Disturbed atrial metabolism, shear stress, and cardiac load contribute to atrial fibrillation after ablation: AXAFA biomolecule study.

Autor:	Chua W; Institute of Cardiovascular Sciences, University of Birmingham, Wolfson Drive, Birmingham, UK., Khashaba A; Institute of Cardiovascular Sciences, University of Birmingham, Wolfson Drive, Birmingham, UK., Canagarajah H; Institute of Cardiovascular Sciences, University of Birmingham, Wolfson Drive, Birmingham, UK., Nielsen JC; Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark., di Biase L; Albert Einstein College of Medicine, Montefiore Hospital, New York, New York, USA.; Texas Cardiac Arrhythmia Institute at St. David's Medical Center, Houston, TX, USA., Haeusler KG; Atrial Fibrillation NETwork (AFNET), Münster, DE.; Department of Neurology, Universitätsklinikum Würzburg, Würzburg, Germany., Hindricks G; Department of Cardiology, German Heart Center Charite, Campus Charite Mitte, Berlin, Germany., Mont L; Hospital Clinic Barcelona, University of Barcelona, Barcelona, ES., Piccini J; Duke Clinical Research Institute (DCRI), Durham, NC, USA.; Division of Cardiology, Duke University Medical Center, Duke University, Durham, NC, USA., Schnabel RB; Atrial Fibrillation NETwork (AFNET), Münster, DE.; German Centre for Cardiovascular Research (DZHK), partner site: Hamburg/Kiel/Lübeck, Germany.; Department of Cardiology, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Building O70, Martinistrasse 52, 20246 Hamburg, Germany., Schotten U; Atrial Fibrillation NETwork (AFNET), Münster, DE.; Department of Physiology, University Maastricht, Maastricht, NL., Wienhues-Thelen UH; Roche Diagnostics, Penzberg, Germany., Zeller T; German Centre for Cardiovascular Research (DZHK), partner site: Hamburg/Kiel/Lübeck, Germany.; University Center of Cardiovascular Sciences, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Fabritz L; Institute of Cardiovascular Sciences, University of Birmingham, Wolfson Drive, Birmingham, UK.; Atrial Fibrillation NETwork (AFNET), Münster, DE.; German Centre for Cardiovascular Research (DZHK), partner site: Hamburg/Kiel/Lübeck, Germany.; Department of Cardiology, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Building O70, Martinistrasse 52, 20246 Hamburg, Germany.; University Center of Cardiovascular Sciences, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany., Kirchhof P; Institute of Cardiovascular Sciences, University of Birmingham, Wolfson Drive, Birmingham, UK.; Atrial Fibrillation NETwork (AFNET), Münster, DE.; German Centre for Cardiovascular Research (DZHK), partner site: Hamburg/Kiel/Lübeck, Germany.; Department of Cardiology, University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Building O70, Martinistrasse 52, 20246 Hamburg, Germany.
Jazyk:	angličtina
Zdroj:	Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology [Europace] 2024 Feb 01; Vol. 26 (2).
DOI:	10.1093/europace/euae028
Abstrakt:	Aims: Different disease processes can combine to cause atrial fibrillation (AF). Their contribution to recurrent AF after ablation in patients is not known. Cardiovascular processes associated with recurrent AF after AF ablation were determined by quantifying biomolecules related to inflammation, metabolism, proliferation, fibrosis, shear stress, atrial pressure, and others in the AXAFA biomolecule study. Methods and Results: Twelve circulating cardiovascular biomolecules (ANGPT2, BMP10, CA125, hsCRP, ESM1, FABP3, FGF23, GDF15, IGFBP7, IL6, NT-proBNP, and hsTnT) were quantified in plasma samples obtained prior to a first AF ablation using high-throughput, high-precision assays. Cox regression was used to identify biomolecules associated with recurrent AF during the first 3 months after AF ablation. In 433 patients (64 years [58, 70]; 33% women), baseline concentrations of ANGPT2, BMP10, hsCRP, FGF23, FABP3, GDF15, and NT-proBNP were elevated in patients with recurrent AF (120/433; 28%). After adjustment for 11 clinical features and randomized treatment, elevated NT-proBNP [hazard ratio (HR) 1.58, 95% confidence interval (1.29, 1.94)], ANGPT2 [HR 1.37, (1.12, 1.67)], and BMP10 [HR 1.24 (1.02, 1.51)] remained associated with recurrent AF. Concentrations of ANGPT2, BMP10, and NT-proBNP decreased in patients who remained arrhythmia free, but not in patients with recurrent AF, highlighting their connection to AF. The other eight biomarkers