Mills N L, Tura O, Padfield G J, Millar C, Lang N N, Stirling D, Ludlam C, Turner M L, Barclay G R, Newby D E
Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, Edinburgh, EH16 4SU, UK.
Heart. 2009 Dec;95(24):2003-8. doi: 10.1136/hrt.2008.163162. Epub 2009 May 28.
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.
Prospective case-control study in a university teaching hospital.
54 patients undergoing elective coronary angiography.
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).
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.
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.
内皮祖细胞(EPCs)是循环单核细胞,具有成熟为内皮细胞并促进血管修复的能力。我们评估了经皮冠状动脉介入治疗(PCI)期间局部血管损伤对冠心病患者循环EPCs的影响。
在一所大学教学医院进行的前瞻性病例对照研究。
54例接受择期冠状动脉造影的患者。
在诊断性血管造影(n = 27)或PCI(n = 27)之前及之后的头24小时内,通过流式细胞术(CD34(+)KDR(+)表型)并辅以实时聚合酶链反应(PCR)以及集落形成单位(CFU-EC)功能测定对EPCs进行定量。
在无明显心肌坏死的情况下,冠状动脉介入治疗而非诊断性血管造影导致血液中性粒细胞计数增加(p<0.001)和C反应蛋白浓度升高(p = 0.001)。PCI后24小时,CFU-ECs增加了两倍(中位数[四分位间距],4.4[1.3 - 13.8]对16.0[2.1 - 35.0],p = 0.01),尽管循环CD34(+)KDR(+)细胞(白细胞的0.019%(标准误0.004%)对0.016%(0.003%),p = 0.62)和白细胞CD34 mRNA(相对量2.3(0.5)对2.1(0.4),p = 0.21)没有增加。CFU-ECs与CD34(+)KDR(+)细胞之间无相关性。
PCI后的局部血管损伤导致全身炎症反应并增加功能性CFU-ECs。这种增加与CD34(+)KDR(+)细胞的早期动员无关,提示这些细胞不是参与血管损伤即时反应的EPCs的主要来源。