Inflammatory proteomics profiling for prediction of incident atrial fibrillation
Börschel, C. S., Ortega-Alonso, A., Havulinna, A. S., Jousilahti, P., Salmi, M., Jalkanen, S., Salomaa, V., Niiranen, T., & Schnabel, R. B. (2023). Inflammatory proteomics profiling for prediction of incident atrial fibrillation. Heart, 109(13), 1000-1006. https://doi.org/10.1136/heartjnl-2022-321959
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2023Copyright
© Author(s) (or their employer(s)) 2023.
Objective Atrial fibrillation (AF) has emerged as a common condition in older adults. Cardiovascular risk factors only explain about 50% of AF cases. Inflammatory biomarkers may help close this gap as inflammation can alter atrial electrophysiology and structure. This study aimed to determine a cytokine biomarker profile for this condition in the community using a proteomics approach.
Methods This study uses cytokine proteomics in participants of the Finnish population-based FINRISK cohort studies 1997/2002. Risk models for 46 cytokines were developed to predict incident AF using Cox regressions. Furthermore, the association of participants’ C reactive protein (CRP) and N-terminal pro B-type natriuretic peptide (NT-proBNP) concentrations with incident AF was examined.
Results In 10 744 participants (mean age of 50.9 years, 51.3% women), 1246 cases of incident AF were observed (40.5% women). The main analyses, adjusted for participants’ sex and age, suggested that higher concentrations of macrophage inflammatory protein-1β (HR=1.11; 95% CI 1.04, 1.17), hepatocyte growth factor (HR=1.12; 95% CI 1.05, 1.19), CRP (HR=1.17; 95% CI 1.10, 1.24) and NT-proBNP (HR=1.58; 95% CI 1.45, 1.71) were associated with increased risk of incident AF. In further clinical variable-adjusted models, only NT-proBNP remained statistically significant.
Conclusion Our study confirmed NT-proBNP as a strong predictor for AF. Observed associations of circulating inflammatory cytokines were primarily explained by clinical risk factors and did not improve risk prediction. The potential mechanistic role of inflammatory cytokines measured in a proteomics approach remains to be further elucidated.
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Additional information about funding
The Biomarker Project was funded by the European Union Seventh Framework Program (FP7/2007-2013) under grant agreement No HEALTH-F2-2011-278913. The MORGAM Project has received funding from EU projects MORGAM (Biomed, BMH4-CT98-3183), GenomEUtwin (FP5, QLG2-CT-2002-01254), ENGAGE (FP7, HEALTH-F4-2007-201413), CHANCES (FP7, HEALTH-F3-2010-242244), BiomarCaRE (FP7, HEALTH-F2-2011-278913), euCanSHare (Horizon 2020, No 825903) and AFFECT-EU (Horizon 2020, No 847770); and Medical Research Council, London (G0601463, No 80983: Biomarkers in the MORGAM Populations). This has supported central coordination, workshops and part of the activities of the MORGAM Data Centre, the MORGAM Laboratories and the MORGAM Participating Centers. The FINRISK surveys were mainly funded by the National Institute for Health and Welfare (THL) budgetary funds. Additional funding has been obtained from numerous non-profit foundations. VS was supported by the Finnish Foundation for Cardiovascular Research and the Juho Vainio Foundation. RBS has received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program under the grant agreement No 648131, from the European Union's Horizon 2020 research and innovation program under the grant agreement No 847770 (AFFECT-EU) and German Centre for Cardiovascular Research (DZHK e.V.) (81Z1710103); German Ministry of Research and Education (BMBF 01ZX1408A) and ERACoSysMed3 (031L0239). TN has received funding from the Academy of Finland (321351), the Emil Aaltonen Foundation, and the Finnish Foundation for Cardiovascular Research. KK reports grants from the European Union and grants from the Medical Research Council, UK, during the development of the study. MS and ASH have received funding from the Academy of Finland (MS 141136, ASH 321356). ...License
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