Association of Fibroblast Growth Factor-23 Levels and Angiotensin-Converting Enzyme Inhibition in Chronic Systolic Heart Failure
Language English Country United States Media print
Document type Journal Article, Observational Study, Research Support, Non-U.S. Gov't
PubMed
26450001
DOI
10.1016/j.jchf.2015.05.012
PII: S2213-1779(15)00425-4
Knihovny.cz E-resources
- Keywords
- adverse events, angiotensin-converting enzyme inhibitor, fibroblast growth factor-23, heart failure, outcome,
- MeSH
- Absorptiometry, Photon methods MeSH
- Survival Analysis MeSH
- Biomarkers MeSH
- Chronic Disease MeSH
- Kidney Failure, Chronic etiology mortality physiopathology MeSH
- Echocardiography, Doppler MeSH
- Fibroblast Growth Factors blood MeSH
- Fibroblast Growth Factor-23 MeSH
- Risk Assessment MeSH
- Angiotensin-Converting Enzyme Inhibitors therapeutic use MeSH
- Kaplan-Meier Estimate MeSH
- Cohort Studies MeSH
- Middle Aged MeSH
- Humans MeSH
- Multivariate Analysis MeSH
- Predictive Value of Tests MeSH
- Prognosis MeSH
- Retrospective Studies MeSH
- Aged MeSH
- Severity of Illness Index MeSH
- Heart Failure, Systolic blood complications drug therapy mortality MeSH
- Kidney Function Tests MeSH
- Treatment Outcome MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Observational Study MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Biomarkers MeSH
- FGF23 protein, human MeSH Browser
- Fibroblast Growth Factors MeSH
- Fibroblast Growth Factor-23 MeSH
- Angiotensin-Converting Enzyme Inhibitors MeSH
OBJECTIVES: The aim of this study was to evaluate the association of fibroblast growth factor (FGF)-23 with clinical and laboratory findings, the prognostic value of FGF-23, and the relationship between angiotensin-converting enzyme inhibitor (ACEi) therapy, FGF-23 levels, and outcomes in patients with chronic systolic heart failure (HF). BACKGROUND: FGF-23 is a bone-derived hormone regulating mineral metabolism. Higher FGF-23 levels are associated with an increased risk of cardiovascular mortality or HF development. Mechanisms leading to increased FGF-23 and its prognostic value have not been thoroughly studied in HF. METHODS: FGF-23 was measured in 369 patients (mean age 59 ± 11 years, 84% male) with systolic HF. Patients were followed for adverse events (e.g., death, urgent heart transplantation, ventricular assist device implantation). RESULTS: Tricuspid regurgitation severity, chronic kidney disease (CKD), alkaline phosphatase concentrations, inferior vena cava dilation, and absence of ACEi therapy were independently associated with FGF-23. FGF-23 was independently associated with outcomes in patients without CKD (hazard ratio [HR]: 1.43, 95% confidence interval [CI]: 1.14 to 1.78), but not in CKD patients (HR: 1.12, 95% CI: 0.87 to 1.45). In patients without CKD and with FGF-23 in the highest tertile, ACEi therapy was associated with a lower risk of adverse events (HR: 0.42, 95% CI: 0.21 to 0.81), whereas no association was seen in the remaining patients (HR: 1.18, 95% CI: 0.52 to 2.70). CONCLUSIONS: In systolic HF, elevated FGF-23 is an independent predictor of adverse events, particularly in patients with preserved renal function. The association of FGF-23 with adverse events likely reflects early alterations of renal hemodynamics and renin-angiotensin system activation. Increased FGF-23 may identify a subset of HF patients benefiting from ACEi therapy.
Department of Cardiology Institute for Clinical and Experimental Medicine Prague Czech Republic
Department of Pathology Brigham and Women's Hospital Harvard Medical School Boston Massachusetts
References provided by Crossref.org
Glucose Homeostasis, Pancreatic Endocrine Function, and Outcomes in Advanced Heart Failure
