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。     

冠心病患者外周血内皮祖细胞数量与心功能的关系

目的探讨冠心病患者外周血内皮祖细胞数量与心功能的关系。方法所有入组病例均为2010年8月至12月在粤北人民医院心内科住院患者,冠心病组(既往行冠脉造影或心脏CTA检查明确诊断为冠心病者)60例,根据ACC/AHA指南,选取心功能为B期组30例,D期组30例,对照组30例(冠脉造影正常),采用流式细胞仪检测循环外周血中CD133+和CD34+双阳性的细胞的数量。结果心功能B期组循环外周血中内皮祖细胞的数量与对照组和心功能D期组相比均显著升高(P<0.05);对照组循环外周血中内皮祖细胞的数量较心功能D期组显著升高(P<0.05)。结论外周血循环内皮祖细胞在未发生心衰的冠心病患者中升高;在严重心衰患者中降低。调节内皮祖细胞的释放可能作为一种治疗心衰的新思路。     

急性冠脉综合征患者内皮祖细胞及C反应蛋白的变化

目的:观察急性冠脉综合征(ACS)患者外周血中内皮祖细胞(EPCs)及C反应蛋白的变化。方法:入选40例ACS(不稳定型心绞痛18例、急性心肌梗死22例)患者与20例行冠状动脉造影术排除冠心病的正常人(正常对照组),取所有研究对象外周血100μl分别加入CD34-PE、AC133-异硫氰酸荧光素(FITC)荧光抗体使与EPCs表面CD34、AC133抗原结合,通过流式细胞仪检测PE、FITC阳性细胞的数量。同时检测高敏C反应蛋白(hsCRP)浓度。结果:与正常对照组比较,不稳定型心绞痛、急性心肌梗死患者外周血中EPCs数量显著增多[(0.48±0.04)%比(0.84±0.31)%比(1.57±0.62)%,P<0.001],hsCRP浓度明显升高[(0.63±011)mg/L比(7.8±0.59)mg/L比(11.2±0.46)mg/L,P<0.001],且上述指标在急性心肌梗死组明显高于不稳定心绞痛组(P<0.001),所有患者外周血中EPCs数量与hsCRP浓度正相关(r=0.82,P<0.001)。结论:急性冠脉综合征患者外周血中内皮祖细胞数量显著增多,可能与炎症因子激活骨髓干细胞分化为内皮祖细胞,参与血管修复有关。     

小鼠内皮祖细胞的分离、培养与定向诱导分化

目的 建立一种稳定、高效,从小鼠骨髓中分离培养与定向诱导分化内皮祖细胞(EPCs)的方法。方法 从小鼠骨髓中密度梯度离心法分离单个核细胞,经差速贴壁结合特殊培养基扩增并向内皮细胞定向诱导分化EPCs。应用免疫荧光和流式细胞技术鉴定内皮细胞系列标志:CD34、CD31、Flk-1和祖细胞标志CD133。并通过检测其对FITC标记的UEA-1的吸附和内吞DiI-ac-LDL来进行细胞功能学的鉴定。对分化细胞行vWF、CD31 免疫组化染色鉴定,并与血管内皮细胞合成前列腺素能力进行比较。结果 经过梯度密度离心和贴壁法选择的细胞表达内皮细胞特异性抗原CD34、CD31、Flk-1,部分表达CD133。分离所得细胞经EBM-2专用培养基培养后,第4天可见集落形成,培养第9天流式细胞仪检测其CD34、CD133、CD31、Flk-1阳性率分别为(44±4)%、(18±3)%、(49±4)%和(79±6)%,细胞能特异性吸附FITC标记的荆豆凝集素并内吞DiI-ac-LDL,约3周左右可融合近80%,形成铺路石样内皮细胞特有形态。传代后vWF、CD31免疫组化染色阳性率分别为(66±5)%和(56±5)%。诱导后的内皮祖细胞的合成前列腺素能力与血管内皮细胞之间无显著差异。结论 从小鼠骨髓中分离培养与定向诱导分化EPCs的方法,效率高,稳定性和重复性好。     

