Michiel Rienstra1, Xiaoyan Yin2, Martin G Larson2, João D Fontes3, Jared W Magnani3, David D McManus4, Elizabeth L McCabe5, Erin E Coglianese6, Michael Amponsah7, Jennifer E Ho3, James L Januzzi5, Kai C Wollert8, Michael G Fradley5, Ramachandran S Vasan9, Patrick T Ellinor10, Thomas J Wang11, Emelia J Benjamin9. 1. Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, MA; Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands; National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA. Electronic address: m.rienstra@umcg.nl. 2. National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA; Department of Mathematics and Statistics, Boston University, Boston, MA. 3. National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA; Section of Cardiovascular Medicine, Department of Medicine, Boston University School of Medicine, Boston, MA. 4. Department of Medicine, Division of Cardiovascular Medicine, University of Massachusetts Medical School, Worcester, MA. 5. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA. 6. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA; Cardiology Division, Loyola University, Chicago, IL. 7. Department of Medicine, Newark Beth Israel Medical Center, Newark, NJ. 8. Division of Molecular and Translational Cardiology, Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany. 9. National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA; Section of Cardiovascular Medicine, Department of Medicine, Boston University School of Medicine, Boston, MA; Department of Preventive Medicine, Boston University School of Medicine, Boston, MA; Department of Epidemiology, Boston University School of Public Health, Boston, MA. 10. Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, MA; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA. 11. National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA; Division of Cardiovascular Medicine, Vanderbilt University, Nashville, TN.
Abstract
BACKGROUND: We investigated whether circulating concentrations of soluble ST2, growth differentiation factor-15 (GDF-15), and high-sensitivity troponin I (hsTnI) are associated with incident atrial fibrillation (AF) and whether these biomarkers improve current risk prediction models including AF risk factors, B-type natriuretic peptide (BNP), and C-reactive protein (CRP). METHODS: We studied the relation between soluble ST2, GDF-15, and hsTnI and development of AF in Framingham Heart Study participants without prevalent AF. We used Cox proportional hazard regression analysis to examine the relation of incident AF during a 10-year follow-up period with each biomarker. We adjusted for standard AF clinical risk factors, BNP, and CRP. RESULTS: The mean age of the 3,217 participants was 59 ± 10 years, and 54% were women. During a 10-year follow-up, 242 participants developed AF. In age- and sex-adjusted models, GDF-15 and hsTnI were associated with risk of incident AF; however, after including the AF risk factors and BNP and CRP, only hsTnI was significantly associated with AF (hazard ratio per 1 SD of loge hsTnI, 1.12, 95% CI 1.00-1.26, P = .045). The c statistic of the base model including AF risk factors, BNP, and CRP was 0.803 (95% CI 0.777-0.830) and did not improve by adding individual or all 3 biomarkers. None of the discrimination and reclassification statistics were significant compared with the base model. CONCLUSION: In a community-based cohort, circulating hsTnI concentrations were associated with incident AF. None of the novel biomarkers evaluated improved AF risk discrimination or reclassification beyond standard clinical AF risk factors and biomarkers.
BACKGROUND: We investigated whether circulating concentrations of soluble ST2, growth differentiation factor-15 (GDF-15), and high-sensitivity troponin I (hsTnI) are associated with incident atrial fibrillation (AF) and whether these biomarkers improve current risk prediction models including AF risk factors, B-type natriuretic peptide (BNP), and C-reactive protein (CRP). METHODS: We studied the relation between soluble ST2, GDF-15, and hsTnI and development of AF in Framingham Heart Study participants without prevalent AF. We used Cox proportional hazard regression analysis to examine the relation of incident AF during a 10-year follow-up period with each biomarker. We adjusted for standard AF clinical risk factors, BNP, and CRP. RESULTS: The mean age of the 3,217 participants was 59 ± 10 years, and 54% were women. During a 10-year follow-up, 242 participants developed AF. In age- and sex-adjusted models, GDF-15 and hsTnI were associated with risk of incident AF; however, after including the AF risk factors and BNP and CRP, only hsTnI was significantly associated with AF (hazard ratio per 1 SD of loge hsTnI, 1.12, 95% CI 1.00-1.26, P = .045). The c statistic of the base model including AF risk factors, BNP, and CRP was 0.803 (95% CI 0.777-0.830) and did not improve by adding individual or all 3 biomarkers. None of the discrimination and reclassification statistics were significant compared with the base model. CONCLUSION: In a community-based cohort, circulating hsTnI concentrations were associated with incident AF. None of the novel biomarkers evaluated improved AF risk discrimination or reclassification beyond standard clinical AF risk factors and biomarkers.
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