Abstract 15374: Contrasting Circulating Endothelial Progenitor Cell Number and Function in Patients Admitted for Acute Dyspnea
Background: Endothelial dysfunction is an important underlying mechanism in the pathophysiology of heart failure (HF). Circulating endothelial progenitor cells (EPCs) may contribute to endogenous vascular repair in HF. We aim to investigate EPC number and function in patients admitted for acute dyspnea.
Methods: Peripheral blood mononuclear cells were isolated from control subjects (Group 1, n=35, outpatient, not dyspneic) or patients admitted acutely with respiratory causes of dyspnea and confirmed non-HF (Group 2, n=40) or acute HF (Group 3, n=45, reduced left ventricular ejection fraction (<50%)) using Ficoll density gradient centrifugation and grown on fibronectin-coated plates. Enumeration of EPCs was performed using flow cytometry of CD34+ and KDR+ markers. Colony forming unit (CFU), migration and tubule formation assays were conducted to determine EPC function.
Results: In HF, the number of CD34+/KDR+ EPCs, CFU and migrated cell distance are higher (all Ps<0.05) with a trend towards longer tubule length compared to Group 1 (Table). In contrast, non-HF acutely dyspneic patients have lower EPC numbers and more EPC dysfunction in terms of CFU, tubule formation (all Ps<0.05) and a trend towards poorer migration capacity (Table).
Conclusion: In HF, circulating EPCs appear to be mobilized and activated whilst in patients acutely admitted for respiratory causes of dyspnea, EPC number and function are reduced. Further studies on the pathophysiology and diagnostic utility of EPC in the acutely breathless patients are warranted.
- © 2013 by American Heart Association, Inc.