循环血液中内皮祖细胞在充血性心力衰竭患者中的表达

目的 研究内皮祖细胞在充血性心力衰竭患者中的表达情况,并进一步研究其与心衰严重程度的相关性.方法 选择心衰患者96例(纽约心功能分级:Ⅰ级22例,Ⅱ级25例,Ⅲ级26例,Ⅳ级23例)及健康正常人25例(对照组),以CD34、CD45为表面标记,用流式细胞仪测量外周血中的内皮祖细胞数,并同时测量脑钠肽(BNP).结果 心衰患者较对照组BNP水平升高(P＜0.01),且心衰的严重程度与BNP呈正相关;在心功能Ⅰ级、Ⅱ级心衰患者中,内皮祖细胞较健康对照组明显升高(P＜0.01);心功能Ⅲ级、Ⅳ级患者较健康对照组降低(P＜0.05或＜0.01).结论 内皮祖细胞在心衰患者中呈现一个双向性改变,即在心衰晚期阶段外周血内皮祖细胞表达较对照组明显下降,而在心衰早期阶段较对照组明显升高,提示受损的内皮祖细胞招募可能参与严重心衰患者的病理生理过程.     

急性心肌梗死伴2型糖尿病患者内皮祖细胞动员障碍

目的观察急性心肌梗死伴2型糖尿病患者血浆缺血相关因子血管内皮生长因子和基质细胞衍生因子水平,骨髓内皮祖细胞动员是否存在障碍,以及基质细胞衍生因子、血管内皮生长因子-内皮祖细胞动员通路是否存在异常。方法采用密度梯度离心法分离外周血单个核细胞,用流式细胞仪检测急性心肌梗死后不同时间点(1、3、5、7、14和28天)外周血CD45-/low /CD34 /CD133 /KDR 早期内皮祖细胞数量。酶联免疫吸附法检测血浆中血管内皮生长因子、基质细胞衍生因子以及高敏C反应蛋白的浓度。结果急性心肌梗死伴2型糖尿病患者外周血内皮祖细胞动员高峰(第7天)较急性心肌梗死非糖尿病患者(第5天)延迟且显著减少[(140±48)/106比(246±100)/106,P<0.05]。糖尿病组血浆血管内皮生长因子(第5天:277±95ng/L比168±35ng/L,P<0.05)、基质细胞衍生因子(第5天:3835±402ng/L比3287±384ng/L,P<0.05)以及高敏C反应蛋白(第3天:55.55±14.88mg/L比36.92±14.83mg/L,P<0.05)在高峰点的水平显著高于非糖尿病组。结论糖尿病患者心肌梗死后组织缺血程度较重,但组织缺血后基质细胞衍生因子、血管内皮生长因子-内皮祖细胞动员通路存在障碍,这可能是糖尿病患者缺血后血管新生功能障碍,发生急性心肌梗死后预后较差的原因之一。     

小鼠骨髓源性内皮祖细胞的分离培养与鉴定

目的 建立一种高效、稳定的从小鼠骨髓中分离培养与定向诱导分化内皮祖细胞的方法.方法 通过密度梯度离心法从小鼠骨髓中分离单个核细胞,经差速贴壁结合特殊培养基扩增,诱导分化为内皮祖细胞.应用流式细胞技术鉴定内皮细胞系列标志:CD34、CD31、Flk-1和祖细胞标志CD133.结果 经密度梯度离心和差速贴壁法分离所得的细胞经EBM-2专用培养基培养后,第4天可见集落形成,培养第12天流式细胞仪检测其CD34、CD133、Flk-1、CD31的阳性率分别为65%±4%、48%±3%、37%±3%和51%±4%.结论 从小鼠骨髓中分离培养与定向诱导分化内皮祖细胞的方法效率高,稳定性和重复性好.     

