Endothelial progenitor cells (CD34+KDR+) and monocytes may provide the development of good coronary collaterals despite the vascular risk factors and extensive atherosclerosis
1From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
2From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
3From Department of Hematology Faculty of Medicine, Gazi University, Ankara-Turkey
4From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
5From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
6From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
7From Department of Hematology Faculty of Medicine, Gazi University, Ankara-Turkey
8From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
9From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
10From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
11From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
12From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
13From Department of Cardiology Faculty of Medicine, Gazi University, Ankara-Turkey
Anatol J Cardiol 2011; 4(11): 290-299 PubMed ID: 21543296 DOI: 10.5152/akd.2011.078
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Abstract

Objective: Endothelial progenitor cells (EPC) have a regenerative role in the vascular system. In this study, we aimed to evaluate simultaneously the effects of EPC and inflammatory cells on the presence and the extent of coronary artery disease (CAD) and the grade of coronary collateral growth in patients with clinical suspicion of CAD. Materials and Methods: This study has a cross-sectional and observational design. We enrolled 112 eligible patients who underwent coronary angiography consecutively (mean age: 59±9 years). The association of circulating inflammatory cells and EPC (defined by CD34+KDR+ in the lymphocyte and monocyte gate) with the presence, severity and extent of CAD and the degree of collateral growth were investigated. Logistic regression analysis was used to define the predictors of collateral flow. Results: Of 112 patients 30 had normal coronary arteries (NCA, 27%, 55±9 years) and 82 had CAD (73%, 61±8 years). Among the patients with CAD, the percent degree of luminal stenosis was <50% in 12 patients; 50-90% in 35 patients; and ≥90% in the other 35 patients. Circulating inflammatory cells were higher (leukocytes, 7150±1599 vs 8163±1588mm-3, p=0.001; neutrophils, 4239±1280 vs 4827±1273mm-3, p=0.021; monocytes, 512±111 vs 636±192mm-3, p=0.001) and EPCs were lower (0.27±0.15% vs 0.17±0.14%, p<0.001; 21±15 vs 13±12mm-3, p=0.004) in CAD group than NCA group. When we investigated the collateral growth in patients having ≥90% stenosis in at least one major coronary artery, we found that the patients with good collateral growth had significantly higher EPC (0.22±0.17% vs 0.10±0.05%, p=0.009; 18±15 vs 7±3mm-3, p=0.003) in comparison to patients with poor collateral growth. Presence of EPC was associated with reduced risk for coronary artery disease (OR: 0.934, 95%CI: 0.883-0.998, p=0.018) and was an independent predictor for good collateral growth (OR: 1.295, 95%CI: 1.039-1.615, p=0.022). A sum of CD34+KDR-, CD34+KDR+ and CD34-KDR+ cells (192±98mm-3), and a CD34-KDR- cell subpopulation within monocyte gate (514±173mm-3) reached to highest counts in good collateral group among all study population. Conclusion: Endothelial progenitor cells can be mobilized from bone marrow to induce the coronary collateral growth in case of myocardial ischemia even in presence of the vascular risk factors and extensive atherosclerosis. This finding may be supportive to investigate the molecules, which can specifically mobilize EPC without inflammatory cells.