Hepcidin in the Pathogenesis of Anemia in Patients With Chronic Heart Failure

Background: Anemia in chronic heart failure (CHF) is directly linked to increased mortality and reduced exercise capacity. The pathomechanism for the development of anemia in CHF is not well understood. Impairment of iron homeostasis is discussed to be one of the major triggers in anemia of chronic disease. Hepcidin was recently described as the central regulator of iron homeostasis.

Main hypothesis: Plasma hepcidin levels are altered in anemic CHF patients compared to non anemic controls and might be a main contributing factor of anemia in CHF.

Iron regulator-hypothesis High levels of cytokines in CHF patients cause up-regulation of hepcidin, which in turn leads to low iron uptake causing anemia. In this case venous hepcidin and hemoglobin concentrations should both correlate with cytokine levels.

Erythropoietin regulator-hypothesis Dysregulation of the erythropoietin system results in anemia, which represses hepcidin. This leads to a negative correlation between hemoglobin and hepcidin in plasma.

Methods: 100 consecutive patients diagnosed with systolic CHF will be prospectively included in the study. Iron status will be assessed and hepcidin, erythropoietin as well as interleukin-1, interleukin-6 and soluble TNF alpha receptor levels will be measured by ELISA.

Patients will be followed up for one year and mortality, rehospitalization and worsening of CHF will be documented.