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Background Anemia and relative iron deficiency (RID) are prevalent in patients with heart failure (HF). The etiology of anemia and RID in HF patients is unclear. Hepcidin expression may be closely related to anemia and RID in HF patients. Although hepcidin is produced mainly by the liver, and the most frequent histologic appearance of liver in HF patients is congestion, the influence of liver congestion (LC) on hepcidin production has not yet been investigated. We investigated whether hepcidin contributed to anemia and RID in rats with LC. Methods and Results LC was induced in rats by ligating the inferior vena cava and compared with bleeding anemia (BA) model induced by phlebotomy and hemolytic anemia (HA) model induced by injection of phenylhydrazine. BA and HA strongly suppressed expression of hepcidin in liver and so did not cause decrease in serum iron and transferrin saturation. However, hepcidin expression did not decrease in LC rats, which resulted in anemia and lower transferrin saturation. In addition, many cells with hemosiderin deposits were observed in the liver and spleen and not in the bone marrow, and this appeared to be related to suppression of hepcidin expression. Iron accumulated in hepatocytes, and bone morphogenetic protein 6, which induces hepcidin, increased. Inflammation was observed in the congestive liver, and there was an increase in interleukin-6, which also induced hepcidin and was induced by free heme and hemoglobin via Toll-like receptor 4. Conclusions We conclude that LC contributes to RID and anemia, and it does so via inappropriate expression of hepcidin.

Background: Some studies suggested that analysis of gene expression in myocardial biopsy promised to improve the differential diagnosis of heart failure. On the other hand, higher serum inflammatory markers are known to predict worse prognosis in heart failure without infectious complication. Objective: We examined whether gene expression of inflammatory markers in myocardial biopsy predicted one subgroup of patients with progressive heart disease, indicative of ongoing immune activation. Method: We examined gene expression of inflammatory markersleukocyte markers, inflammatory cytokine and chemokineby quantitative RT-PCR in heart samples from patients admitted to our hospital due to heart failurecardiac biopsy, 55; autopsy, 5. Result: Gene expression of several inflammatory markers was detectable from a small piece of cardiac biopsy. Expression levels of inflammatory markers in samples of myocarditis were higher than those of non-myocarditis. But expression levels of inflammatory markers in some samples of non-myocarditis, progressive heart diseases like fabry disease and mitochondrial cardiomyopathy, were the same as those of myocarditis. Conclusion: High expression of leukocyte marker, inflammatory cytokines and chemokine may predict progressive heart disease, abeit infiltrating immunocompetent cells are not detected histopathologically.