Inflammatory mediated chronic anemia in patients supported with a mechanical circulatory assist device.

It is widely accepted and clinically anticipated that the patient implanted with a mechanical circulatory assist device (MCAD) will develop a state of chronic anemia that will last throughout the duration of MCAD support. Large-scale hemolysis mediated by the high sheer stress transmitted to the erythrocytes (RBCs) from the mechanical action of most MCAD systems is the accustomed mechanism responsible for this anemic status. MCAD patients exhibiting chronic anemia require frequent blood transfusions placing the patients at a high infectious risk to maintain an acceptable hematocrit. It is also acknowledged that the biomaterial interaction of the MCAD with the immune system precipitates a chronic inflammatory state in this patient population. Taken together, we hypothesize that inflammatory mediation of the erythropoiesis pathway at multiple sites-limiting the replacement of lysed RBCs-dictates the extent of chronic anemia in MCAD patients more than mechanical trauma to the blood. Hematological parameters were retrospectively analyzed for 78 patients implanted with a mechanical circulatory assist device for greater than 30 days at the University of Arizona Health Sciences Center between the years 1996 to 2002. Analysis demonstrates that the rate of hemolysis slows after MCAD implantation, marked by a progressively decreasing plasma hemoglobin concentration. In addition, the absolute reticulocyte count, a marker of juvenile RBC production, increases and remains above maximum normal values after MCAD implantation. Furthermore, the mean cell hemoglobin concentration indicates sufficient substrate for RBC development and maturation. However, hematocrit, a conventional marker of anemia, drops and remains below minimum normal value throughout the measured time period. A state of anemia in the MCAD supported patient results initially from the effect of hemolysis associated with the mechanical action of the MCAD, then chronically persists as the result of another undetermined mechanism. Given the state of chronic inflammation in the patient population, immunological activation most likely limits the full production of RBCs to their mature state.