Abstract 2361: Bone Marrow Dysfunction In Chronic Heart Failure Patients Contributes To Impaired Erythropoiesis

Abstract

Background: We hypothesised that anemia in chronic heart failure (CHF) patients is caused by bone marrow dysfunction. Methods: Bone marrow was harvested during cardiac surgery from 17 patients with CHF (LVEF 32 ± 1.8 %) and 17 age matched control patients with normal cardiac function (LVEF ≥ 55%). Early hematopoietic progenitor cells (CD34 + ) and committed erythroid cells (CD71 bright ), apoptosis (Annexin-V + /DAPI + ) and EPO-receptor (EPO-R) density were quantified by FACS. Erythroid and myeloid colony formation of isolated CD34 + cells was assessed in methylcellulose containing incrementing doses of erythropoietin (EPO) or myeloid cytokines. After 14 days Burst Forming Units Erythroid (BFU-E) or granulocyte and monocyte colonies were quantified. Results: Patients with CHF had lower hemoglobin levels and 35% of CHF patients had anemia. The numbers of CD34 + and CD71 bright cells were 2 fold lower in CHF patients (P < 0.05). Throughout the EPO dose-response range, CD34+ cells of CHF patients produced a 3-fold lower number of BFU-E colonies than controls (figure 1 , P < 0.02). Concomittantly, myeloid colony formation was 2 fold lower in CHF patients as well (P < 0.05). This was associated with markedly increased apoptosis (P < 0.01), but equivalent EPO-receptor expression. Lower BFU-E numbers were independently associated with higher NTproBNP levels (R = − 0.5, P = 0.03). However, BFU-E formation was comparable in anemic and non-anemic CHF patients (P = 0.8). Conclusions : General bone marrow dysfunction in CHF patients contributes to impaired erythropoiesis. Although this might render patients more susceptible to anemia, it does not exclusively explain its occurrence. Impaired erythropoiesis in heart failure patients