脐血MSCs移植对急性心肌梗死大鼠心肌的修复作用

目的:观察体内心肌缺血微环境诱导下人脐血间充质干细胞(umbilical cord blood mesenchymal stem cells,UCBMSCs)向心肌样细胞的定向分化及对急性心肌梗死(acute myocardial infarction,AMI)大鼠心功能、新生血管的影响。方法:收集健康产妇脐血细胞,采用密度梯度离心结合差速贴壁的方法分离MSCs;健康成年SD大鼠30只,制备成AMI大鼠模型后分为2组,移植组在心肌梗死周边区注射移植GFP标记的UCBMSCs;对照组在心肌梗死周边区注射等量生理盐水。术后4周行超声心动图检测及血流动力学检查,并取心脏组织行冰冻切片,免疫荧光染色检测UCBMSCs心肌特异性蛋白cTnT和Connexin43的表达;并进行抗Ⅷ因子抗体免疫组化染色,观察心肌毛细血管密度(myocardial capillary density,MCD)的变化。结果:与对照组相比,术后4周移植的UCBMSCs表达心肌特异性蛋白cT-nT和Connexin43,对照组无心肌特异蛋白表达;移植组LVEDD、LVESD明显减小,而LVEF、LVFS明显增加,血流动力学指标明显改善;免疫组化染色结果显示,移植组梗死周边区MCD较对照组明显增加,移植组为(4.16±0.2)个/HP(×400),对照组为(2.29±0.3)个/HP,两组比较差异有统计学意义(P<0.01)。结论:UCBMSCs移植可在大鼠AMI部位存活,并向心肌样细胞分化;UCBMSCs移植后明显改善AMI大鼠心功能及心室重构,促进毛细血管新生。     

多种细胞移植治疗心肌梗死的比较

目的通过横向比较乳鼠心肌细胞、骨髓单个核细胞、骨髓间充质干细胞及诱导后的骨髓间充质干细胞移植治疗大鼠急性心肌梗死的疗效,确定更优异的移植细胞。方法分离培养和鉴定新生心肌细胞、骨髓单个核细胞、骨髓间充质干细胞,并在体外用5-氮杂胞苷诱导骨髓间充质干细胞向心肌细胞分化。二脒苯基吲哚(DAPI)标记移植细胞,5组(包括4组细胞处理组和对照组)大鼠急性心肌梗死后一周,可直视下在梗死中央区和周边区注射同等数量级细胞(2×106／只),4周后行心功能检测。处死动物,免疫荧光法检测移植细胞缝隙连接蛋白(connexin-43)、横纹肌肌动蛋白、血管平滑肌肌动蛋白(α-SMA)和Ⅷ因子相关抗原(vWF)以确定移植细胞的分化情况,免疫组化法检测心肌组织中血管平滑肌肌动蛋白和vD因子相关抗原以确定血管新生情况。结果体外实验显示经5-氮杂胞苷诱导的骨髓间充质干细胞能部分表达横纹肌肌动蛋白:体内试验,移植4周后,间充质干细胞组、乳鼠心肌细胞组、骨髓单个核细胞组大鼠心功能均较对照组大鼠心功能明显提高,其中间充质干细胞组优于其他处理组,间充质干细胞,能表达血管平滑肌肌动蛋白,促进血管新生,但未见其表达心肌细胞特异抗原,而诱导后骨髓间充质干细胞对心功能无显著作用。结论在乳鼠心肌细胞、骨髓单个核细胞、骨髓间充质干细胞、诱导后的骨髓间充质干细胞移植治疗大鼠的急性心肌梗死的比较中,间充质干细胞对心功能的保护效果最显著,其机制与血管新生等有关。     