主动脉夹层患者循环内皮祖细胞或许经由氧化应激机制加速细胞衰老

目的探讨主动脉夹层患者循环内皮祖细胞是否经由氧化应激机制加速衰老。方法临床选取疑似主动脉夹层患者并经主动脉CTA检查后分为对照组和主动脉夹层组,抽取外周血分离单个核细胞群,流式细胞分选术分离和计数内皮祖细胞,应用层粘连蛋白粘附法、改良的Boyden小室及MTT法测定内皮祖细胞的粘附、迁移和增殖功能,应用Western blot检测内皮祖细胞衰老相关的p16INK4a和SIRT1蛋白水平,并测定细胞内反应氧类物质水平。结果与对照组相比,主动脉夹层组循环CD34+CD133+KDR+内皮祖细胞数量明显减少(P0.01),且细胞粘附、迁移和增殖功能明显降低(P0.05);Western blot结果显示细胞衰老相关的p16INK4a蛋白水平明显升高,而抗衰老蛋白SIRT1表达水平明显降低,细胞内反应氧类物质水平明显增加(P0.05)。结论不断增加的细胞内反应氧类物质致主动脉夹层患者循环内皮祖细胞的粘附、增殖和迁移功能受损,最终加速循环内皮祖细胞衰老。     

出血性卒中患者急性期外周血CD34阳性细胞不同亚群的变化及意义

目的探讨出血性卒中患者急性期外周血CD34、KDR/CD34、CD133/CD34和CD117/CD34阳性细胞水平变化及其意义。方法回顾性纳入2013年9月—2014年4月江苏省海门市人民医院神经外科收治的急性出血性卒中患者30例,同时选取20名健康者作为对照组,利用FACSCalibur流式细胞仪分别于急性出血性卒中患者脑出血后第1~7天和对照组体检当天对外周血中CD34+、KDR+/CD34+、CD133+/CD34+和CD117+/CD34+细胞水平进行检测,使用CELLQuest软件获取数据并进行分析。结果外周血CD34+细胞与KDR+/CD34+、CD133+/CD34+、CD117+/CD34+细胞在出血性卒中后1~7d时均低于对照组,差异均有统计学意义(均P0.05)。CD34+和CD117+/CD34+在1~2d时先下降,后逐渐上升;KDR+/CD34+和CD133+/CD34+细胞在1~5 d时逐渐升高,均在5 d达到最大值,分别为(14.8±3.5)×105和(16.7±3.3)×105。与1 d时相比,CD34+细胞在5、6 d时分别为(27.4±6.3)×105和(25.4±5.7)×105,KDR+/CD34+、CD133+/CD34+细胞在4、5、6d时分别为(10.2±3.1)×105、(14.8±3.5)×105、(12.1±3.4)×105和(14.3±3.6)×105、(16.7±3.3)×105、(13.1±4.0)×105,CD117+/CD34+细胞在5d时为(21.3±4.2)×105,均高于脑出血后第1天,差异均有统计学意义(均P0.05)。在CD34+群体中,与对照组相比,KDR+/CD34+细胞比例在1~7 d时均降低,差异均具有统计学意义(均P0.05);CD133+/CD34+细胞比例在4d时为(65±4)%,高于对照组,差异有统计学意义(P0.05);与1 d相比,KDR+/CD34+细胞比例在5 d时为(55±6)%,CD133+/CD34+细胞比例在4 d时为(65±4)%,CD117+/CD34+细胞比例在4d和5d时,分别为(69±6)%和(72±6)%,均出现升高,差异均有统计学意义(均P0.05)。结论出血性卒中患者急性期外周血CD34+细胞及其细胞亚群发生了变化,推测不同细胞亚群可能具有不同的功能与潜能,KDR+/CD34+和CD133+/CD34+可能是急性出血性卒中的早期敏感指标,而CD117+/CD34+则在早期即被大量动员。     

壳聚糖/肝素层层自组装涂层与CD133^＋内皮祖细胞生物相容性的实验研究

目的研究壳聚糖/肝素层层自组装涂层对CD133＋内皮祖细胞的黏附、增殖相关基因表达的影响,并从分子生物学角度探讨其作为促内皮修复功能药物洗脱支架涂层材料的可行性。方法（1）分离人脐血单个核细胞,免疫磁珠分选CD133＋内皮祖细胞;（2）制备壳聚糖/肝素层层自组装涂层,1%明胶涂层以及玻璃对照皿,接种并培养分选所得内皮祖细胞;（3）免疫荧光鉴定内皮祖细胞;（4）抽提总RNA,RT-PCR法比较不同培养介质中细胞的eNOS、VE-cadherin、KDR、PECAM-1、Sirtuin-1、Thrombomodulin等基因的表达差异。结果（1）重力梯度离心及磁珠分选法所得CD133＋内皮祖细胞纯度较高（92.88%±0.51%（n=4）,在VEGF诱导下能较好的分化为内皮细胞;（2）eNOS、VE-cadherin、KDR、PECAM-1和Sirtuin-1在壳聚糖/肝素层层自组装涂层组表达丰度较玻璃对照组显著增高（P〈0.05）,与明胶组差异不明显,Thrombomodulin在壳聚糖涂层表达丰度较明胶组、玻璃组表达均增高（P〈0.05）结论壳聚糖涂层能促进内皮祖细胞的黏附、增殖,生物相容性好,为理想的生物材料。     

