Fibroblast Growth Factor 23 is a strong independent marker of worse cardiovascular outcomes after an acute coronary syndrome
Kallmeyer, A.; Pello Lazaro, A. M.; Canovas, E.; Acena, A.; Gonzalez-Casaus, M. L.; Tarin, N.; Cristobal, C.; Gutierrez-Landaluce, C.; Huelmos, A.; Rodriguez-Valer, A.; GONZALEZ LORENZO, O.; Alonso, J. J.; Lopez Bescos, L.; Egido, J.; Mahillo-Fernandez, I.; Lorenzo, O.; Tunon, J.
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Background and aimsThis study aimed to assess the role of plasmatic fibroblast growth factor 23 (FGF23) as a prognostic marker after an acute coronary syndrome (ACS). MethodsThis prospective and multicentric study included 1,190 patients with ACS. FGF23 plasma levels and other components of mineral metabolism (calcidiol, parathormone [PTH], klotho, and phosphate), lipids, troponin, high-sensitivity C-reactive protein, N-terminal-pro-brain natriuretic peptide and estimated glomerular filtration rate (eGFR) were measured at discharge. The primary outcome was a combination of acute ischemic events, heart failure (HF) and death. Secondary outcomes were the separate components of the primary outcome. ResultsMedian follow-up was 5.44 (3.03-7.46) years. 294 patients developed the primary outcome. Patients with FGF23 levels below the median were predominantly males, younger, and with lower load of cardiovascular risk factors. Calcidiol and PTH levels were lower among them. Multivariable analysis showed that FGF23 (HR 1.18 [1.08-1.29], p<0.001), calcidiol (HR 0.86 [0.74-1.00], p=0.046), previous CAD or cerebrovascular accidents, and hypertension were independent predictors of the primary outcome. The predictive power of FGF23 was homogeneous across different subgroups of population. FGF23 resulted an independent predictor of HF (HR 1.38 [1.22-1.57], p<0.001), and death (HR 1.21 [1.07-1.37], p=0.002), but not of acute ischemic events. According to renal function, FGF-23 was an independent predictor for the primary outcome in patients with estimated glomerular filtration rate (eGFR) above 60 ml/min/1.73m2. ConclusionsFGF23 is a strong, independent predictor of HF and death among patients with ACS. This effect is homogeneous across different subgroups of population and not limited to patients with chronic kidney disease (CKD).
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