showed unchanged concentrations. Conclusion: Elevated concentrations of ANGPT2, BMP10, and NT-proBNP are associated with recurrent AF after a first AF ablation, suggesting that processes linked to disturbed cardiomyocyte metabolism, altered atrial shear stress, and increased load contribute to AF after AF ablation in patients. Competing Interests: Conflict of interest: K.G.H. reports lecture fees/advisory board fees from Abbott, Alexion, Amarin, AstraZeneca, Bayer, Biotronik, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, Edwards Lifesciences, Medtronic, Pfizer, Premier Research, SUN Pharma, and W. L. Gore & Associates. R.B.S. has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme under the grant agreement no. 648131, from the European Union’s Horizon 2020 research and innovation programme under the grant agreement no. 847770 (AFFECT-EU), German Center for Cardiovascular Research (DZHK e.V.; 81Z1710103), German Ministry of Research and Education (BMBF 01ZX1408A), and ERACoSysMed3 (031L0239). R.B.S. has received lecture fees and advisory board fees from BMS/Pfizer outside this work. P.K. receives research support for basic, translational, and clinical research projects from the European Union, British Heart Foundation, Leducq Foundation, Medical Research Council (UK), and German Centre for Cardiovascular Research, from several drug and device companies active in atrial fibrillation, and has received honoraria from several such companies in the past, but not in the last 3 years. P.K. is listed as inventor on two patents held by University of Birmingham (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783). U.S. received research grants from the Netherlands Heart Foundation (CVON2014-09, RACE V Reappraisal of Atrial Fibrillation: Interaction between hyperCoagulability, Electrical remodeling, and Vascular Destabilisation in the Progression of AF) and the European Union (ITN Network Personalize AF: Personalized Therapies for Atrial Fibrillation: a translational network, grant number 860974; CATCH ME: Characterizing Atrial fibrillation by Translating its Causes into Health Modifiers in the Elderly, grant number 633196; MAESTRIA: Machine Learning Artificial Intelligence Early Detection Stroke Atrial Fibrillation, grant number 965286; REPAIR: Restoring cardiac mechanical function by polymeric artificial muscular tissue, grant number 952166). U.S. received consultancy fees or honoraria from Università della Svizzera Italiana (USI, Switzerland), Roche Diagnostics (Switzerland), EP Solutions Inc. (Switzerland), Johnson & Johnson Medical Limited (UK), and YourRhythmics BV. U.S. is co-founder and shareholder of YourRhythmics BV, a spin-off company of the University Maastricht. U.-H.W.-T. is an employee of Roche Diagnostics. T.Z. received funding from the German Science Foundation, German Center for Cardiovascular Research (DZHK e.V.; 81Z1710101, partner site project), The European Union euCanSHare project (grand agreement 825903), the ERA CVD project PREMED-CAD (FKZ01KL1807), and the ERA PerMed project (01KU1910B) outside this work. L.M. reports honoraries as consultant, lecturer, and advisory board from Boston Scientific, Abbott Medical, Johnson & Johnson, and Medtronic. He is a shareholder of Galgo Medical SL. J.P. is supported by R01AG074185 from the National Institutes of Aging, grants for clinical research from Abbott, American Heart Association, the Association for the Advancement of Medical Instrumentation, Bayer, Boston Scientific, iRhythm, and Philips, and serves as a consultant to Abbott, AbbVie, Bayer, Biotronik, Boston Scientific, Bristol Myers Squibb, Element Science, Itamar Medical, LivaNova, Medtronic, Milestone, ElectroPhysiology Frontiers, ReCor, Sanofi, Philips, and Up-to-Date. The other authors have nothing to disclose. L.F. received institutional research support from EU Horizon 2020 CATCH ME (grant agreement number 633196), and MAESTRIA (grant agreement number 965286). L.F. has received funding from Accelerator Award by the British Heart Foundation AA/18/2/34218. L.F. is further part-funded by National Institute for Health and Care Research (NIHR) award 1002898 (APRAISE-AS) at University of Birmingham, AFFECT-EU grant agreement number 847770 and German Center for Cardiovascular Research (DZHK). (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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