Association between mobilization of circulating endothelial progenitor cells and time or degree of injury from angioplasty in patients with exertional angina: A prospective study

Abstract

The aim of the present study was to investigate the effect of coronary artery angioplasty on the recruitment of circulating endothelial progenitor cells (EPCs) in patients with angina pectoris. A total of 66 patients treated by coronary stenting were enrolled in the PCI group and 17 patients that underwent angiography alone were enrolled in the control group. The EPC count in the blood was measured by flow cytometry prior to and at 1, 3, 5, 7 and 24 h following angioplasty in the percutaneous coronary intervention (PCI) group, and at three time-points following angiography in the control group. Differences between the two groups included the characteristics of the coronary artery lesions, the incidence of diabetes and family history of coronary heart disease. The mean surface area of the stent deployed was 335.59±234.99 mm. No significant change in EPC count was measured in the control group. In the PCI group, a moderate and delayed increase in the number of cluster of differentiation (CD)34/kinase domain receptor (KDR) EPCs occurred at 24 h post-balloon inflation compared with the baseline level. The CD133/CD34/KDR subpopulations showed undulating changes at 3, 7 and 24 h post-PCI (P=0.016, P=0.01 and P=0.032, respectively). An arch shape was displayed in CD133/KDR cells; initially, a reduction occurred at 3 h and was maintained constantly until 7 h (P=0.003, P=0.013 and P=0.033 at 3, 5 and 7 h, respectively), after which a slight increase to the baseline level occurred at 24 h (P=0.084). The CD133/CD34 cells increased in stepwise manner until 24 h. The CD34/KDR EPC change magnitude correlated significantly with a global damage index by partial correlation analysis (P<0.001). The results suggested that a time-dependent mobilization of EPCs may be initiated by PCI; the change magnitude of the CD34/KDR cells was associated particularly with endothelial injury degree from the PCI procedure.

Substance P ameliorates tumor necrosis factor‐alpha‐induced endothelial cell dysfunction by regulating eNOS expression in vitro

“…Genetic or environmental factors such as diabetes and smoking induce vascular injury to cause functional deficiency of the vascular endothelium; moreover, clinical treatment, including balloon expansion or a stenting process, can also provoke damage to the endothelium . This endothelial injury results in an excessive inflammatory response leading to vascular diseases, including acute myocardial infarction and aortic dissection.…”

“…Genetic or environmental factors such as diabetes and smoking induce vascular injury to cause functional deficiency of the vascular endothelium; moreover, clinical treatment, including balloon expansion or a stenting process, can also provoke damage to the endothelium. 34 This endothelial injury results in an excessive inflammatory Previous reports have shown that activation of the survivalrelated PI3K/Akt signaling pathway and endothelial-specific eNOS/ NO system is closely associated with endothelial cell function and dysfunction. 35 Notably, Akt-mediated NO secretion was proven to inhibit caspase-3 activation and consequently prevent apoptosis.…”

Percutaneous Transluminal Angioplasty in Patients with Peripheral Arterial Disease Does Not Affect Circulating Monocyte Subpopulations

“…It is minimally invasive and is still a very efficient way to combat arterial stenosis and occlusion. Acute changes in circulating cell populations were demonstrated in course of endovascular treatment [32]. Moreover, endovascular procedure is a unique opportunity to access and evaluate direct vicinity of atherosclerotic plaque in vivo .…”

Endothelial progenitor cells mobilisation after percutaneous coronary intervention: a pilot study

“…[17] More recently, Gao et al have found the same EPC kinetics than us during the first 24 h post-PCI for CD133+, CD34+, KDR+ cells. [18] They also described that EPC mobilisation is influenced by the degree of endothelial injury.…”