循环内皮祖细胞与血管内皮功能在2型糖尿病和2型糖尿病合并冠心病患者中的相关性研究

目的 对比研究2型糖尿病(T2DM)和T2DM合并稳定型冠心病(T2DM CAD)患者的循环内皮祖细胞(EPCs)与血管内皮功能的变化.方法 测取88例健康对照组、73例T2DM和79例T2DM-CAD患者的内皮依赖性血管舒张功能(FMD),非内皮依赖性血管舒张功能(GTN)和循环EPCs水平.结果 T2DM和T2DM-CAD组的循环EPCs水平较健康对照组明显降低(P＜0.001),T2DM组循环CD133+KDR+EPCs％与循环CD34+KDR+ EPCs％高于T2DM-CAD组(分别为0.519％±0.288％ vs 0.303％±0.357％,P=0.042和1.038％±1.252％ vs 0.672％±0.220％,P=0.028).T2DM和T2DM-CAD组相比,肱动脉FMD没有显著性差异(6.62％±2.86％ vs 6.13％00±2.51％,P=0.335),然而,肱动脉GTN有显著性差异(16.80％±6.47％00 vs 13.26％±4.49％,P=0.017).3组中CD34+ KDR+ EPCs％和CD133 +KDR+EPCs％与肱动脉FMD有着较高的相关关系,多元回归分析循环CD133+KDR+EPCs％、CD34+ KDR+ EPCs％和HbAlc是肱动脉FMD的独立预测指标.结论 高血糖状态可以减少循环EPCs的数量,减弱糖尿病患者的血管内皮细胞功能.与T2DM组相比,T2DMCAD组的循环EPCs水平和肱动脉GTN明显降低,血管平滑肌层受损程度更加严重.     

PCl治疗对急性心肌梗死患者CD34+单个核细胞及血管内皮功能的影响

目的：研究经皮冠状动脉内介入治疗（PCI）对急性心肌梗死（AMI）患者CD34+单个核细胞及血管内皮功能的影响。方法采用流式细胞分析法对40例PCI治疗的AMI患者、40例非PCI治疗的AMI患者及20例无心脏病的对照组的CD34+单个核细胞百分率进行动态监测。内皮功能采用动脉流量介导舒张（FMD）指标评价。结果 AMI患者（PCI组和非PCI组）CD34+单个核细胞百分率在AMI后第2～3天开始升高,在第3天后持续升高,在第7天达到最高峰后持续下降,第30天CD34+单个核细胞百分率仍高于第2天。在第90天时,已基本回降至第2天水平。在第120天时,基本恢复正常水平。PCI组的CD34+单个核细胞胞百分率明显高于非PCI组,差异有统计学意义（χ2=5.44,P＜0.05）。PCI组的CD34+单个核细胞数量在PCI术后第1天与术前比较开始升高,差异有统计学意义（χ2=7.30, P＜0.05）,术后第2天开始明显升高,差异有统计学意义（χ2=6.74,P＜0.05）。AMI发病1周时,PCI组和非PCI组的FDM均低于对照组,差异均有统计学意义（t分别=3.19、8.51, P均＜0.05）。结论 PCI能促进AMI后CD34+单个核细胞的表达,能改善AMI患者的血管内皮功能。     

