Abstract
(1) Background: Fibroblast growth factor 23 (FGF23) is associated with mortality in patients with heart failure (HF); however, less is known about mortality associations in patients with myocardial infarction (MI). (2) Methods: FGF23 was assessed in 180 patients with acute MI, 99 of whom presented with concomitant acute HF. Patients were followed up for one year, and outcome estimates by FGF23 were compared to GRACE score estimates. (3) Results: Log-transformed serum levels of intact FGF23 (logFGF23) did not differ between MI patients with and without HF, and no difference in logFGF23 was observed between 14 MI patients who died and those who survived. However, when only MI patients with concomitant HF were considered, logFGF23 was significantly higher among non-survivors compared to that in survivors. While logFGF23 was not associated with the outcome in the entire cohort, logFGF23 was fairly predictive for one-year mortality in patients with concomitant HF (AUC 0.78; 95%CI 0.61–0.95), where it outperformed GRACE score estimates (AUC 0.70; 95%CI 0.46–0.94). (4) Conclusions: FGF23 was associated with one-year mortality only in MI patients who concomitantly presented with HF, surpassing the predictive ability of GRACE score estimates. No associations were observed in patients without HF despite similar FGF23 levels at admission. Further studies are warranted to investigate whether FGF23 is causal for dismal outcome of HF.
Highlights
Fibroblast growth factor 23 (FGF23) is a bone-marrow-derived hormone secreted by osteoblasts and osteocytes in response to increased phosphate levels, preventing phosphate reuptake in the renal proximal tubule
FGF23 is a potent suppressor of vitamin D hormone production, inhibiting conversion of 25-hydroxyvitamin D to its active form
Besides its role in mineral metabolism, FGF23 has been shown to have a role in cardiovascular diseases
Summary
Fibroblast growth factor 23 (FGF23) is a bone-marrow-derived hormone secreted by osteoblasts and osteocytes in response to increased phosphate levels, preventing phosphate reuptake in the renal proximal tubule. Increased FGF23 levels have been associated with structural myocardial damage, including impaired left-ventricular (LV) function and adverse LV remodeling [1,2,3,4], and with alterations in myocyte calcium handling [5], upregulation of the renin–angiotensin system [6], and promotion of vascular calcification [7]. Experimental myocardial infarction (MI) resulted in the upregulation of circulating intact FGF23 along with a suppression of vitamin D hormone levels in mice and in rat models [10]. Local myocardial upregulation of FGF23 and its receptor has been shown early after MI in mice, sustained by inflammatory cytokines [11], suggesting FGF23 has a crucial role in the healing and remodeling processes after MI. FGF23 knockout mice develop rapid calcification and exhibit a markedly short life span [12], suggesting that any detrimental effects of FGF23 mainly occur through the myocardium
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