Levels of circulating endothelial progenitor cells in systemic sclerosis

OBJECTIVE: Contradictory results have been reported regarding vasculogenesis in systemic sclerosis (SSc). Our aim was to investigate bone marrow-derived circulating endothelial precursors (EPCs) and activated circulating endothelial cells (CECs) in SSc patients. METHODS: Peripheral blood from consecutive patients with SSc hospitalised for systemic follow-up was analysed and compared with blood from patients with active refractory rheumatoid arthritis (RA) and osteoarthritis (OA). EPCs were quantified by cell sorting and flow cytometry and were identified as circulating CD34+CD133+ cells. Activated CECs were defined as CD105+CD62+CD105+CD102+CD105+CD106+ cells. RESULTS: Patients with SSc had higher putative EPC levels than OA patients, but lower levels than RA patients. In SSc patients, EPC levels increased with European disease activity score. Activated CEC levels were high in SSc patients and RA patients, but not correlated with EPC levels. CONCLUSION: These results together and previous data suggest that EPCs may be recruited during active vascular disease but that the sustained ischaemic conditions of SSc may eventually lead to EPCs depletion.     

急性心肌梗塞循环内皮祖细胞与冠状动脉病变严重程度的分析

目的：研究急性心肌梗塞（AMI）患者外周血中内皮祖细胞（EPCs）的水平与冠状动脉病变程度之间的关系。方法：选取55例AMI患者，以定量冠状动脉造影评估冠状动脉的血管狭窄程度，同时选取30名冠状动脉造影阴性的患者为对照组。所有患者均在入院后即刻[AMI发病平均时间（2．5±1．5）h]，第24h、48h、72h、7d、14d及一个月时采血，以CD133作为EPCs标记物，用流式细胞仪检测患者外周血中CD133标记细胞数量。结果：AMI组患者及对照组均有EPCs（CD133）的表达，AMI患者EPCs数目明显低于非冠心病患者（P〈0．05）。多支病变者较单支病变者有降低趋势，但无显著性差异（P〉0．05）。EPCs数目和Gensini评分呈明显负相关（n=55，r=-0．619，P〈0．05）。结论：急性心肌梗塞患者EPCs数目和冠状动脉病变程度有关。     

冠心病患者外周血内皮祖细胞数量及生物学功能与肝细胞生长因子的关系

目的观察冠心病患者外周血内皮祖细胞（EPCs）数量及生物学功能的变化,进一步探讨肝细胞生长因子（HGF）对其影响,为临床应用HGF提供理论依据。方法收集50例非冠心病患者（对照组）、50例冠心病患者（冠心病组;每例分为HGF干预组和非HGF干预组）外周血,应用流式细胞仪和ELISA法分别检测各组CD133＋／CD34＋细胞的数量和HGF水平;采用密度梯度离心法分离培养各组外周血中EPCs,通过MTT法、Transwell迁移试验、黏附能力测定试验及PI—AnnexinV双重染色法来分别检测EPCs的增殖、迁移、黏附能力和凋亡水平。结果与对照组比较,冠心病组外周血中CD133＋／CD34＋细胞数量减少[（2．15±0．69）％1）S（5．26±1．16）％,P〈0．011,血浆中HGF浓度升高[（6．80±1．22）w（2．62±0．83）gg／L,P〈0．01],EPCs增殖、迁移、黏附等生物学功能减弱（P〈0．05）;HGF干预组EPCs增殖、迁移、黏附等生物学功能显著改善（P〈0．05）。各组细胞凋亡水平差异无统计学意义（P〉0．05）。结论外周血中CD133＋／CD34＋细胞数量和血浆中HGF水平的变化可能成为冠心病患者新的危险评估因素。     

