下肢动脉硬化性闭塞症患者外周血内皮祖细胞数量和功能的变化

目的 研究下肢动脉硬化性闭塞症患者外周血内皮祖细胞数量及其功能的改变.方法 入选对象60例分为实验组(n=30)和对照组(n=30).密度梯度法分离人外周血单个核细胞,诱导分化培养7天后,荧光染色和流式细胞术鉴定贴壁细胞为内皮祖细胞.采用吉姆萨染色法计算细胞个数、集落数目,MTT比色法、改良Boyden小室及黏附能力实验测定内皮祖细胞增殖、迁移和黏附能力.结果 下肢动脉硬化性闭塞症患者外周血内皮祖细胞数量较对照组(27.2±3.6:52.6±5.9,细胞/×200倍视野,P<0.05)减少,集落个数较对照组(16.6±4.8:22.3±4.9,集落/×40倍视野,P<0.05)也减少,而且增殖能力 (0.193±0.064:0.243±0.078,P<0.05)、迁移能力(12.1±2.7:17.8±4.2,细胞/×200倍视野,P<0.05)、黏附能力(47.3±4.3:51.9±3.7,细胞/×200倍视野,P<0.05)受损.结论 下肢动脉硬化性闭塞症患者外周血内皮祖细胞数量减少,生物学功能减退.     

急性心肌梗死患者外周血内皮祖细胞早晚期集落数目和功能的变化

目的:探讨急性心肌梗死(AMI)患者外周血内皮祖细胞早晚期集落数目及功能的变化。方法:我院心内科住院患者74例,分成3组:AMI组28例、稳定性心绞痛组(心绞痛组)26例、非冠心病组(对照组)20例。密度梯度离心法获得外周血单个核细胞(MNCs),EGM-2MV培养液培养扩增。第7天和21天后通过形态学、双荧光染色及细胞表面分子标志鉴定内皮祖细胞,分别计数早期、晚期内皮祖细胞集落数目,酶联免疫吸附法测定上清液中基质细胞衍生因子-1(SDF-1)浓度。采用二苯基四氮唑嗅盐(MTT)比色法、改良的Boyden小室和黏附能力测定观察内皮祖细胞的增殖、迁移和黏附能力。结果:AMI组早期内皮祖细胞集落数目显著高于心绞痛组和对照组(P0.01),但SDF-1水平显著低于心绞痛组(P0.05)和对照组(P0.01);心绞痛组早期内皮祖细胞集落数目和SDF-1水平显著低于对照组(P0.05或0.01)。AMI组晚期内皮祖细胞集落数目,增殖、迁移细胞和贴壁细胞显著低于心绞痛组(P0.05)和对照组(P0.01),心绞痛组显著低于对照组(P0.01)。结论:AMI患者急性期早期内皮祖细胞集落数目增加,但其分泌功能严重受损,晚期内皮祖细胞集落数目减少,增殖、迁移和黏附功能下降。     

冠心病患者内皮祖细胞变化与冠状动脉病变的相关性

目的观察冠心病患者外周血中提取的内皮祖细胞的细胞形态、数量、集落数与正常对照组的区别。并研究冠心病患者冠状动脉狭窄的不同范围和程度与内皮祖细胞数量变化的相关性。方法选择冠心病患者57例和对照组30例,从外周血获取单个核细胞,体外培养后进行细胞分析和计数。并分析冠状动脉狭窄的不同范围和程度,患者内皮祖细胞数量和成集落数量的区别,并进行相关分析。结果 (1)冠心病患者外周血内皮祖细胞数量(23.1±1.8比56.7±2.4)和细胞集落数(14.7±2.5比24.2±1.7)较对照组明显减少;(2)随着冠状动脉狭窄范围的扩大和狭窄程度的加重,内皮祖细胞的数量和活性明显下降。结论冠心病患者外周血内皮祖细胞的数量和成集落的数量明显降低;冠心病患者外周血内皮祖细胞的数量与冠状动脉病变的范围和狭窄程度呈负相关。     

