Dataset Information

Fibroblast growth factor-23 and death, heart failure, and cardiovascular events in community-living individuals: CHS (Cardiovascular Health Study).

ABSTRACT: OBJECTIVES:This study sought to determine the association of fibroblast growth factor (FGF)-23 with death, heart failure (HF), and cardiovascular disease (CVD) in the general population, as well as the influence of chronic kidney disease (CKD) in this setting. BACKGROUND:FGF-23 increases renal phosphorus excretion and inhibits vitamin D activation. In end-stage renal disease, high FGF-23 levels are associated with mortality. The association of FGF-23 with death, HF, and CVD in the general population, and the influence of CKD in this setting, are unknown. METHODS:Plasma FGF-23 was measured in 3,107 community-living persons ? 65 years of age in 1996 and 1997, and participants were followed through 2008. HF and CVD events were adjudicated by a panel of experts. Associations of FGF-23 with each outcome were evaluated using Cox proportional hazards models, and we tested whether associations differed by CKD status. RESULTS:Both lower estimated glomerular filtration rate and higher urine albumin to creatinine ratios were associated with high FGF-23 at baseline. During 10.5 years (median) follow-up, there were 1,730 deaths, 697 incident HF events, and 797 incident CVD events. Although high FGF-23 concentrations were associated with each outcome in combined analyses, the associations were consistently stronger for those with CKD (p interactions all <0.006). In the CKD group (n = 1,128), the highest FGF-23 quartile had adjusted hazards ratios (HR) of 1.87 (95% confidence interval [CI]: 1.47 to 2.38) for all-cause death, 1.94 (95% CI: 1.32 to 2.83) for incident HF, and 1.49 (95% CI: 1.02 to 2.18) for incident CVD events compared with the lowest quartile. Corresponding HRs in those without CKD (n = 1,979) were 1.29 (95% CI: 1.05 to 1.59), 1.37 (95% CI: 0.99 to 1.89), and 1.07 (95% CI: 0.79 to 1.45). CONCLUSIONS:FGF-23, a hormone involved in phosphorous and vitamin D homeostasis, is independently associated with all-cause death and incident HF in community-living older persons. These associations appear stronger in persons with CKD.

SUBMITTER: Ix JH

PROVIDER: S-EPMC3396791 | biostudies-literature | 2012 Jul

REPOSITORIES: biostudies-literature

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Fibroblast growth factor-23 and death, heart failure, and cardiovascular events in community-living individuals: CHS (Cardiovascular Health Study).

Ix Joachim H JH Katz Ronit R Kestenbaum Bryan R BR de Boer Ian H IH Chonchol Michel M Mukamal Kenneth J KJ Rifkin Dena D Siscovick David S DS Sarnak Mark J MJ Shlipak Michael G MG

Journal of the American College of Cardiology 20120613 3

<h4>Objectives</h4>This study sought to determine the association of fibroblast growth factor (FGF)-23 with death, heart failure (HF), and cardiovascular disease (CVD) in the general population, as well as the influence of chronic kidney disease (CKD) in this setting.<h4>Background</h4>FGF-23 increases renal phosphorus excretion and inhibits vitamin D activation. In end-stage renal disease, high FGF-23 levels are associated with mortality. The association of FGF-23 with death, HF, and CVD in the ...[more]

PMID: 22703926

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Project description:Background Fibroblast growth factor 23 (FGF-23) is crucial in regulating phosphate and vitamin D metabolism and is moreover associated with an increased cardiovascular risk. The specific objective of this study was to investigate the influence of FGF-23 on cardiovascular outcomes, including hospitalization for heart failure (HHF), postoperative atrial fibrillation, and cardiovascular death, in an unselected patient population after cardiac surgery. Methods and Results Patients undergoing elective coronary artery bypass graft and/or cardiac valve surgery were prospectively enrolled. FGF-23 blood plasma concentrations were assessed before surgery. A composite of cardiovascular death/HHF was chosen as primary end point. A total of 451 patients (median age 70 years; 28.8% female) were included in the present analysis and followed over a median of 3.9 years. Individuals with higher FGF-23 quartiles showed elevated incidence rates of the composite of cardiovascular death/HHF (quartile 1, 7.1%; quartile 2, 8.6%; quartile 3, 15.1%; and quartile 4, 34.3%). After multivariable adjustment, FGF-23 modeled as a continuous variable (adjusted hazard ratio for a 1-unit increase in standardized log-transformed biomarker, 1.82 [95% CI, 1.34-2.46]) as well as using predefined risk groups and quartiles remained independently associated with the risk of cardiovascular death/HHF and the secondary outcomes, including postoperative atrial fibrillation. Reclassification analysis indicated that the addition of FGF-23 to N-terminal pro-B-type natriuretic peptide provides a significant improvement in risk discrimination (net reclassification improvement at the event rate, 0.58 [95% CI, 0.34-0.81]; P<0.001; integrated discrimination increment, 0.03 [95% CI, 0.01-0.05]; P<0.001). Conclusions FGF-23 is an independent predictor of cardiovascular death/HHF and postoperative atrial fibrillation in individuals undergoing cardiac surgery. Considering an individualized risk assessment, routine preoperative FGF-23 evaluation may improve detection of high-risk patients.

