|M.Sc Student||Solomon Aya|
|Subject||The Influence of Anemia on Endothelial Progenitor Cells|
(EPC) Circulating in Peripheral Blood in
Patients with Acute Coronary Syndrome
|Department||Department of Medicine||Supervisors||Mr. Yonathan Hasin|
|Mr. Arnon Blum|
Background: Anemia is an independent predictor of poor prognosis in patients with acute coronary syndrome (ACS). Endothelial progenitor cells (EPCs) are bone marrow-derived cells that are mobilized into the circulation in response to tissue ischemia. The present paradigm is that one of the roles of EPCs is to repair damaged endothelium. We know that the number of circulating EPCs increase within days of an ACS. Still, the mechanism leading to a grave prognosis in patients with anemia after ACS is not well understood.
Aim: To study a possible mechanism that may explain the association between the grave clinical outcome of anemic ACS patients and their ability to produce and mobilize EPCs on demand.
Methods: EPCs levels and function were examined in 26 ACS patients. Fifteen patients had chronic non-progressive anemia (not related to any known cause) and 11 patients had normal blood count. Blood samples were drawn on the first day of admission (within 24 hours) and upon discharge (4-7 days later). Mononuclear cells (MNC) were separated and cultured on Fibronectin coated plates with Endocult medium for 5 days. Colony forming units (CFU) were identified and counted to measure the ability to produce EPCs by the bone marrow. Endothelial lineage was confirmed by immunostaining (CD31 and Tie-2), and migration assays was performed to study EPCs’ ability to migrate into the circulation in each time point.
Results: Baseline CFU in the non-anemic group was significantly higher than in the anemic group (p<0.0001).There was a highly significant correlation between admission Hemoglobin (Hb) level and CFU count (R= 0.83, P< 0.0001). CFUs increased in both groups, non-anemic and anemic, on the second measurement (P<0.0001 and P=0.0001, respectively) but to a lower extent in the anemic group (p=0.0004 for the average delta). There was a highly significant correlation between discharge Hb level and CFU count on the second measurement (R= 0.75, P< 0.0001). Migration assay in the non-anemic group was higher than the anemic group, at baseline (p=0.017) and 4-7 days later (p=0.0054).
Conclusions: ACS patients with chronic non-progressive anemia demonstrated a reduced ability to produce and recruit EPCs on demand, possibly due to an impaired bone marrow function. These observations may partly explain the inability to heal and repair the damaged vascular endothelium, and explain the grave prognosis of ACS patients with chronic non-progressive anemia.