冠心病患者外周血内皮祖细胞的数量和活性

目的研究冠心病患者外周血中内皮祖细胞的数量、形态和活性。方法选择冠心病患者57例和正常对照者30例,用密度梯度离心法从外周血获取单个核细胞,将其接种在人纤维连接蛋白包被的培养板,用加入血管内皮生长因子165和碱性成纤维细胞生长因子的1640培养基培养细胞,并分析细胞形态和形成集落的数量,7d后贴壁细胞进行细胞分析和计数。用激光共聚焦显微镜鉴定FITC标记的荆豆凝集素和Dil标记的乙酰化低密度脂蛋白,双染色阳性细胞为正在分化的内皮祖细胞;用流式细胞仪检测细胞表面抗原CD34和KDR;采用MTT比色法检测细胞的生长状态。结果冠心病患者外周血内皮祖细胞数量较对照组明显减少(23.1±1.8个/200倍比56.7±2.4个/200倍,P<0.05),形成细胞集落数(14.7±2.5个/40倍比24.2±1.7个/40倍,P<0.05)、细胞增殖能力和生长曲线也明显降低。结论冠心病患者外周血内皮祖细胞的数量和活性明显降低。     

冠心病患者内皮祖细胞tPA和PAI表达的变化

目的探讨冠心病患者外周血中内皮祖细胞(EPC)的变化及其组织型纤溶酶原激活物(tPA)和纤溶酶原激活剂抑制剂(PAI)的表达。方法选择冠心病患者57例和对照组30例,提取内皮祖细胞进行数量和细胞集落的比较。利用ELISA法和底物发光法检测EPC分泌tPA和PAI的浓度和活性;用RT-PCR法检测EPC的tPA和PAI mRNA表达。结果冠心病患者EPC数量较对照组明显减少(23.1±1.8比56.7±2.4,P<0.05),形成细胞集落数(14.7±2.5比24.2±1.7,P<0.05)、细胞增殖能力也明显降低,冠心病患者EPC的tPA表达较对照组下降,PAI表达增强。结论冠心病患者外周血EPC数量减少和功能障碍可能在疾病的发生发展中起作用。     

外周血两种不同类型内皮祖细胞与颈动脉狭窄的关系

目的探讨外周血中早期内皮祖细胞和晚期内皮祖细胞数量和功能变化与颈动脉狭窄程度之间的关系。方法入组对象60例,根据全脑血管造影术分成颈动脉狭窄组40例(其中轻度狭窄组20例,中重度狭窄组20例),对照组20例。在全脑血管造影术中抽取患者股动脉血,采用密度梯度离心法分离外周血单个核细胞,分别培养至7天和21天鉴定为早期内皮祖细胞、晚期内皮祖细胞,计数细胞集落数量并分别用MTT比色法、改良的Boyden小室法和HFN培养板测定早期内皮祖细胞、晚期内皮祖细胞的增值、迁移、黏附功能。结果颈动脉狭窄组患者吸烟、高血压、甘油三酯、低密度脂蛋白明显高于对照组,高密度脂蛋白低于对照组(P<0.05);而年龄、性别、血糖、总胆固醇与对照组比较,差异无统计学意义(P>0.05)。与对照组比较,颈动脉狭窄组外周血早期内皮祖细胞、晚期内皮祖细胞数量及功能均下降(P<0.05),晚期内皮祖细胞数量与功能改变与颈动脉狭窄程度呈负相关(P<0.05)。结论颈动脉狭窄患者外周血晚期内皮祖细胞数量减少,功能受损,其数量与功能变化与颈动脉狭窄程度呈负相关。对于颈动脉狭窄患者,检测晚期内皮祖细胞数量及功能可间接预测颈动脉狭窄严重程度。     

叶酸对老年冠心病患者外周血内皮祖细胞数量及功能的影响

目的探讨老年冠心病患者口服叶酸治疗对外周血内皮祖细胞(EPCs)数量及功能的影响。方法选择初次诊断为冠心病的老年患者60例,随机分为治疗组和对照组,每组30例,在规范的冠心病二级预防基础上,治疗组给予叶酸5 mg/d口服,对照组口服安慰剂。在入院时、服药4 w及8 w时检测两组患者的同型半胱氨酸(Hcy)和血流介导的内皮舒张功能(FMD)水平,并利用外周血分离单个核细胞进行体外诱导培养,分别观察其集落形成、增殖及迁移能力。结果 Di L-ac LDL(红色)和FITC-UEA-1(绿色)染色双阳性的细胞可鉴定为EPCs。与对照组比较,治疗组治疗8 w EPCs数量、迁移及增殖能力显著增高[(67.70±4.09)个vs(48.92±3.55)个,(34.03±3.43)%vs(27.54±4.24)%,(0.67±0.04)%vs(0.54±0.04)%,P<0.05],FMD水平显著增高[(7.63±1.67)%vs(5.36±1.33)%,P<0.05],Hcy水平显著降低[(10.37±0.84)μmol/L vs(12.23±0.74)μmol/L,P<0.05]。EPCs数量、迁移、增殖能力与Hcy水平呈负相关(r=-0.668,P<0.05;r=-0.657,P<0.05;r=-0.775,P<0.05),FMD水平与Hcy水平呈负相关(r=-0.718,P<0.05)。结论老年冠心病患者口服叶酸可增高外周血EPCs的数量、迁移及增殖能力,改善血流介导的FMD,这可能与叶酸降低Hcy水平有关。     