体内外诱导人脐血间充质干细胞向心肌细胞的定向分化

目的观察在体外5-氮胞苷诱导和体内心肌缺血微环境诱导下,人脐血间充质干细胞（mesenchymal stem cells,MSCs）向心肌细胞的定向分化。方法收集健康产妇脐血细胞,采用密度梯度离心结合差速贴壁的方法分离MSCs,传代培养至第三代,应用流式细胞术分析MSCs表面分子CD34、CD45、CD44和CD90的表达。体外应用5-氮胞苷（5-aza）诱导MSCs四周后,免疫荧光染色和RT-PCR分别检测MSCs心肌标志物cTnT（肌钙蛋白）和Connexin43（缝隙连接蛋白）的表达;体内将GFP标记的MSCs移植入心肌梗死大鼠模型心肌梗死周边区,移植后1周,取大鼠心脏行冰冻切片,免疫荧光染色检测MSCs心肌特异性蛋白cTnT和Connex-in43的表达。结果分离的MSCs表达表面分子CD44和CD90,不表达CD34和CD45;MSCs体外经5-氮胞苷诱导后在mRNA和蛋白水平均表达心肌标志物cTnT和Connexin43;MSCs体内移植后1周,免疫荧光染色检测发现移植的MSCs表达心肌特异性蛋白cTnT和Connexin43。结论人脐血间充质干细胞可在体外诱导和体内心肌缺血微环境下向心肌细胞分化。     

VEGF基因转染骨髓间充质干细胞对大鼠心梗区血管新生的影响

目的：探讨转染血管内皮细胞生长因子（vascular endothelial growth factor，VEGF）基因的骨髓间质干细胞（mesenchymal stem cell，MSC）心肌移植及其对大鼠心梗区血管新生的影响。方法：以Wistar近交系大鼠建立心肌缺血模型，实验动物随机分为4组（n=12）。冠脉结扎2周后，联合组（A组）于心梗区移植转染VEGF基因的MSC，细胞组（B组）移植等量的MSC，基因组（c组）注射脂质体-pcDNA3.1-VEGF165DNA复合物，对照组（D组）注射等容积培养液，移植4周后通过Ⅷ因子染色检测血管新生，RT-PCR检测VEGF基因的体内表达。结果：Ⅷ因子染色示A组动物心梗区毛细血管密度明显高于B组和D组，较C组亦有一定程度的升高；RT—PCR显示VEGF基因的体内表达从高到低依次为A组、C组、B组、D组。结论：BMMSC有利于VEGF基因的稳定表达，可作为VEGF基因的良好细胞载体。     

骨髓间质干细胞在梗死心肌移植后心肌再生的实验研究

目的：研究骨髓间质干细胞在梗死心肌移植后的心肌再生作用。方法：贵州香猪24只，随机分为对照组（C组），实验组（E组）。抽取骨髓液3ml，按照Wakitani的方法培养出骨髓间质干细胞，经5-氮胞苷诱导后，BrdU标记备用。开胸结扎冠状动脉前降支，自体骨髓间质干细胞分别经局部注射和结扎的左冠状动脉前降支远端灌注移植入自体急性心肌梗死区域，C组以DMEM对照。术后3，6周取心肌标本行免疫组化、电镜检测。结果：梗死区域可观察到标记的骨髓间质干细胞，这些细胞能表达肌球蛋白重链（MHC），缝隙连接蛋白-43（Cx-43），心肌特异性肌钙蛋白1（cTnTI），电镜下有肌丝形成。结论：骨髓间质干细胞在梗死心肌内移植具有分化再生的能力。     

骨髓间质干细胞分离培养及向心肌细胞的转化

目的:探讨骨髓间质干细胞(MsCs)诱导分化为心肌细胞的可能性,为干细胞移植治疗心肌梗死寻求理想的细胞材料.方法:体外分离培养大鼠骨髓MSCs,5-氮胞苷(5-aza)诱导24 h后继续培养,免疫细胞化学染色和RT-PCR检测心肌细胞特异性蛋白的表达.结果:MSCs经5-aza诱导后3周心肌肌钙蛋白T和连接蛋白43免疫细胞化学染色阳性表达;RT-PCR显示诱导3周细胞有心肌肌钙蛋白I、α心肌肌动蛋白表达.结论:MsCs可在体外经5-aza诱导定向分化为心肌细胞.     

