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FGF-23 as a predictor of 6-month outcome and response to therapy in acute heart failure


 
 
 Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work was supported by a grant from the Institute of Medical Sciences, Univeristy of Opole, Poland
 
 
 
 FGF-23 is a well-known marker for phosphate metabolism and independent risk marker for cardiovascular mortality. FGF-23 can stimulate pro-fibrotic factors in myocytes and finally promote cardiac fibrosis. There is also evidence that FGF-23 levels can predict the response to the therapies in acute heart failure (AHF) patients. The aim of the study was to assess whether FGF-23 level change during an episode of AHF as well as its long-term prognostic utility in population of AHF patients. Additionally, we also aimed to evaluate correlations of FGF-23 levels with the response to therapy.
 
 
 
 We analysed 112 consecutive patients admitted to ICCU between June 2019 and January 2021 due to high-risk AHF. Guidelines guided therapy of heart failure was introduced. Blood samples were collected on admission, at discharge as well as at the 30-day. Patients were then followed-up for all-cause mortality and rehospitalisations due to heart failure.
 
 
 
 Patients (N=112; median age 68 years, 75% men, median left ventricular ejection fraction 30% [IQR 20-38%]) had median admission levels of FGF-23 = 1278 pg/ml [283-4429], Klotho protein = 670 pg/ml [501-851], NT-proBNP = 5361 ng/l [3019-13182], and GDF-15 = 4582 pg/ml [3028-9081]. FGF-23 decreased by 70% from admission to discharge (P<0.001) and then remain relatively stable up to 30-day. During median 478 days follow-up 40 patients (36%) died or were hospitalised due to heart failure - they were older, more often with new onset AHF, of ischaemic aetiology and diabetics. Patients with high levels of FGF-23 (in the 4th quartile, both on admission or at discharge) had higher mortality (Figure A and B). Model combining FGF-23, Klotho protein, NT-pro BNP, and GDF-15 adjusted for age and sex showed satisfactory predictive value of unfavourable prognosis in ROC analysis (Figure C).
 
 
 
 Levels of FGF-23 on admission in patients with AHF are significantly elevated and lowers during appropriate effective therapy what indicates the utility of FGF-23 as a typical biomarker. High values of FGF-23 are associated with higher 6-month mortality. Reduction of the FGF-23 during hospitalization can serve as a marker of AHF compensation, thus FGF-23 could be a valuable tool for assessing response to treatment.
