence interval 1.08 to 1.56, p = 0.006). Adjusting for interim myocardial infarction or heart failure attenuated the association between osteoprotegerin and incident AF (hazard ratio 1.18, 95% confidence interval 0.98 to 1.43, p = 0.09). In conclusion, circulating osteoprotegerin concentration was significantly associated with incident AF in our community-based sample, possibly mediated by interim cardiovascular events.Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory biomarkers (i.e., C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor II) with incident AF in 2863 Framingham Offspring Study participants (mean age 60.7 years, SD = 9.4, 55% women). During follow-up (median 6 years), 148 participants (43% women) developed incident AF. In the multivariable proportional hazards models, the inflammatory biomarker panel was associated with incident AF (p = 0.03). With stepwise selection (p <0.01 for entry and retention), log-transformed osteoprotegerin was associated with incident AF (hazard ratio per SD 1.30, 95% confidence interval 1.08 to 1.56, p = 0.006). Adjusting for interim myocardial infarction or heart failure attenuated the association between osteoprotegerin and incident AF (hazard ratio 1.18, 95% confidence interval 0.98 to 1.43, p = 0.09). In conclusion, circulating osteoprotegerin concentration was significantly associated with incident AF in our community-based sample, possibly mediated by interim cardiovascular events. |
| Author | Keaney, John F. Vasan, Ramachandran S. Wang, Thomas J. Yamamoto, Jennifer F. Larson, Martin G. Kathiresan, Sekar Rong, Jian Levy, Daniel Schnabel, Renate B. Benjamin, Emelia J. |
| AuthorAffiliation | m Department of Medicine II, Johannes Gutenberg-University, Mainz, Germany j Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA a NHLBI’s Framingham Study, Framingham, MA b Boston University’s Department of Mathematics and Statistics Department, School of Medicine, Boston, MA d Department of Biostatistics, Boston University Public School of Health, Boston, MA l Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA c Department of Mathematics and Statistics, Boston University Public School of Health, Boston, MA h Center for Population Studies, National Heart, Lung, and Blood Institute, Bethesda, MD e Evans Memorial Medicine Department, School of Medicine, Boston, MA f Section of Preventive Medicine, School of Medicine, Boston, MA k University of Massachusetts Medical School, Massachusetts Institute of Technology, Cambridge, MA |
| AuthorAffiliation_xml | – name: a NHLBI’s Framingham Study, Framingham, MA – name: d Department of Biostatistics, Boston University Public School of Health, Boston, MA – name: b Boston University’s Department of Mathematics and Statistics Department, School of Medicine, Boston, MA – name: e Evans Memorial Medicine Department, School of Medicine, Boston, MA – name: l Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA – name: h Center for Population Studies, National Heart, Lung, and Blood Institute, Bethesda, MD – name: m Department of Medicine II, Johannes Gutenberg-University, Mainz, Germany – name: f Section of Preventive Medicine, School of Medicine, Boston, MA – name: c Department of Mathematics and Statistics, Boston University Public School of Health, Boston, MA – name: j Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA – name: k University of Massachusetts Medical School, Massachusetts Institute of Technology, Cambridge, MA |
| Author_xml | – sequence: 1 givenname: Renate B. surname: Schnabel fullname: Schnabel, Renate B. organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts – sequence: 2 givenname: Martin G. surname: Larson fullname: Larson, Martin G. organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts – sequence: 3 givenname: Jennifer F. surname: Yamamoto fullname: Yamamoto, Jennifer F. organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts – sequence: 4 givenname: Sekar surname: Kathiresan fullname: Kathiresan, Sekar organization: Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts – sequence: 5 givenname: Jian surname: Rong fullname: Rong, Jian organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts – sequence: 6 givenname: Daniel surname: Levy fullname: Levy, Daniel organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts – sequence: 7 givenname: John F. surname: Keaney fullname: Keaney, John F. organization: University of Massachusetts Medical School, Boston, Massachusetts – sequence: 8 givenname: Thomas J. surname: Wang fullname: Wang, Thomas J. organization: Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts – sequence: 9 givenname: Ramachandran S. surname: Vasan fullname: Vasan, Ramachandran S. organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts – sequence: 10 givenname: Emelia J. surname: Benjamin fullname: Benjamin, Emelia J. email: melia@bu.edu organization: National Heart Lung Blood Institute Framingham Study, Framingham, Massachusetts |
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| Keywords | Multiple Arrhythmia Heart disease Atrial fibrillation Biological marker Cardiovascular disease Inflammation Circulatory system Cardiology Excitability disorder |
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| Snippet | Basic and clinical studies have suggested that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory... Basic and clinical studies suggest that inflammation predisposes to atrial fibrillation (AF). We assessed the association of 12 circulating inflammatory... |
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| SubjectTerms | Atrial Fibrillation - epidemiology Atrial Fibrillation - etiology Atrial Fibrillation - microbiology Biological and medical sciences Biomarkers C-Reactive Protein Cardiac arrhythmia Cardiac dysrhythmias Cardiology Cardiology. Vascular system Cardiovascular Cell adhesion & migration Confidence Intervals Correlation analysis Female Germany - epidemiology Heart Heart attacks Heart failure Humans Incidence Inflammation - complications Inflammation - diagnosis Male Medical sciences Middle Aged Multivariate Analysis Odds Ratio Osteoprotegerin - blood Prospective Studies Proteins Risk Factors Survival Analysis |
| Title | Relation of Multiple Inflammatory Biomarkers to Incident Atrial Fibrillation |
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