冠心病患者冠状动脉病变严重程度与内皮祖细胞及血管内皮功能的相关性分析

目的探讨冠心病患者循环血内皮祖细胞(EPCs)数量、血流介导的内皮依赖性血管舒张功能(FMD)的变化及其与冠状动脉病变严重程度的相关性。方法对159例患者根据冠状动脉造影结果,分为冠心病组(101例)及对照组(58例),采用流式细胞术检测所有入选者EPCs水平,并采用高分辨率血管超声法检测其肱动脉FMD。冠心病组依据SYNTAX积分进一步分为低危、中危和高危3个亚组,比较高危、中危、低危三组之间EPCs数量及FMD的差异及与冠状动脉病变程度的相关性。结果与对照组比较,冠心病组患者EPCs数量显著减少,肱动脉FMD亦明显减低(P<0.05),循环血EPCs数量与肱动脉FMD呈显著正相关趋势(r=0.41,P<0.01)。各亚组之间,低危组与高危组比较,EPCs数量水平及FMD有统计学差异(P<0.05),中危组与低危组、中危组与高危组之间比较,EPCs数量水平及FMD均无显著性差异(P>0.05)。EPCs数量及FMD均与冠状动脉造影SYNTAX评分呈负相关(r=-0.381,P<0.01;r=-0.317,P<0.01)。结论冠心病患者循环血EPCs数量较健康人群显著减少,血管内皮功能显著低下,且与冠状动脉病变严重程度呈负相关。     

系统性硬皮病患者外周血内皮祖细胞数量及分化功能的研究

目的探讨系统性硬皮病（Systemic scleroderma,SSc）患者外周血内皮祖细胞（endothelial progenitor cells,EPCs）数量和分化功能的变化。方法选取女性SSc患者及健康志愿者各20例,抽取外周血20 ml,密度梯度离心法分离单个核细胞,以CD133/CD34、CD133/VEGFR2双荧光标记鉴定细胞,CD34/CD133/VEGFR2三荧光标记流式检测EPCs数量;分别以PE标记抗人CD14,FITC标记抗人CD64,PerCP/Cy5.5标记抗人VEGFR2,流式细胞仪检测单阳性细胞率,进而比较分化功能。结果 SSc患者外周血EPCs表达阳性率（3.18±1.97）%,较健康对照的（20.56±4.37）%明显下降,差异有统计学意义（P〈0.01）;培养7天后,外周血单个核细胞表达单核细胞表面标志CD14＋、CD64＋细胞百分率（32.49±5.41）%、（30.57±4.83）%,与对照组的（14.76±2.37）%、（15.39±2.09）%比较明显增加,差异均有统计学意义（均P〈0.01）,而内皮细胞表面标记KDR＋细胞百分率（68.38±4.65）%与对照组的（89.81±5.13）%比较明显减低,差异有统计学意义（P〈0.01）。结论 SSc患者循环内皮祖细胞数量减少,分化功能降低。     

不同他汀类药物对介入治疗后内皮功能的干预作用

目的了解冠心病（CHD）患者介入治疗（PCI）前后血管内皮功能状态及比较不同他汀类药物（普伐他汀、阿托伐他汀）对PCI后内皮功能的影响.方法选择经冠状动脉造影证实冠状动脉单支或双支以上≥70%狭窄患者60例,于成功行PCI后在常规治疗（阿司匹林、血管紧张素转化酶抑制剂、硝酸酯类）的基础上按分层随机分配法分为普伐他汀组（30例）和阿托伐他汀组（30例）.全部患者采用高分辨超声技术分别在PCI前、PCI后3天（干预前）和8周（干预后）检测肱动脉舒张功能：反应性充血后血管舒张（FMD）、含服硝酸甘油后的血管舒张（NID）,且同步检验血内皮素（ET）、一氧化氮（NO）及肝肾功能、血脂等指标并进行对比分析.结果①两组PCI后3天的FMD、NO均较PCI前显著下降 （均P〈0.05）,ET则升高（均P〈0.05）;两组间PCI前、后的上述指标比较差异均无统计学意义（P〉0.05）.②两组干预后的FMD、NO较干预前显著上升（均P〈0.05）,ET则降低（P〈0.05）;两组间干预前、后的上述指标比较差异均无统计学意义（P〉0.05）.③NID在各组PCI前后、干预前后及组间比较差异均无统计学意义（P〉0.05）.④干预后的血总胆固醇：阿托伐他汀组较普伐他汀组明显降低（P〈0.05）.结论 CHD患者 PCI后均出现明显的血管内皮舒张功能障碍;FMD、 NO、ET为反映CHD患者PCI后血管内皮功能的指标;血管内皮功能障碍在PCI后血管再狭窄起始机制中可能具有重要意义;应用不同他汀类药物（普伐他汀、阿托伐他汀）均能改善PCI后血管内皮功能,且安全性好;阿托伐他汀还具明显的降脂的作用.     