Project description:BackgroundElevated fibroblast growth factor 23 (FGF23) levels have been associated with mortality in adults with heart failure (HF), but data on FGF23 levels in paediatric HF are limited. In this prospective cohort study, we aimed to assess the prognostic value of FGF23 in children with chronic HF.MethodsWe prospectively enrolled 40 children with chronic HF and 20 matched healthy controls. In each patient, a complete diagnostic workup was performed, including transthoracic echocardiography to evaluate cardiac systolic and diastolic functions. Serum FGF23, renal function tests, parathyroid hormone, serum calcium and phosphate were measured in patients and controls. N-terminal probrain natriuretic peptide (NT-proBNP) was measured in patients. The severity of symptoms was assessed using the modified Ross HF classification for children. Patients were followed for 1 year, and clinical worsening events such as death and HF hospitalisation were recorded.ResultsPatients with HF had significantly higher FGF23 levels compared with controls (355.68±97.27 pg/mL and 60.20±11.04 pg/mL, respectively; p<0.001). Three patients died and 11 were admitted with HF. In comparison with patients without clinical worsening events, these 14 patients exhibited significantly higher FGF23 levels (320.04±89.56 pg/mL and 421.86±75.50 pg/mL, respectively; p<0.001). FGF23 was positively correlated with NT-proBNP and left ventricular end-diastolic diameter and negatively correlated with ejection fraction and fractional shortening. The ability of FGF23 to predict clinical worsening events in patients was analysed using a receiver operating characteristic curve. The optimal cut-off point was 375 pg/mL, with 85.71% sensitivity, 84.62% specificity, positive predictive value of 75.0, negative predictive value of 91.7 and area under the curve (AUC) of 0.878. Multivariable regression analysis revealed that FGF23 is the only independent predictor of clinical worsening events in children with chronic HF.ConclusionFGF23 levels were elevated in children with chronic HF and increased significantly as Ross score class increased. FGF23 levels increased in patients who experienced clinical worsening events.

Project description:BACKGROUND:Elevated fibroblast growth factor 23 (FGF-23) concentrations are associated with greater risk of cardiovascular events and mortality, especially among people with chronic kidney disease (CKD). Because individuals with CKD are at an increased risk of sudden cardiac death (SCD), we sought to understand whether FGF-23 level is a stronger risk factor for SCD versus non-SCD. STUDY DESIGN:Cohort study. SETTING & PARTICIPANTS:3,244 participants 65 years or older in the community-based Cardiovascular Health Study. PREDICTOR:Plasma FGF-23 concentrations. OUTCOMES:We assessed SCD and non-SCD in these analyses. SCD was adjudicated rigorously and was defined as a sudden pulseless condition of cardiac origin in a previously stable person occurring out of hospital or in the emergency department. MEASUREMENTS:We estimated associations of baseline FGF-23 concentrations with SCD and non-SCD using Cox proportional hazards models after adjustment for demographics, cardiovascular risk factors, comorbid conditions, and kidney function. We also tested whether associations differed by CKD status. RESULTS:During a median follow-up of 8.1 years, there were 118 adjudicated SCD and 570 non-SCD events. After multivariable adjustment for demographics, cardiovascular risk factors, comorbid conditions, and parameters of kidney function, higher FGF-23 concentrations were an independent risk factor for non-SCD (HR [per doubling], 1.17; 95% CI, 1.06-1.30). However, elevated FGF-23 concentrations were not associated independently with SCD (HR [per doubling], 1.07; 95% CI, 0.85-1.35). In stratified analysis by CKD status (36.5% of cohort), doubling of FGF-23 concentrations was associated independently with non-SCD (adjusted HR, 1.26; 95% CI, 1.10-1.45). A similar magnitude of association was observed between FGF-23 level and SCD in the CKD subgroup; however, it was not significant (HR, 1.20; 95% CI, 0.89-1.62). LIMITATIONS:Limited power to detect moderate-sized effects between FGF-23 level and SCD in both the primary and stratified analyses. CONCLUSIONS:In this population-based study, FGF-23 level elevations were associated independently with non-SCD. Among individuals with CKD, the associations between FGF-23 level and SCD and non-SCD were similar.

Dataset Information

Fibroblast growth factor-23 and death, heart failure, and cardiovascular events in community-living individuals: CHS (Cardiovascular Health Study).

Publications

Fibroblast growth factor-23 and death, heart failure, and cardiovascular events in community-living individuals: CHS (Cardiovascular Health Study).

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