Association of bone morphogenetic protein 10 and recurrent atrial fibrillation after catheter ablation
- PMID: 37314197
- PMCID: PMC10265951
- DOI: 10.1093/europace/euad149
Association of bone morphogenetic protein 10 and recurrent atrial fibrillation after catheter ablation
Abstract
Aims: Atrial remodelling, defined as a change in atrial structure, promotes atrial fibrillation (AF). Bone morphogenetic protein 10 (BMP10) is an atrial-specific biomarker released to blood during atrial development and structural changes. We aimed to validate whether BMP10 is associated with AF recurrence after catheter ablation (CA) in a large cohort of patients.
Methods and results: We measured baseline BMP10 plasma concentrations in AF patients who underwent a first elective CA in the prospective Swiss-AF-PVI cohort study. The primary outcome was AF recurrence lasting longer than 30 s during a follow-up of 12 months. We constructed multivariable Cox proportional hazard models to determine the association of BMP10 and AF recurrence. A total of 1112 patients with AF (age 61 ± 10 years, 74% male, 60% paroxysmal AF) was included in our analysis. During 12 months of follow-up, 374 patients (34%) experienced AF recurrence. The probability for AF recurrence increased with increasing BMP10 concentration. In an unadjusted Cox proportional hazard model, a per-unit increase in log-transformed BMP10 was associated with a hazard ratio (HR) of 2.28 (95% CI 1.43; 3.62, P < 0.001) for AF recurrence. After multivariable adjustment, the HR of BMP10 for AF recurrence was 1.98 (95% CI 1.14; 3.42, P = 0.01), and there was a linear trend across BMP10 quartiles (P = 0.02 for linear trend).
Conclusion: The novel atrial-specific biomarker BMP10 was strongly associated with AF recurrence in patients undergoing CA for AF.
Clinicaltrials.gov identifier: NCT03718364; https://clinicaltrials.gov/ct2/show/NCT03718364.
Keywords: Atrial fibrillation; BMP10; Biomarker; Bone morphogenetic protein 10; Catheter ablation; Pulmonary vein isolation.
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.
Conflict of interest statement
Conflict of interest: P.B. received research funding from the University of Basel, the ‘Stiftung für Herzschrittmacher und Elektrophysiologie’, the ‘Freiwillige Akademische Gesellschaft Basel’, and the Swiss Heart Foundation and Johnson&Johnson, all outside the submitted work, and reports personal fees from Abbott, Boston Scientific, and Pfizer BMS. D.C. received consultancy fees from Roche Diagnostics and Trimedics and speaker fees from Servier and BMS/Pfizer. S.K. received funding from the ‘Stiftung für Herzschrittmacher und Elektrophysiologie’. M.K. received personal fees from Daiichi Sankyo and grants from the Swiss National Science Foundation, Swiss Heart Foundation, Foundation for CardioVascular Research Basel, Bayer, Pfizer, Boston Scientific, BMS, Biotronik, and Daiichi Sankyo. S.O. received research grants from the Swiss National Science Foundation and Swiss Heart Foundation, Foundation for CardioVascular Research Basel, and F. Hoffmann-La Roche Ltd and educational and speaker grants from F. Hoffmann-La Roche Ltd, Bayer, Novartis, Sanofi, AstraZeneca, Daiichi Sankyo, and Pfizer. C.S. is a member of the Advisory Board of Medtronic Europe and Advisory Board of Boston Scientific Europe and has received educational grants from Biosense Webster and Biotronik, research grants from the European Union’s FP7 program and Biosense Webster, and lecture and consulting fees from Abbott, Medtronic, Biosense Webster, Boston Scientific, Micro-Port, and Biotronik. All remaining authors have declared no conflicts of interest.
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