老年冠心病与血管内皮功能及血清肌钙蛋白相关性分析

目的：探讨老年冠心病患者血管内皮功能与肌钙蛋白的变化及相关性。方法：对55例老年冠心病组，50例无冠心病老年对照组，采用高分辨率超声测算内皮依赖性血流介导的舒张功能（FMD）和非内皮依赖性硝酸甘油介导的舒张功能（NMD），全自动化学发光仪对上述组别进行血清cTnI含量测定。结果：老年冠心病组中FMD、NMD明显低于老年对照组（P〈0．01），且血清cTnI含量明显高于老年对照组（P〈0．01）。结论：老年冠心病与血管内皮功能的失调及肌钙蛋白的变化密切相关。。     

超声检测表浅血管功能和形态改变在预测冠心病中的作用

目的 应用高频超声探头检测表浅血管的功能和形态，探讨它们在预测冠心病中的作用。 方法 用高频探头检测135例有胸痛并经冠状动脉造影确诊的冠心病患者颈动脉内-中膜厚度（IMT）和肱动脉内皮依赖及非内皮依赖性功能（FMD、NMD），作组间方差分析、多因素Logistic分析及ROC分析，与冠状动脉病变程度及范围作相关性分析。 结果 冠状动脉造影阳性组颈动脉IMT增厚、斑块分级（CPS）高，肱动脉FMD及NMD减低，差异有显著性意义（P〈0．01）；各血管参数指标与冠脉病变程度、范围均相关，以颈总动脉分叉处内-中膜厚度（IMTB）相关性最大；Logistic分析示FMD、NMD、IMTB及CPS（Odds ratio OR分别为0．81，0．82，6．28，2．75）均可作为冠心病独立影响因素，而ROC分析则显示IMTB和CPS[-Roe曲线下面积（Az）分别为0．77、0．74]较肱动脉FMD、NMD（Az分别为0．27、0．28）诊断冠心病价值高。 结论 外周表浅血管超声检测可反映冠状动脉病变发生、发展、范围、程度，以颈动脉IMT和CPS预测冠心病价值高，表浅血管结构和功能的综合评价则有利于冠心病早期动脉硬化发现和疗效判断。     

血管内皮祖细胞生物学活性与血管内皮祖细胞捕获支架的研究进展

血管内皮祖细胞（EPCs）作为内皮细胞的前体细胞,具有"持续"的自我更新及定向分化的能力。EPCs捕获支架,如表面包被CD34^＋抗体的支架,能够识别循环血液中EPCs表面特异性性结合位点,捕获并促使EPCs归巢、分化为内皮细胞,参与病变血管内皮修复、促进血管新生、改善冠脉血流。EPCs的生物学活性是决定EPCs捕获支架临床应用的关键,本文从EPCs生物学特性、功能、冠状动脉微环境对EPCs的调控机制、EPCs捕获支架的研究进展等方面进行综述,探讨EPCs捕获支架的治疗价值。     

