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RESEARCH PRODUCT

0126: New regulators of iron metabolism, Hepcidin and Erythroferrone, in acute myocardial infarction.

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Background Dysfunctional iron storage and transport are common in patients with chronic heart failure and associated with poor prognosis. Body iron could contribute to the pathogenesis of coronary artery disease (CAD) through its ability to induce oxidative stress. However, studies on the relationship between iron metabolism and CAD have yielded conflicting results. Patients and Methods From the obseRvatoire des Infarctus de Cote d’Or (RICO) survey, 31 consecutive patients admitted in Intensive Care Unit for a first AMI were included. Serum concentrations of iron, transferrin, ferritin, the iron-regulatory hormone hepcidin and erythroferrone (a new hepcidin-regulating hormone), transferrin saturation and total iron binding capacity were assessed on admission. Results Mean age was 65±16 yrs, 61% were male, 51% had hypertension, 23% diabetes, 45% dyslipidemia and 32% were smokers. There was a trend toward a higher serum hepcidin concentration in men (99.8 versus 56.3 ng/ml, p=0.181). Heart rate on admission was negatively associated with an erythroferrone concentration (r=–0.428, p=0.023). Haemoglobin level and hematocrit were positively correlated with erythroferrone concentration (p=0.027 and p=0.021). Moreover, a lower serum transferrin concentration was found in patients with heart failure on admission (1.93±0.16g/l, vs 2.32±0.42, p=0.001). Ferritin concentration was positively related with infarct size, as assessed by Creatine Kinase peak (r=0.535, p=0.002) and there was a trend toward a positive correlation with erythroferrone concentration (r=0.314, p=0.085). Conclusion Elucidating the metabolic circuits regulated by peptidic hormones will provide valuable insights into complex networks governing iron availability in acute myocardial infarction.