Bone marrow endothelial progenitors are defective in systemic sclerosis

OBJECTIVE: Vascular abnormalities represent the main component of the pathobiology of systemic sclerosis (SSc), progressing from structural derangements of the microcirculation with abortive neoangiogenesis to final vessel loss. Since circulating endothelial progenitor cells (EPCs) are important in the vascular repair process, we undertook this study to examine their numbers in the peripheral blood (PB) of SSc patients and to evaluate whether their status is related to impaired quantitative and/or qualitative aspects of the bone marrow (BM) microenvironment. METHODS: Circulating EPCs from 62 SSc patients were evaluated by flow cytometry and characterized as CD45 negative and CD133 positive. BM EPCs, identified as CD133 positive, were isolated from 14 SSc patients and grown to induce endothelial differentiation. In addition, progenitor numbers and functional properties of hematopoietic and stromal compartments were analyzed by various assays. RESULTS: We found that EPCs were detectable in the PB of patients with SSc, and their number was significantly increased in patients with early-stage disease but not in those with late-stage disease. All of the examined BM samples contained reduced numbers of EPCs and stromal cells, both of which were functionally impaired. Both endothelial and stromal progenitors expressed vascular endothelial growth factor receptor, indicating that BM is strongly induced to differentiate into the endothelial lineage; furthermore, only BM EPCs from patients with early disease led to endothelial differentiation in vitro. CONCLUSION: This study provides the first demonstration that in SSc, there is a complex impairment in the BM microenvironment involving both the endothelial and mesenchymal stem cell compartments and that this impairment might play a role in defective vasculogenesis in scleroderma.     

Circulating endothelial progenitor cells are reduced in SLE in the absence of coronary artery calcification

Circulating endothelial progenitor cells (EPCs) are reduced in patients with systemic lupus erythematosus (SLE). A reduced number of EPCs are associated with the presence of atherosclerosis in other populations. We sought to determine whether the reduction in EPC numbers in SLE is dependent on the presence of advanced coronary artery calcification (CAC). Patients with SLE had previous coronary calcium scores which placed them in either the >75th percentile or <25th percentile for their age. Seventeen patients with SLE and 13 healthy controls (HC) were included in the study. White blood cells were stained for EPC and progenitor cell markers including CD34, CD133, and VEGFR and analyzed by flow cytometry. SLE patients had repeated coronary imaging as well as carotid ultrasound. There was no difference in age between groups. SLE patients with advanced CAC were more likely to be hypertensive, to be smokers, and to have longer disease duration than SLE patients without CAC. SLE patients without evidence of CAC had a significantly lower number of EPCs (CD34+/CD133+/VEGFR+) compared to HC (median (IQR)) 0 (0, 6.7) vs. 10.2 (5.8, 12.3) (P = 0.02). Total numbers of PCs (CD133+/CD34+) were not significantly decreased in patients with SLE ((mean ± SEM) 1,007 ± 154 vs. 824 ± 170 (P = 0.20)). No significant difference was seen in EPC number between SLE patients without CAC and those with advanced CAC. Increased carotid intima-media thickness did not correlate with CAC or EPC number in SLE patients. Reduced numbers of EPCs in SLE patients may be observed compared to HC even in the absence of CAC. Differences in measured risk factor profiles and depletion of total circulating PCs do not fully explain this finding.     