经皮冠状动脉介入术后康复运动结合体外反搏对血管内皮功能及侧枝循环的改善作用

目的探讨康复运动结合体外反搏对冠心病患者经皮冠状动脉介入术（PCI）后侧枝循环和内皮功能的影响。方法选择63例PCI后患者，其中25例采用三阶段康复运动程序，作为康复运动组（运动组），18例在此基础上同时给予体外反搏治疗，作为康复运动＋体外反搏治疗组（运动反搏组），20例为单纯PCI对照组（对照组）。3个月后采用Bruce方案亚极量分级运动试验进行康复评定，采用多普勒超声检测肱动脉内皮功能，并于术后第6个月行冠状动脉造影术判定侧枝循环情况。结果（1）与对照组相比，运动组和运动反搏组患者的康复训练进展均较快，其中运动反搏组第3阶段RPP和RPE值明显低于运动组（P〈0．05）。（2）活动平板运动试验评定结果显示，运动组和运动反搏组均达较高康复程度，运动耐量和运动时间显著高于对照组（P〈0．05和P〈0．01）。（3）运动组和运动反搏组内皮依赖性舒张功能指标FMD较治疗前提高（P〈0．05和P〈0．01），而且运动反搏组的NMD也较治疗前明显增高（P〈0．05），对照组治疗前、后相关指标差异无统计学意义（P〉0．05）。（4）运动组和运动反搏组侧枝循环计分均明显高于对照组（P〈0．01）。且运动反搏组明显高于运动组（P〈0．05）。结论PCI术后给予康复运动训练可有效改善血管内皮功能，促进冠状动脉侧枝循环，从而提高心功能和生活质量，配合体外反搏治疗效果更好。     

小剂量辛伐他汀对老年冠心病患者血管内皮功能的影响——附42例分析

目的:探讨小剂量辛伐他汀(10 mg)对老年冠状动脉粥样硬化性心脏病(冠心病)患者血管内皮功能作用的影响.方法:将42例老年冠心病患者随机分为2组:10 mg组21例, 辛伐他汀10 mg/d;20 mg组21例,辛伐他汀20 mg/d,均治疗8周.治疗前后采用彩色多普勒超声检测肱动脉血管内皮的血流介导的舒张功能(flow-mediated dilation,FMD)、肱动脉血管内皮的硝酸甘油介导的舒张功能(nitroglycerin-mediated dilation,NMD),同时观察2组治疗前后血脂水平的变化,并对血脂水平与血管内皮功能改善的相关性进行分析.结果:2组血清总胆固醇、LDL-C水平治疗后均下降,与本组治疗前比较差异有统计学意义(均为P＜0.01),2组间比较差异无统计学意义(P﹥0.05);2组的FMD均较治疗前明显改善,但2组间FMD变化值比较差异无统计学意义(P＞0.05).单因素相关分析结果显示,2组的FMD的改善程度与患者治疗前、后的血清总胆固醇、LDL-C水平均无相关性(均为P﹥0.05).2组治疗前、后NMD比较差异无统计学意义(P﹥0.05).结论:辛伐他汀10 mg、20 mg均可显著改善老年冠心病患者的血管内皮功能,对于需长期服用他汀类药物、血脂水平不太高甚至偏低的老年患者,可考虑使用较小剂量的他汀类调脂药,以发挥其改善血管内皮细胞功能等非调脂作用,降低心脏不良事件的发生率,从而改善冠心病老年患者的预后.     

维持性血液透析患者循环内皮祖细胞变化的临床分析

目的 观察维持性血液透析患者循环内皮祖细胞(circulating endothelial progenitor cells,CEPCs)的变化.方法 以外周血中CD34+/CD133+/KDR + 为循环内皮祖细胞的标志物,对44例维持性血液透析患者和36例健康体检者采用流式细胞仪检测 CEPCs数量;将维持性血液透析患者的CEPCs数量与对照组比较,并根据维持性血液透析患者有无高血压或冠心病史、透析是否充分、血红蛋白水平进一步作亚组分析.结果维持性血液透析患者外周血CEPCs数量显著低于对照组( tCD34+=2.205,tCD34+/CD133+/KDR+ =2.148;均P＜0.05);合并高血压的维持性血液透析患者CEPCs数量较无高血压者显著降低(tCD34+ =2.183,tCD34+/CD133+/KDR+=2.023;均 P＜0.05);有冠心病史的维持性血液透析患者CEPCs数量低于无冠心病史者 (tCD34+=2.136,tCD34+/CD133+/KDR+ = 2.072;均P＜0.05);Kt/V≥1.3组患者CEPCs 数量明显高于Kt/V＜1.3组(tCD34+ =2.276,tCD34+/CD133+/KDR+=2.086;均 P＜0.05);血红蛋白≥110g/L组患者较血红蛋白＜110g/L组患者 CEPCs数量为高(tCD34+=2.707,t CD34+/CD133+/KDR+=2.859;均P＜0.05).结论 充分血液透析、积极控制高血压、改善肾性贫血使血红蛋白达标有助于提高维持性血液透析患者循环内皮祖细胞数量,有助于降低发生心血管并发症的风险.     

