Number and migratory activity of circulating endothelial progenitor cells inversely correlate with risk factors for coronary artery disease
M Vasa1, S Fichtlscherer, A Aicher
1Division of Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Germany.
Insights
Coronary artery disease (CAD) patients have fewer and less functional endothelial progenitor cells (EPCs), which are crucial for blood vessel repair. This reduction is linked to CAD risk factors like smoking and hypertension.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Regenerative Medicine
Background:
- Postnatal neovascularization relies on bone marrow-derived endothelial progenitor cells (EPCs).
- The role and regulation of EPCs in coronary artery disease (CAD) remain unclear.
- EPCs are vital for repairing ischemic tissues.
Purpose of the Study:
- To quantify and assess the functional activity of EPCs in CAD patients.
- To investigate the correlation between CAD risk factors and EPC levels/function.
- To identify independent predictors of impaired EPC function in CAD.
Main Methods:
- Compared EPC numbers and CD34+/KDR+ cells in 45 CAD patients and 15 healthy controls.
- Assessed EPC migratory function in vitro.
- Calculated a risk factor score (age, sex, hypertension, diabetes, smoking, family history, LDL).
- Utilized multivariate analysis to identify independent predictors.
Main Results:
- CAD patients showed significantly reduced EPC numbers (approx. 40%) and CD34+/KDR+ cells (approx. 48%).
- Reduced EPC levels correlated with a higher number of risk factors (R=-0.394) and CD34+/KDR+ cells (R=-0.537).
- Smokers had significantly lower EPC and CD34+/KDR+ cell levels.
- EPCs from CAD patients exhibited impaired migration, inversely correlated with risk factors (R=-0.484).
- Hypertension was an independent predictor of impaired EPC migration (P=0.043).
Conclusions:
- Patients with CAD exhibit decreased levels and impaired function of EPCs.
- This EPC dysfunction is associated with CAD risk factors.
- Reduced EPC number and activity may contribute to impaired vascularization in CAD patients.
Abstract:
Recent studies provide increasing evidence that postnatal neovascularization involves bone marrow-derived circulating endothelial progenitor cells (EPCs). The regulation of EPCs in patients with coronary artery disease (CAD) is unclear at present. Therefore, we determined the number and functional activity of EPCs in 45 patients with CAD and 15 healthy volunteers. The numbers of isolated EPCs and circulating CD34/kinase insert domain receptor (KDR)-positive precursor cells were significantly reduced in patients with CAD by approximately 40% and 48%, respectively. To determine the influence of atherosclerotic risk factors, a risk factor score including age, sex, hypertension, diabetes, smoking, positive family history of CAD, and LDL cholesterol levels was used. The number of risk factors was significantly correlated with a reduction of EPC levels (R=-0.394, P=0.002) and CD34-/KDR-positive cells (R=-0.537, P<0.001). Analysis of the individual risk factors demonstrated that smokers had significantly reduced levels of EPCs (P<0.001) and CD34-/KDR-positive cells (P=0.003). Moreover, a positive family history of CAD was associated with reduced CD34-/KDR-positive cells (P=0.011). Most importantly, EPCs isolated from patients with CAD also revealed an impaired migratory response, which was inversely correlated with the number of risk factors (R=-0.484, P=0.002). By multivariate analysis, hypertension was identified as a major independent predictor for impaired EPC migration (P=0.043). The present study demonstrates that patients with CAD revealed reduced levels and functional impairment of EPCs, which correlated with risk factors for CAD. Given the important role of EPCs for neovascularization of ischemic tissue, the decrease of EPC numbers and activity may contribute to impaired vascularization in patients with CAD. The full text of this article is available at http://www.circresaha.org.
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