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Title: 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
Authors: ter Maaten, Jozine M.
Voors, Adriaan A.
Damman, Kevin
van der Meer, Peter
Anker, Stefan D.
Cleland, John G.
Dickstein, Kenneth
Filippatos, Gerasimos
van der Harst, Pim
Hillege, Hans L.
Lang, Chim C.
Metra, Marco
Navis, Gerjan
Ng, Leong
Ouwerkerk, Wouter
Ponikowski, Piotr
Samani, Nilesh J.
van Veldhuisen, Dirk J.
Zannad, Faiez
Zwinderman, Aeilko H.
de Borst, Martin H.
First Published: 3-Jan-2018
Publisher: Elsevier, International Society for Adult Congenital Heart Disease
Citation: International Journal of Cardiology, 2018, 253, pp. 84-90 (7)
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.
DOI Link: 10.1016/j.ijcard.2017.10.010
ISSN: 0167-5273
eISSN: 1874-1754
Embargo on file until: 3-Jan-2019
Version: Post-print
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2018, Elsevier, International Society for Adult Congenital Heart Disease. Deposited with reference to the publisher’s open access archiving policy.
Description: The file associated with this record is under embargo until 12 months after publication, in accordance with the publisher's self-archiving policy. The full text may be available through the publisher links provided above.
Appears in Collections:Published Articles, Dept. of Cardiovascular Sciences

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