Fibroblast growth factor 23 is related to profiles indicating volume overload, poor therapy optimization and prognosis in patients with new-onset and worsening heart failure

ter Maaten, J. M. et al. (2018) Fibroblast growth factor 23 is related to profiles indicating volume overload, poor therapy optimization and prognosis in patients with new-onset and worsening heart failure. International Journal of Cardiology, 253, pp. 84-90. (doi: 10.1016/j.ijcard.2017.10.010) (PMID:29306478)

Abstract

Background: Fibroblast growth factor (FGF) 23 is a hormone that increases urinary phosphate excretion and regulates renal sodium reabsorption and plasma volume. We studied the role of plasma FGF23 in therapy optimization and outcomes in patients with new-onset and worsening heart failure (HF). Methods: We measured plasma C-terminal FGF23 levels at baseline in 2399 of the 2516 patients included in the BIOlogy Study to Tailored Treatment in Chronic HF (BIOSTAT-CHF) trial. The association between FGF23 and outcome was evaluated by Cox regression analysis adjusted for potential confounders. Results: Median FGF23 was 218.0 [IQR: 117.1–579.3] RU/ml; patients with higher FGF23 levels had a worse NYHA class, more signs of congestion, and were less likely to use an ACE-inhibitor (ACEi) or angiotensin receptor blocker (ARBs) at baseline (all P < 0.01). Higher FGF23 levels were independently associated with higher BNP, lower eGFR, the presence of oedema and atrial fibrillation (all P < 0.001). In addition, higher FGF23 was independently associated with impaired uptitration of ACEi/ARBs after 3 months, but not of beta-blockers. In multivariable Cox regression analysis, FGF23 was independently associated with all-cause mortality (hazard ratio: 1.17 (1.09–1.26) per log increase, P < 0.001), and the combined endpoint of all-cause mortality and HF hospitalization (1.15 (1.08–1.22) per log increase, P < 0.001). Conclusions: In patients with new-onset and worsening HF, higher plasma FGF23 levels were independently associated with volume overload, less successful uptitration of ACEi/ARBs and an increased risk of all-cause mortality and HF hospitalization.

• Item Type: Articles
• Additional Information: This project was funded by a grant from the European Commission: FP7-242209-BIOSTAT-CHF. This study was supported by the Dutch Heart Foundation, CVON 2014-11 RECONNECT.
• Status: Published
• Refereed: Yes
• Glasgow Author(s) Enlighten ID: Cleland, Professor John and Damman, Dr Kevin
• Authors: ter Maaten, J. M., Voors, A. A., Damman, K., van der Meer, P., Anker, S. D., Cleland, J. G.F., Dickstein, K., Filippatos, G., van der Harst, P., Hillege, H. L., Lang, C. C., Metra, M., Navis, G., Ng, L., Ouwerkerk, W., Ponikowski, P., Samani, N. J., van Veldhuisen, D. J., Zannad, F., Zwinderman, A. H., and de Borst, M. H.
• Subjects: R Medicine > R Medicine (General)
• College/School: College of Medical Veterinary and Life Sciences > School of Cardiovascular & Metabolic Health; College of Medical Veterinary and Life Sciences > School of Health & Wellbeing > Robertson Centre
• Journal Name: International Journal of Cardiology
• Publisher: Elsevier
• ISSN: 0167-5273
• ISSN (Online): 1874-1754
• Published Online: 03 January 2018
• Copyright Holders: Copyright © 2017 Elsevier B.V.
• First Published: First published in International Journal of Cardiology 253: 84-90
• Publisher Policy: Reproduced in accordance with the publisher copyright policy