原代骨髓间充质干细胞治疗创伤性脑损伤大鼠模型

目的移植大鼠原代骨髓间充质干细胞治疗创伤性脑损伤模型,探索该方法的疗效及临床可行性。方法体外培养大鼠原代骨髓间充质干细胞,造模成功7d后将其移植入受损脑组织边缘,移植后养育14d,神经功能评分后处死模型取脑组织,记录实验组及对照组（未移植干细胞）的神经功能评分、组织形态学、Ⅷ因子表达血管计数。结果实验组脑组织受损坏死区域较对照组小,受损周边脑水肿较轻;数据显示实验组神经功能恢复优于对照组,血管计数多于对照组。神经功能评分及Ⅷ因子表达血管计数提示实验组与对照组有统计学差异,实验组有明显疗效（P〈0.05）。结论移植原代骨髓间充质干细胞治疗创伤性脑损伤能够帮助神经功能恢复,并促进血管生长。推测骨髓间充质干细胞通过促进血管新生帮助脑组织修复。实验验证最短培养周期的原代干细胞早期移植即可应用于治疗急性创伤性脑损伤。     

骨髓间充质干细胞移植对大鼠心肌梗死后细胞凋亡的作用

目的：探讨骨髓间充质干细胞心肌移植对大鼠心肌梗死区细胞凋亡的影响。方法：取大鼠骨髓间充质干细胞进行体外培养、增殖和标记，同时以液氮冷冻左室游离壁建立心肌梗死模型，4周后分别将2×106个细胞悬液或冷D-Hanks液注入心肌梗死区数个不同部位。于移植后1周、2周和4周依次获取心肌梗死区标本。随机于第2周实验组与对照组中各抽取两个标本进行透射电镜检查，凋亡细胞计数，RT-PCR检测所有标本bcl-2 mRNA的表达。结果：部分心肌细胞呈调亡细胞初期形态改变，实验组和对照组调亡指数分别为0.02和0.08。bcl-2 mRNA在术后第1，2及4周的表达水平实验组与对照组相比均增加（P<0.01），且随着时间的推移其表达量两组均呈迅速降低的趋势（P<0.01）。结论：骨髓间充质干细胞心肌移植可促进心肌梗死区Bcl-2蛋白表达，并减轻大鼠心肌梗死后细胞凋亡。     

骨髓间质干细胞移植治疗急性心肌梗死的实验研究

目的通过两种不同移植途径研究骨髓间质干细胞治疗急性心肌梗死可行性及疗效对比。方法骨髓间质干细胞培养传至5代后,制备成浓度4×106/ml悬液备用。39只SD大鼠均结扎冠状动脉左前降支,制备成急性心肌梗死模型,随机分为3组每组各13只。Ⅰ为对照组:从尾静脉注射生理盐水。Ⅱ为直接经心外膜移植组:模型制备成功后1~3 h梗死周边区分六点注射骨髓间质干细胞,每点50μl。Ⅲ为通过静脉移植组:模型制备成功后24h,从尾静脉注射骨髓间质干细胞0.5 ml(含2×106个)连续7 d,Ⅰ和Ⅱ组注射等量生理盐水7 d作为对照。5周后,观察3组的大鼠死亡率以及心脏的结构和功能。结果Ⅰ组有3只大鼠死亡,其他组无死亡。与Ⅰ组相比,Ⅱ组和Ⅲ组的左心室结构与功能明显改善(P<0.05),Ⅱ组和Ⅲ组相比无明显差别(P>0.05)。结论骨髓间质干细胞移植治疗急性心肌梗死有效;静脉注射与直接经心外膜心肌注射两种途径无明显差别,静脉注射移植相对简单易行。     

脐血间质干细胞移植后梗死心肌细胞的凋亡及意义

目的 探讨脐血间质干细胞移植对梗死心肌残存心肌细胞凋亡的影响.方法 无菌条件下采集成年杂种妊娠犬脐血,体外分离、纯化、培养、扩增脐血间质干细胞,经5-氮杂胞苷(5-aza)体外诱导向肌源性细胞分化,DAPI荧光标记,经左冠状动脉前降支灌注移植入成年杂种犬急性心肌梗死模型区域,2、4、8周取心肌标本,采用HE染色及TUNEL法检测犬心肌梗死模型中脐血间质干细胞移植后心肌细胞的凋亡情况.结果 免疫组化法检测结果表明,培养的细胞为脐血间质干细胞,在5-aza诱导作用下可向肌源性细胞定向分化,2、4、8周后在移植区域观察到带荧光的心肌纤维和细胞核,排列方向与残留心肌组织基本一致,荧光标记的肌纤维相互连接.经TUNEL法检测可见在脐血间质干细胞移植组和对照组心肌梗死区域均有凋亡的心肌细胞分布,但移植组凋亡细胞明显低于非移植组;HE染色有相似的阳性率,阳性细胞多具有凋亡的形态特征.结论 脐血间质干细胞移植梗死心肌除能形成心肌再生外,尚能减少心肌梗死后梗死区域的心肌细胞凋亡,达到延缓心室重构的目的.应用TUNEL法检测心肌细胞凋亡有较强的实用性.     