肝细胞生长因子对冠心病患者内皮祖细胞功能的影响

目的观察肝细胞生长因子(HGF)对体外培养冠心病患者外周血内皮祖细胞(EPCs)生物学功能的影响,为HGF在冠心病治疗方面的应用提供研究基础。方法选择冠心病患者(冠心病组)和非冠心病患者(对照组)各15例,每组再随机分为重组人HGF(rhHGF)干预组和非rhHGF干预组,ELISA法检测血浆中HGF水平。流式细胞仪检测EPCs数量,并体外选择培养EPCs,检测rhHGF对EPCs增殖、迁移和黏附能力的影响。结果与对照组比较,冠心痛组患者外周血EPCs数量明显减少,血浆HGF含量明显升高(P0.01);EPCs增殖、黏附和迁移能力明显下降(P0.05,P0.01)。在冠心病组,与非rhHGF干预组比较,rhHGF干预组能明显促进冠心病患者FPCs增殖、黏附和迁移(P0.05,P0.01);在对照组,与非rhHGF干预组比较,rhHGF干预组仅促进对照组患者EPCs增殖,对黏附和迁移虽有促进作用,但差异无统计学意义(P0.05)。结论 HGF可增强冠心病患者EPCs的各项生物学功能,有望将HGF刺激EPCs的生物学活性的作用应用于冠心病的治疗。     

高胆固醇对内皮祖细胞数量和功能的影响

目的　观察高胆固醇血症患者外周血内皮祖细胞 (EPC)数量和功能的变化。方法选择高胆固醇血症患者和非高胆固醇血症患者各 2 0例 ,用密度梯度离心法从外周血获取单个核细胞 ,将其接种在人纤维连接蛋白包被培养板 ,培养 7d后贴壁细胞进行细胞化学分析。激光共聚焦显微镜鉴定FITC UEA Ⅰ和DiI acLDL双染色阳性细胞为正在分化的EPC。采用MTT比色法、改良的Boyden小室和黏附能力测定实验观察EPC的增殖、迁移和黏附能力。结果　高胆固醇血症患者外周血EPC数量明显减少 [(41 8± 8 7比 6 4 5± 16 6 )EPCs/× 2 0 0视野 ,P <0 0 5 ],且EPC数量与血总胆固醇水平 (r =- 0 6 5 9,P <0 0 0 1)和低密度脂蛋白胆固醇水平 (r =- 0 6 11,P <0 0 0 1)呈反向线性关系。高胆固醇血症患者EPC的增殖、迁移和黏附能力也明显受损。结论　高胆固醇患者外周血内皮祖细胞数量减少、功能减退。     

长期血液透析的CRF患者外周血内皮祖细胞数量和功能检测及意义

采用密度梯度离心法分离培养长期行血液透析的慢性肾功能衰竭(CRF)患者(CRF组)和健康人(对照组)外周血单个核细胞,将其接种在人纤维连接蛋白包被培养板,培养7 d后取贴壁细胞进行Di-LDL和FITC-UEA-I双染色鉴定内皮祖细胞(EPCs),采用二苯基四氮唑嗅盐比色等方法 评价其增殖、迁移和黏附能力.结果 CRF组透析前后EPCs的数量和增殖、迁移、黏附功能均低于对照组(P<0.05和0.01);CRF组血液透析后EPCs数量及黏附能力较透析前增高(P<0.05).认为长期行血液透析的CRF患者存在血管新生和内皮修复缺陷,此可能为其心血管并发症发病率和病死率较高的原因之一.     

