The relationship between Fibroblast Growth Factor 23 (FGF23) and cardiac MRI findings following primary PCI in patients with acute first time STEMI

Background Fibroblast growth factor 23 (FGF23) is a regulator of mineral metabolism, that has been linked to myocardial remodeling including development of left ventricular (LV) hypertrophy and myocardial fibrosis. The aim of this study was to investigate the relationship between intact FGF23 (iFGF23), myocardial infarct size and LV remodeling following a first acute ST-elevation myocardial infarction (STEMI). Methods and results Forty-two consecutive patients with first-time STEMI, single vessel disease, successfully treated with primary percutaneous coronary intervention were included. Cardiac magnetic resonance (CMR) imaging was performed at day 2, 1 week, 2 months and 1 year post MI, and blood samples were drawn at admittance and at the same time points as the CMRs. The cohort was divided according to the presence or not of heart failure post MI. In the total cohort, iFGF23 (mean ± SD) was significantly lower at day 0 (33.7 ± 20.6 pg/ml) and day 2 (31.5 ± 23.4 pg/ml) compared with a reference interval based on 8 healthy adults (43.9 pg/ml ± 19.0 pg/ml). iFGF23 increased to normal levels (55.8 ± 23.4 pg/ml) seven days post MI. In the subset of patients with signs of acute heart failure, FGF23 was higher at all measured timepoints, reaching significantly higher FGF23 levels at 2 months and 1 year following revascularization. Conclusion There was a reduction in iFGF23 levels during the acute phase of MI, with a normalization at seven days following revascularization. During one-year follow-up, there was a gradual increase in iFGF23 levels in patients with heart failure.publishedVersio

Clustering of 37 circulating biomarkers by exploratory factor analysis in patients following complicated acute myocardial infarction

<p>Background: The objective of this study was to elucidate the complex interactions between families of circulating biomarkers representing different biochemical responses to the pathophysiology following complicated acute myocardial infarction (AMI).</p><p>Methods: Blood samples, drawn at a median of 3 days post AMI were obtained from 236 patients with complicated AMI and evidence of heart failure or left ventricular dysfunction. Using exploratory factor analysis, 37 biomarkers were grouped according to their collinearity to each other into clusters. The clusters were used as a model to elucidate interdependencies between individual biomarkers. Each cluster defines a specific pathophysiological process, called factor. These factors were used as covariates in multivariable Cox-proportional hazard regression analyses for prediction of all-cause death and the combined endpoint of cardiovascular death and re-infarction.</p><p>Results: Exploratory factor analysis grouped the biomarkers under 5 factors. The composition of these groups was partially unexpected but biological plausible. In multivariable analysis, only 1 factor proved to be an independent predictor of outcome. Major contributions (factor loadings>0.50) in this cluster came from: midregional pro-adrenomedullin, tumor necrosis factor receptor, pro-endothelin-1, growth differentiation factor 15, C-terminal pro arginine vasopressin, uric acid, chromogranin A and procollagen type III N-terminal.</p><p>Conclusion: Clustering of multiple biomarkers by exploratory factor analysis might prove useful in exploring the biological interactions between different biomarkers in cardiovascular disease and thus increase our understanding of the complicated orchestral interplay at the molecular level. (C) 2011 Elsevier Ireland Ltd. All rights reserved.</p>