Mobilization of CD34+KDR+ endothelial progenitor cells predicts target lesion revascularization

Summary. Background: Endothelial lesion and regeneration are critical events in the process leading to in‐stent restenosis (ISR) after bare metal stent (BMS) percutaneous coronary intervention (PCI). Objectives: To prospectively investigate the relationship between biomarkers reflecting endothelial turnover and the occurrence of ISR. Methods: We performed a multicenter prospective observational study that included 156 patients undergoing elective PCI with BMS. Endothelial lesion was assessed by the enumeration of circulating endothelial cells (CECs). Endothelial regeneration was evaluated by enumeration of circulating CD34⁺ progenitor cells (CD34⁺ PCs) and CD34⁺KDR⁺ endothelial progenitor cells (EPCs). Measurements were performed before PCI, and 6 and 24 h after PCI. Dynamic changes were evaluated by calculating the delta value of each marker. The primary and secondary endpoints of the study were clinical target lesion revascularizations (TLRs) and major adverse cardiovascular events (MACEs) after 6 months of follow‐up. Results: During follow‐up, 28 MACEs were recorded, including 27 TLRs. PCI induced a significant rise in the numbers of CECs, CD34⁺ PCs, and CD34⁺KDR⁺ EPCs. Baseline, 6‐h and 24‐h levels of these markers did not differ between patients with and without TLR. The delta percentage of CD34⁺KDR⁺ EPCs was significantly reduced in patients with TLR as compared with patients without TLR (? 0.56 ± 8.1 vs. 2.91 ± 6.2; P = 0.015). In multivariate analysis, the delta percentage of CD34⁺KDR⁺ EPCs independently predicted the occurrence of TLR and MACEs (P = 0.02 and P = 0.014, respectively). Conclusion: The endothelial regenerative response to injury induced by PCI, assessed by CD34⁺KDR⁺ EPCs mobilized among progenitor cells, determines the risk of TLR and MACEs in stable coronary artery disease patients.     

中青年原发性高血压患者循环内皮祖细胞CD34+水平与颈动脉粥样硬化的相关性研究

目的 探讨中青年原发性高血压患者循环内皮祖细胞(EPCs)CD34+水平与颈动脉内膜中层厚度(IMT)和Framingham心血管危险因素积分标准(FRFC)的相关性及其评估高血压患者早期血管病变的价值.方法选择62例年龄25～45岁原发性高血压患者(高血压组)及20例健康体检者(健康对照组).高血压组患者采用FRFC分层方法分为低危组18例,中危组14例,高危组17例,极高危组13例.测定各组的外周循环EPCs CD34+水平及颈动脉IMT,并对EPCs CD34+水平与FRFC积分及颈动脉IMT进行相关性分析.结果 高血压各亚组患者外周循环EPCs CD34+水平随心血管危险程度的增加逐步下降[低危组(0.12±0.02)%,中危组(0.07±0.03)%,高危组(0.04±0.03)%,极高危组(0.01±0.01)%],各组间比较差异有统计学意义(P＜0.05或P＜0.01),且均明显低于健康对照组[(0.15±0.03)%,均P＜0.01];颈动脉IMT随心血管危险程度增加明显增厚[低危组(0.80±0.07)mm,中危组(1.11±0.08)mm,高危组(1.26±0.10)mm,极高危组(1.45±0.09)mm],各组间比较差异有统计学意义(P＜0.05或P＜0.01),且与健康对照组[(0.73±0.08)mm]比较差异有统计学意义(均P＜0.01).高血压患者外周循环EPCs CD34+水平与FRFC积分呈负相关(r=-0.875,P＜0.01),与颈动脉IMT呈负相关(r=-0.852,P＜0.01).结论 中青年原发性高血压患者循环EPCs CD34+水平与心血管危险因素及颈动脉IMT呈负相关;外周循环EPCs CD34+水平可以作为评估高血压患者早期血管病变的标志之一.     