降糖治疗对老年冠心病合并糖尿病患者外周血内皮祖细胞影响的研究

目的探讨降糖药物对老年冠心病合并糖尿病患者外周血CD34与血管内皮生长因子受体2(VEGFR-2)共同标记的血管内皮祖细胞(EPC)水平的影响。方法选择确诊的冠心病患者85例,根据口服葡萄糖耐量试验结果分为冠心病组41例,冠心病合并糖尿病组(合并组)44例,采用流式细胞仪检测2组外周血CD34及VEGFR 2双阳性的EPC(CD34~+/VEGFR-2~+EPC)水平;合并组患者降糖治疗,血糖稳定4周后门诊随访,观察外周血CD34~+/VEGFR-2~+EPC水平的变化。结果合并组外周血CD34~+/VEGFR-2~+EPC水平较冠心病组明显降低(P<0.05);合并组治疗后外周血CD34~+/VEGFR-2~+EPC水平较治疗前明显上升(P<0.05);EPC百分比与糖化血红蛋白水平呈负相关(r=-0.771,P<0.05)。结论降糖治疗可减轻高血糖水平对CD34~+/VEGFR-2~+的影响,使EPC耗损减少,有利于减缓冠状动脉粥样硬化进程。     

The comparison of EPC count and function in the situation of vascular repair at early and late stage

To investigate the relationship between the changes in the number and function of the late endothelial progenitor cells (EPC) in peripheral blood and the carotid artery stenosis. 60 cases were selected and were divided into the carotid artery stenosis group of 40 cases (mild stenosis in 20 cases, moderate/severe stenosis in 20 cases), normal control group of 20 cases with the global cerebral angiography. Extracted the blood of femoral artery from the patients during the global cerebral angiography, mononuclear cells were isolated from peripheral blood by density-gradient centrifugation and were cultured to 21 days when they were identified as late endothelial progenitor cells, counted the colony numbers of late EPC. Then the proliferation, migration and adherentce ability of late EPC were determined by the MTT assay, modified Boyden and the HFN culturing plates. The amount of the late EPC colonies(34.30 ± 4.90, 25.38 ± 6.33) were significantly reduced in the patients with carotid artery stenosis compared with the control group (46.00 ± 5.64) (P < 0.05); the function of proliferation, migration, adhesion of the late EPC in patiens with cerebral artery stenosis were significantly lower (P < 0.05), the number and function of late EPC decreased with the worsening of vascular stenosis (P < 0.05). The number of EPC in peripheral blood of patients with the carotid artery stenosis decreased, the function was impaired, and number and function changes of late EPC were negatively correlated with the degree of carotid artery stenosis.     

Circulating endothelial progenitor cells and coronary collaterals in patients with non-ST segment elevation myocardial infarction

BACKGROUND: Endothelial progenitor cells (EPCs) are bone marrow-derived cells that are augmented in response to ischemia and incorporated into neovascularization sites. We sought to determine whether circulating EPCs are related to collateral formation following non-ST segment elevation myocardial infarction (NSTEMI). METHODS: Twenty patients who underwent percutaneous coronary intervention (PCI) within a week of NSTEMI were divided into two groups: patients without collaterals (coll-, n=10) and patients with Rentrop grade 3--4 collaterals (coll+, n=10). Blood samples were drawn before PCI and 24+/- 2 h after PCI. EPC colonies were grown from peripheral blood mononuclear cells, characterized, and counted. Using flow cytometry the percentage of cells co expressing vascular endothelial growth factor receptor-2 and CD 133 was determined. RESULTS: The coll+ group had higher degree of culprit vessel stenosis and lower initial thrombolysis in myocardial infarction flow grade. The relative number of EPCs before PCI was significantly higher in the coll+ group than in the coll- group (1.49 +/- 0.9% vs. 0.77+/- 0.4%, p= 0.045). There were no significant intergroup differences in the number of EPC colony-forming cells. The number of EPC colonies increased in the coll- group after PCI (9.5 +/- 4.8 to 14.0 +/- 5.9/10(6) cells, p=0.01). CONCLUSIONS: This study supports an association between circulating EPC levels and collateral formation in patients with an NSTEMI.     

