Objective
In this study, we investigated whether or not the number and function of endothelial progenitor cells (EPCs) were associated with the development of collateral formation in patients with single-vessel coronary artery disease of chronic total occlusion (CTO). We aimed also to examine the ability of EPCs to decrease the size of myocardial infarction, and test formation of neovascularization in an experimental model (dogs) with acute myocardial infarctions (AMI).
Methods
The patients who had CTO in one major coronary artery ( n =20) were undergoing coronary angiography (CAG). EPCs were isolated from peripheral blood samples and cultured. Their phenotypes were confirmed by uptake of acetylated LDL and binding of fluorescein isothiocyanate (FITC)-labeled Ulex europaeus agglutinin 1 (UEA-1) lectin. The numbers of colony-forming units (CFUs) were counted. The expressed angiogenic genes [human vascular endothelial growth factor receptor-2 (hVEGFR-2) and endothelial nitric oxide synthase (eNOS)] from the culture cells were also measured by real-time qPCR. Isolated EPCs from CTO patients were transplanted intramyocardially in an experimental model (dogs) with AMI. ECG was done and cardiac enzymes (CK and CK-MB) were measured for the animals to assess cardiac activity. Scarification was done after 1 month of EPCs injection .Histopathology was done to assess neovascularization and cardiac repair in peri-infarct cardiac tissue. Real-time qPCR for human genes (hVEGFR-2, and eNOS) was done to assess homing of transplanted EPCs.
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