Darbepoetin enhances endothelium-dependent vasomotor function in patients with stable coronary artery disease only after preceding ischaemia/reperfusion

Vasoprotective effects of erythropoietin in animal models are mediated by endothelium-derived NO and/or mobilization of EPCs (endothelial progenitor cells) and may be enhanced by ischaemia: whether they are present in humans is unknown. We examined whether the erythropoietin analogue darbepoetin improves FMD (flow-mediated dilatation), a measure of endothelium-derived NO, and whether this is influenced by preceding I/R (ischaemia/reperfusion). A total of 36 patients (50-75 years) with stable coronary artery disease were randomized to receive a single dose of darbepoetin (300 μg) or saline placebo. FMD was measured at the brachial artery using high-resolution ultrasound. CD133?/CD34?/VEGFR2? (vascular endothelial growth factor receptor 2) circulating EPCs were enumerated by flow cytometry. Measurements were made immediately before darbepoetin/placebo and at 24 h, 72 h and 7 days. At 24 h, FMD was repeated after 20 min of I/R of the upper limb. A further group of 11 patients was studied according to the same protocol, all receiving darbepoetin, with omission of forearm I/R at 24 h. Immunoreactive erythropoietin peaked at 24 h and remained elevated at approximately 50-fold of baseline at 72 h. FMD did not differ significantly between groups at 24 h (before I/R). At 72 h (48 h after I/R), FMD was greater (by 2.3±0.5% in the darbepoetin compared with the placebo group, a 66% increase over baseline; P<0.001) and greater than FMD at the same time point without preceding I/R (P<0.01). Increases in CD133?/CD34?/VEGFR2? cells after darbepoetin did not differ according to the presence or absence of preceding I/R. Preceding I/R is required for darbepoetin to enhance endothelial function, possibly by increasing expression of the erythropoietin receptor and by a mechanism likely to involve Akt/NO rather than circulating EPCs.     

Reduced endothelial progenitor cells in European and South Asian men with atherosclerosis

BACKGROUND: Circulating endothelial progenitor cells (EPCs) play a role in the repair and regeneration of the endothelium and may represent a novel cardiovascular risk factor. South Asian subjects have an increased risk of cardiovascular disease which is not fully explained by known risk factors. This study examined associations of EPCs with atherosclerosis and possible ethnic differences in EPCs. MATERIALS AND METHODS: A population sample of 58 European and South Asian adult men was enriched with the recruitment of an additional 59 European and South Asian men with known coronary disease. The coronary artery calcification score was measured by multi-slice computerized tomography (CT), carotid and femoral intima-media thickness (IMT), and femoral plaques were measured by ultrasound. The subjects were further subdivided into three categories of coronary artery disease on the basis of coronary artery calcification score and clinical history. Total EPCs and non-senescent EPCs (ns-EPCs) were quantified after 5 days cell culture and the number of late outgrowth colonies was measured over a 6-week test period. Circulating CD34+ haematopoietic precursor cells were measured by flow cytometry. RESULTS: Individuals with femoral plaques had reduced total and ns-EPCs. The number of ns-EPCs were reduced in individuals with the most coronary atheroma and were inversely related to the coronary calcification score and femoral IMT. These relationships persisted after multivariate adjustment for other risk factors. The numbers of late outgrowth colonies or circulating CD34+ cells were unrelated to the presence of atherosclerosis. There were no differences in the number of EPCs between European and South Asian subjects. CONCLUSION: The number of EPCs are reduced in subjects with atherosclerosis independent of other risk factors. Reduction in EPC numbers may be an independent risk factor for atherosclerosis but does not explain ethnic differences in cardiovascular risk.     