2型糖尿病外周血内皮祖细胞的诱导分化及影响因素的研究

目的观察2型糖尿病（T2DM）外周血内皮祖细胞（endothelial progenitor cell，EPC）在体外的分化增殖能力及影响因素。方法取20例T2DM无并发症患者、19例T2DM合并血管并发症患者和21例对照人群外周血EPC培养，观察细胞形态学变化并计数，用流式细胞仪检测贴壁细胞的特异性标志。结果糖尿病血管并发症组培养获得的EPC和EPC集落低于糖尿病无并发症组（P〈0．05）和对照组（P〈0．01）。EPC数量与SBP及FPG呈负相关（R=-0.266，P〈0.05；R=-0.619，P〈0．01），糖尿病人EPC集落生成数量与HbA1C水平呈负相关（R=-0．749，P〈0.05），与糖尿病病程年呈负相关（R=-0.406，P〈0．01）。结论FPG和SBP与EPC的增殖分化有关，T2DM外周血EPC数目减少，与HbA1c、SBP及病程相关。     

血内皮祖细胞与降钙素基因相关肽在慢性阻塞性肺疾病并发肺动脉高压中的变化及意义

目的 观察慢性阻塞性肺疾病(chronie obstructive pulmonary disease,COPD)并发肺动脉高压(pulmonary arterial hypertension,PAH)患者外周血内皮祖细胞(endothelial progenitor cells,EPC)数量和功能及降钙素基因相关肽(calcitonin gene-related peptide,CGRP)的变化,并探讨其在COPD并PAH发病中的作用.方法 选择聊城市人民医院住院的COPD患者60例,其中COPD并PAH(COPD+PAH组)患者30例,COPD非PAH患者30例(COPD组);正常对照20名(非COPD组)、用密度梯度离心法从外周血获取单个核细胞,将其接种在人纤维连接蛋白包被培养板,培养7 d后对贴壁细胞进行细胞化学分析.通过集落形成试验、改良的Boyden小室和黏附能力测定实验计数EPC的数量、测定EPC的迁移和黏附能力.用放射免疫法检测人选患者血浆CGRP水平.结果 与正常对照组及COPD组相比,COPD+PAH组外周血EPC数量明显减少,黏附和迁移能力显著降低(F＝9.52～14.35,q=3.36～8.12,P＜0.05),且EPC数量及黏附、迁移能力与肺动脉压力呈负相关(r＝0.73、-0.79、-0.81,P＜0.01).COPD+PAH组患者血浆CGRP水平明显低于对照组(P＜0.01),CGRP浓度与循环EPC数量及迁移能力呈正相关(γ=0.71,0.73),与循环血EPC黏附能力无相关性.结论 COPD患者PAH的发生可能与循环EPC数量减少、迁移和黏附能力降低有关,这种变化可能与血浆CGRP水平减少有关.     

Endothelial progenitor cell mobilization after percutaneous coronary intervention

BACKGROUND: In animal models, circulating endothelial progenitor cells (EPC) have been shown to participate in repair of damaged or degenerating vascular surfaces. In humans, reduced EPC counts correlate with cardiovascular risk and disease outcome; yet it has been difficult to establish that EPC are in fact mobilized in response to vascular injury as a physiologic response. We therefore studied early (<12h) mobilization of EPCs into the peripheral circulation after a defined vascular manipulation, percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) and non-ACS patients. METHODS AND RESULTS: CD34/CD31 positive EPC colony forming units (EPC-CFU) were quantified by a blinded observer in peripheral blood samples from eight control patients with angiographically normal coronary arteries, and in 30 patients with coronary artery lesions before and 12h after PCI. All patients (n=38) had one or more CV risk factors. Ten patients presented with acute coronary syndrome (PCI(ACS)), and the rest (n=20) underwent elective PCI (PCI(Elect)). Despite the presence of an acute coronary syndrome, patients in the PCI(ACS) group did not present with increased EPC-CFU compared with either the PCI(Elect) or control groups (P>0.05). In addition, EPC-CFU (colonies/ml blood) increased significantly in the PCI(Elect) group after stent placement (11.8+1.6 before versus 16.5+1.9 after, P=0.0009), while in contrast, PCI did not stimulate EPC mobilization in patients in the PCI(ACS) group (9.6+3.2 before versus 6.5+1.8, P=0.20). We found a higher presenting vascular endothelial growth factor (VEGF) level in the PCI(Elect) group compared to PCI(ACS) (78.7+25.2 versus 15.3+7.9 pg/ml blood, P=0.02). However, VEGF levels increased after PCI only in the PCI(ACS) group (15.3+7.9 to 133.3+27.5 pg/ml, P=0.003) and not in the PCI(Elect) group (78.7+25.2 to 79.7+12.2 pg/ml, P=0.97). CONCLUSION: Our findings suggest that focal coronary endothelial injury as a result of PCI triggers early mobilization of EPC into the peripheral circulation in patients presenting for an elective PCI, without a corresponding rise in VEGF levels. In contrast, patients with an acute coronary syndrome fail to respond to PCI with early EPC mobilization despite a significant rise in VEGF. The results of the present study may suggest a novel mechanism for early EPC augmentation after PCI.     

