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. (15th February 2018)

• Record Type: Journal Article
• 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.
• Is Part Of: International journal of cardiology. Volume 253(2018)
• Page Start: 84
• Page End: 90
• Publication Date: 2018-02-15
• Subjects: ACEi angiotensin converting enzyme inhibitor -- ARB angiotensin receptor blocker -- BNP Brain Natriuretic Peptide -- BIOSTAT-CHF BIOlogy Study to Tailored Treatment in Chronic Heart Failure -- CKD chronic kidney disease -- eGFR estimated Glomerular Filtration Rate -- FGF23 fibroblast growth factor 23 -- HF heart failure -- JVP jugular venous pressure -- NT-pro BNP N terminal pro Brain Natriuretic Peptide -- RAAS Renin Angiotensin Aldosterone System; Heart failure -- FGF23 -- Volume overload -- Prognosis; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2017.10.010
• Languages: English
• ISSNs: 0167-5273

Abstract

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.