磁共振心肌灌注成像评价心肌梗死PTCA治疗前后心肌存活

目的 评价磁共振心肌灌注成像(MRMPI) 检测心肌梗死存活心肌的作用. 方法 选择心肌梗死患者51 例.采用1.5 T MR扫描仪,反转恢复快速小角度激励( IR-turbo FLASH) 序列,全部患者均在静脉注射钆喷替酸葡甲胺(Gd-DTPA) 0.1 mmol/kg、MRMPI 首过期及5~30 min 延迟期成像.21 例行静息、负荷99锝单光子发射计算机体层摄影术( single photon emission computed tomography, SPECT) 进行对照研究.首过期行短轴面成像,延迟期行短轴面及长轴面成像.结果 51例心肌梗死患者,42 例(82.3%) 首过期显示灌注减低;50 例(98%) 延迟增强.在21例168个心肌段SPECT诊断无活性心肌段48个,MRMPI 示梗死区均有延迟增强,SPECT诊断存活心肌段120 个,MRMPI 示97段无延迟增强.以静息、负荷99m锝SPECT 作为参考标准,MRMPI 的敏感度、特异度分别为100%、80.8%. 结论 MRMPI 可有效地检测心肌梗死的存活和非存活心肌,以及其程度和范围.     

Acute myocardial infarction due to myocardial bridge

Myocardial bridge (MB) is regarded as a common anatomic variant rather than a congenital condition anomaly,defined as the intramyocardial course of a portion of the coronary artery.It was first mentioned by Rayman in 1737 and first described by Grainicianu in the early 1920s.The current gold standard for diagnosing     

Acute myocardial infarction: myocardial salvage assessment

Primary coronary revascularization by means of percutaneous coronary intervention(PCI)is a highly effective treatment of acute myocardial infarction re-establishing coronary perfusion and stopping the ongoing necrosis in the dependent myocardium.Single-photon emission computed tomography(SPECT)is the most widely used modality assessing myocardial salvage as the difference between the acute perfusion defect before intervention and the remaining scar size measured in a second scan several days after the event.SPECT allows quantification of area at risk(AAR)and final infarct size(FIS)by tracer injection prior to revascularization and after 1 month,respectively.SPECT provides the most validated measure of myocardial salvage and has been utilized in multiple randomizedclinical trials.However,SPECT is logistically challenging,expensive,and includes radiation exposure.More recently,a large number of studies have suggested that cardiac magnetic resonance(CMR)can determine salvage in a single examination by combining measures of myocardial oedema in the AAR exposed to ischaemia reperfusion with FIS quantification by late gadolinium enhancement.     

Evaluation of Myocardial Viability after Myocardial Infarction with Intravenous Real-time Myocardial Contrast Echocardiography

The myocardial viability after myocardial infarction was evaluated by intravenous myocardial contrast echocardiography. Intravenous real-time myocardial contrast echocardiography was performed on 18 patients with myocardial infarction before coronary revascularization. Follow-up echocardiography was performed 3 months after coronary revascularization. Segmental wall motion was assessed using 18-segment LV model and classified as normal, hypokinesis, akinesis and dyskinesis. Viable myocardium was defined by evident improvement of segmental wall motion 3 months after coronary revascularization. Myocardial perfusion was assessed by visual interpretation and divided into 3 conditions： homogeneous opacification; partial or reduced opaciflcation or subendocardial contrast defect; contrast defect. The former two conditions were used as the standard to define the viable myocardium. The results showed that 109 abnormal wall motion segments were detected among 18 patients with myocardial infarction, including 47 segments of hypokinesis, 56 segments of akinesis and 6 segments of dyskinesis. The wall motion of 2 segments with hypokinesis before coronary revascularization which showed homogeneous opacification, 14 of 24 segments with hypokinese and 20 of 24 segments with akinese before coronary revascularization which showed partial or reduced opaciflcation or subendocardial contrast defect was improved 3 months after coronary revascularization. In our study, the sensitivity and specificity of evaluation of myocardial viability after myocardial infarction by intravenous real-time myocardial contrast echocardiography were 94.7% and 78.9%, respectively. It was concluded that intravenous real-time myocardial contrast echocardiography could accurately evaluate myocardial viability after myocardial infarction.     

