Dissociation of phenotypic and functional endothelial progenitor cells in patients undergoing percutaneous coronary
N L Mills1, O Tura, G J Padfield
1Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, Edinburgh, EH16 4SU, UK. nick.mills@ed.ac.uk
Insights
Percutaneous coronary intervention (PCI) increases functional endothelial progenitor cells (EPCs), specifically colony-forming units (CFU-ECs), after vascular injury. This rise in CFU-ECs was not linked to circulating CD34(+)KDR(+) cells, suggesting they are not the primary source of EPCs in the immediate response.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Cell Biology
Background:
- Endothelial progenitor cells (EPCs) are crucial for vascular repair.
- Percutaneous coronary intervention (PCI) involves local vascular injury.
- Understanding EPC response to PCI is vital for cardiovascular disease management.
Purpose of the Study:
- To assess the impact of local vascular injury during PCI on circulating EPCs.
- To investigate the changes in EPCs following PCI in patients with coronary artery disease.
Main Methods:
- Prospective case-control study involving 54 patients undergoing coronary angiography.
- Quantification of EPCs using flow cytometry (CD34(+)KDR(+)) and CFU-EC assays.
- Comparison of EPC levels before and 24 hours after diagnostic angiography or PCI.
Main Results:
- PCI, unlike diagnostic angiography, increased neutrophil count and C-reactive protein.
- A threefold increase in functional CFU-ECs was observed 24 hours post-PCI (p=0.01).
- No significant change in circulating CD34(+)KDR(+) cells or their mRNA levels was detected post-PCI.
Conclusions:
- Local vascular injury from PCI triggers a systemic inflammatory response.
- Functional CFU-ECs increase post-PCI, but not CD34(+)KDR(+) cells.
- CD34(+)KDR(+) cells may not be the primary source of EPCs in the immediate response to vascular injury.
Objectives:
Endothelial progenitor cells (EPCs) are circulating mononuclear cells with the capacity to mature into endothelial cells and contribute to vascular repair. We assessed the effect of local vascular injury during percutaneous coronary intervention (PCI) on circulating EPCs in patients with coronary artery disease.
Design And Setting:
Prospective case-control study in a university teaching hospital.
Patients:
54 patients undergoing elective coronary angiography.
Interventions And Main Outcome Measures:
EPCs were quantified by flow cytometry (CD34(+)KDR(+) phenotype) complemented by real-time polymerase chain reaction (PCR), and the colony forming unit (CFU-EC) functional assay, before and during the first 24 hours after diagnostic angiography (n = 27) or PCI (n = 27).
Results:
Coronary intervention, but not diagnostic angiography, resulted in an increase in blood neutrophil count (p<0.001) and C-reactive protein concentrations (p = 0.001) in the absence of significant myocardial necrosis. Twenty-four hours after PCI, CFU-ECs increased threefold (median [IQR], 4.4 [1.3-13.8] vs 16.0 [2.1-35.0], p = 0.01), although circulating CD34(+)KDR(+) cells (0.019% (SEM 0.004%) vs 0.016% (0.003%) of leucocytes, p = 0.62) and leucocyte CD34 mRNA (relative quantity 2.3 (0.5) vs 2.1 (0.4), p = 0.21) did not. There was no correlation between CFU-ECs and CD34(+)KDR(+) cells.
Conclusions:
Local vascular injury following PCI results in a systemic inflammatory response and increases functional CFU-ECs. This increase was not associated with an early mobilisation of CD34(+)KDR(+) cells, suggesting these cells are not the primary source of EPCs involved in the immediate response to vascular injury.