老年心肌梗死患者循环血内皮祖细胞数目和功能的变化及其对心功能的影响

目的 比较不同年龄组心肌梗死患者循环血内皮祖细胞（EPCs）数目及功能的差异,分析蛋白激酶B（Akt）和间质细胞源因子1（SDF-1）表达的差异,探讨老年患者EPCs修复梗死心脏功能的可能机制及临床意义.方法 抽取老年心肌梗死患者（n=26）和中青年心肌梗死患者（n=24）动脉血8 ～10 ml,流式细胞仪检测各组EPCs含量,酶联免疫吸附法检测Akt及SDF-1表达变化情况;利用冠状动脉左前降支结扎术制备大鼠心肌梗死模型后,尾静脉注射老年EPCs、中青年EPCs（1×107/200 ml）或等体积盐水（PBS组）,观察终点时间为28 d,超声心动评价心脏功能,荧光显微镜下观察EPCs在梗死心脏的归巢情况,免疫荧光法计数缺血心肌局部血管数量.结果 老年心肌梗死患者循环血EPCs数量明显少于中青年组（47.23％±14.92％比89.76％ ±7.27％,P＜0.001）;心肌梗死后老年组Akt磷酸化水平和SDF-1表达水平明显低于中青年组（Akt：19.04％±6.41％比43.96％±15.91％;SDF-1：25.81％ ±6.32％比64.04％±16.35％,均为P＜0.001）.将EPCs移植至梗死大鼠后,移植的老年EPCs在梗死心脏的归巢数量明显少于移植的中青年EPCs（3.69±1.97/mm2比12.01 ±5.44/mm2,P ＜0.001）.移植老年EPCs的大鼠梗死心脏的血管密度明显少于移植中青年EPCs的大鼠（42±9/mm2 比96±15/mm2,P ＜0.001）.移植老年EPCs组心功能指标[左心室射血分数（LVEF）和左心室缩短分数（LVFS）]显著低于移植中青年EPCs组（LVEF：58.1％±5.0％比73.8％±7.9％;LVFS：35.4％±3.8％比59.0％±7.6％.均为P＜0.001）.结论 老年心肌梗死患者的循环血EPCs数量及其修复功能均不如中青年患者,可能与Akt-SDF-1信号通路受损有关.     

大鼠外周血晚期内皮前体细胞体外培养研究

目的体外培养大鼠外周血内皮前体细胞（EPCs）,观察细胞克隆形态并进行鉴定。方法密度梯度离心法分离SD大鼠外周血单个核细胞,EGM-2培养基离体培养。免疫荧光染色鉴定细胞CD34、CD31、CD133、FLk-1、vwF细胞表面标志。Real—TimePCR检测细胞CD34、CD133、FLk-1、eNOSmRNA表达。结果细胞培养10天后可见“铺路石样细胞”和少数“紊乱生长细胞”,传代培养后经免疫荧光及Real—TimePCR鉴定“铺路石样细胞”符合晚期EPCs特点,紊乱生长细胞不表达相应标志。结论通过体外分离长时培养可从大鼠外周血获得晚期内皮前体细胞,具有内皮细胞的特征。     

Smoking is associated with depletion of circulating endothelial progenitor cells and elevated pulmonary artery systolic pressure in patients with coronary artery disease

Smoking is associated with depletion of endothelial progenitor cells (EPCs) and may subsequently contribute to the development of vascular dysfunction. The aim of this study was to investigate the relation between circulating EPCs and pulmonary artery systolic pressure (PASP) as determined by flow cytometry and echocardiography in 174 patients (mean age 69 ± 9 years, 95 smokers) with established coronary artery disease. Smokers had significantly lower circulating log CD34/KDR(+) (0.86 ± 0.03 vs 0.96 ± 0.03 × 10?3/ml, p = 0.032) and log CD133/KDR(+) (0.68 ± 0.03 vs 0.82 ± 0.03 × 10?3/ml, p = 0.002) EPCs and a higher prevalence of elevated PASP >30 mm Hg (52% vs 30%, p = 0.001) than nonsmokers. Smokers with elevated PASP also had significantly lower circulating log CD34/KDR(+) (0.74 ± 0.04 vs 0.88 ± 0.06 × 10?3/ml, p <0.001) and log CD133/KDR(+) (0.61 ± 0.04 vs 0.78 ± 0.05 × 10?3/ml, p <0.001) EPCs, higher pulmonary vascular resistance, and larger right ventricular dimensions with impaired function (all p values <0.05). Log CD34/KDR(+) and log CD133/KDR(+) EPC counts were significantly and negatively correlated with PASP (r = -0.30, p <0.001, and r = -0.34, p <0.001, respectively) and pulmonary vascular resistance (r = -0.29, p = 0.002, and r = -0.18, p = 0.013, respectively). In conclusion, this study demonstrated that in patients with coronary artery disease, smoking was associated with a reduced number of EPCs and elevated PASP. This suggests that in smokers, depletion of circulating EPCs might be linked to the occurrence of pulmonary vascular dysfunction.