他汀类药物对不同类型冠心病患者外周血中内皮祖细胞数量的影响

目的：研究他汀类药物对不同类型冠心病患者外周血中内皮祖细胞（EPCs）数量的影响。方法：选择127例冠心病患者,分为急性心肌梗死（AMI）介入治疗组（A组,45例）,AMI保守治疗组（B组,29例）,不稳定型心绞痛组（C组,31例）,稳定型心绞痛组（D组,22例）,入院后均给予阿托伐他汀治疗;同时选择30例非冠心病患者作为非冠心病对照组,不给予阿托伐他汀治疗。上述所有患者在入院即刻、14d、30d采血,检测患者外周血中CD133标记的EPCs数量。结果：冠心病各组及非冠心病对照组患者外周血中均有EPCs（CD133）的表达,与入院即刻相比,冠心病各组患者服用阿托伐他汀后EPCs（CD133）的表达在14d和30d后明显上升[A组：（0.015±0.016）%比（0.411±0.361）%比（0.472±0.384）%,B组：（0.009±0.010）%比（0.250±0.031）%比（0.413±0.035）%,C组：（0.421±0.814）%比（1.065±2.014）%比（1.325±2.321）%,D组：（1.387±0.021）%比（2.153±0.167）%比（3.052±0.086）%],P均〈0.05;非冠心病对照组患者EPCs（CD133）的表达在14d和30d后无明显变化（P〉0.05）。结论：他汀类药物能增加冠心病患者外周血内皮祖细胞数量。     

Functional impairment of hematopoietic progenitor cells in patients with coronary heart disease

The circulating form of endothelial progenitors cells (EPCs) are derived from bone marrow (BM)-derived hematopoietic stem cells (HSCs). Enhanced mobilization of EPCs was shown to be linked to cardiac diseases. This study investigated whether reduced EPC levels in advanced coronary heart disease (CHD) are secondary to a functional exhaustion of HSCs in the BM or to reduced mobilization. Number and functional properties of EPCs were assessed in 15 healthy controls, and 40 patients with CHD. The colony-forming unit (CFU) capacity of BM-derived mononuclear cells and the CD34+ HSC number were examined in four healthy volunteers, and 15 CHD patients. EPC number was reduced in CHD patients (P < 0.01 vs. controls). Moreover, the migratory capacity was significantly impaired in EPCs of CHD patients (P < 0.05 vs. controls). On multivariate analysis, CHD was an independent predictor of functional EPC impairment. CFUs were reduced in CHD patients (59.6 +/- 21.2 vs. 75.4 +/- 25.8 in controls, P < 0.05). CHD was also predictor of impaired CFU capacity. In this small clinical study, CHD is associated with selective impairment of HSC function in the BM and in the peripheral blood, which may contribute to impairment of cardiac function.     

循环内皮祖细胞与冠心病关系的Meta分析

目的采用Meta分析综合评价循环内皮祖细胞(EPC)的数量与冠心病的关系。方法利用计算机检索国内发表的有关EPC与冠心病关系的文献,经质量评价后按一定标准纳入文献,应用RevMan 6.0软件进行分析。用漏斗图分析发表偏倚。结果共纳入14项研究,包括890例研究对象。Meta分析结果显示,稳定型冠心病患者循环EPC明显低于对照组,计数集落数的合并后标准化均数差(SMD)=-2.81,95%CI(-4.03,-1.59),Z=4.50(P<0.01);流式细胞分析结果的合并后SMD=-1.85,95%CI(-2.95,-0.76),Z=3.33(P<0.01)。急性心肌梗死患者EPC的集落数却高于对照组,合并后SMD=3.89,95%CI(1.44,6.34),Z=3.11(P<0.01)。三个Meta分析存在异质性,均采用随机效应模型分析。漏斗图提示无明显发表偏倚。结论循环EPC数量的降低与稳定型冠心病密切相关,而急性心肌梗死患者EPC数量增加。