Reduced circulating endothelial progenitor cells in reversible cerebral vasoconstriction syndrome

Background

The pathophysiology of reversible cerebral vasoconstriction syndrome (RCVS) remains elusive. Endothelial dysfunction might play a role, but direct evidence is lacking. This study aimed to explore whether patients with RCVS have a reduced level of circulating circulating endothelial progenitor cells (EPCs) to repair the dysfunctional endothelial vasomotor control.

Methods

We prospectively recruited 24 patients with RCVS within one month of disease onset and 24 healthy age- and sex-matched controls. Flow cytometry was used to quantify the numbers of circulating EPCs, defined as KDR⁺CD133⁺, CD34⁺CD133⁺, and CD34⁺KDR⁺ double-positive mononuclear cells. The Lindegaard index, an index of vasoconstriction, was calculated by measuring the mean flow velocity of middle cerebral arteries and distal extracranial internal carotid arteries via color-coded sonography on the same day as blood drawing. A Lindegaard index of 2 was chosen as the cutoff value for significant vasoconstriction of middle cerebral arteries based on our previous study.

Results

Patients with RCVS had a reduced number of CD34⁺KDR⁺ cells (0.009 ± 0.006% vs. 0.014 ± 0.010%, p = 0.031) but not KDR⁺CD133⁺ cells or CD34⁺CD133⁺ EPCs, in comparison with controls. The number of CD34⁺KDR⁺ cells was inversely correlated with the Lindegaard index (rs = -0.418, p = 0.047). Of note, compared to controls, patients with a Lindegaard index > 2 (n = 13) had a reduced number of CD34⁺KDR⁺ cells (0.007 ± 0.005% vs. 0.014 ± 0.010%, p = 0.010), but those with a Lindegaard index ≤ 2 did not.

Conclusions

Patients with RCVS had reduced circulating CD34⁺KDR⁺ EPCs, which were correlated with the severity of vasoconstriction. Endothelial dysfunction might contribute to the pathogenesis of RCVS.     

Differential increase of CD34, KDR/CD34, CD133/CD34 and CD117/CD34 positive cells in peripheral blood of patients with acute myocardial infarction

Objective Circulating progenitor cells (CPC) may contribute to cardiac regeneration and neovascularization after acute myocardial infarction (AMI). For potential therapeutic use, understanding the endogenous mechanisms after ischemia is inevitable. We investigated the absolute number, but also the subset composition of CD34+ CPC after AMI. Methods CD34+, KDR+/ CD34+, CD133+/CD34+ and CD117+/CD34+ CPC were analyzed by FACS in peripheral blood of 10 patients with acute MI (59±5 yrs, m/f=8/2) at day of AMI (day 0) and days 1–5. For comparison patients with stable coronary artery disease (CAD, n=12, 66±2 yrs, m/f=10/2) and young healthy volunteers (n=7, 26±2 yrs, m/f=3/4) were studied. Results CD34 and KDR/CD34, CD133/CD34, CD117/CD34 were increased day 3 and 4 after AMI. KDR+ fraction within CD34+ population remained unchanged (58.3±7.8% vs 55.3±10.6%), whereas CD133+ (64.9±3.1% vs 43.5±5.9%, P=0.006) and CD117+ fractions (71.7±5.6% vs 50.1±5.5%, P=0.02) were elevated. In CAD, all CPC and fractions were similar as AMI day 0. Healthy volunteers had more CD34+ than CAD and AMI day 0. Double positive CPC were also higher, but fractions were unchanged vs CAD with more KDR/CD34 in trend (72.8±10.6% vs 50.5±5.6%, P=0.058). After AMI both absolute numbers of CD34+ and their subset composition change, suggesting selective mobilization of CPC. Increased CPC after AMI never reach numbers of young healthy volunteers.