心肌声学造影对急性心梗PCI术后心肌灌注的评价

目的:通过心肌声学造影(MCE)对急性心梗经皮冠状动脉支架术(PCI)后心肌灌注的情况进行判断,了解其对左心功能及左室重构的影响.方法:采用病例对照的研究方法,根据PCI术后1周的MCE检查,将急性心梗患者分为灌注正常组、灌注稀疏组和灌注缺失组,并随访检查3个月、6个月的左室射血分数(LVEF)及左室舒张末内径(LVDd)的变化情况,比较组内及组间不同时段LVEF与LVDd的变化.结果:PCI术后3个月灌注稀疏组LVEF恢复到正常;灌注缺损组PCI术后LVEF的平均水平随时间变化而逐渐降低;灌注缺损组患者的LVEF低于灌注稀疏组和灌注正常组(P<0.05);术后6个月灌注缺损组LVDd平均水平高于灌注正常组和灌注稀疏组(P<0.05),灌注缺损组随时间的变化左室内径逐渐增大(P<0.05).结论:急性心梗患者PCI术后心肌微循环较差时,其左室射血分数降低,左室内径增大;MCE有利于对急性心梗患者PCI术后左心功能及左室重构评估.     

水飞蓟素通过抑制心肌细胞凋亡减轻心肌梗死

目的：观察水飞蓟素对心肌梗死小鼠的血流动力学、梗死面积及梗死边缘区凋亡蛋白表达情况。方法：将60只小鼠随机分为心肌梗死组、假手术组、心肌梗死+水飞蓟素组和心肌梗死溶剂组。建模成功4周后检测小鼠血流动力学变化,进行心脏超声检查,评价梗死面积、细胞凋亡指数以及凋亡蛋白Bcl-2、Bax、Cleaved-Caspase3的表达。结果：与心肌梗死组小鼠相比,水飞蓟素可显著减轻心肌梗死,改善心梗小鼠心功能,降低心肌细胞凋亡指数,增强Bcl-2蛋白表达和减弱Bax和Cleaved-Caspase3蛋白表达。结论：水飞蓟素能够减轻心肌梗死,改善心梗小鼠心室收缩功能,保护心肌,减少心肌细胞的凋亡,其机制与升高Bcl-2蛋白、降低Bax和Cleaved-Caspase3蛋白表达水平有关。     

“肾阳虚证”下心肌梗死模型与单纯心肌梗死模型大鼠心肌形态学、心肌酶学及血液流变学的比较

目的：建立大鼠“肾阳虚证”下心肌梗死模型,探讨其与单纯心肌梗死模型大鼠在心肌形态学、心肌酶学及血液流变学方面的差异,为评价治疗胸痹心痛中药的药效学提供理论依据。方法：60只Wistar大鼠随机分为空白对照组、肾阳虚模型组、心肌梗死假手术组、单纯心肌梗死模型组及“肾阳虚证”下心肌梗死模型组,每组12只。在大鼠 “肾阳虚”情况下复制急性心肌梗死模型,测定各组大鼠心肌梗死面积 (MIS),血清天门冬氨酸氨基转化酶（AST）、肌酸磷酸激酶（CK）及乳酸脱氢酶（LDH）活性,同时测定血小板黏附率（PAR）、血小板聚集率（PAG）、红细胞沉降率（ESR）、红细胞压积（HCT）、体外血栓长度、血栓干重与湿重以及血栓弹力图等参数。结果： 大鼠“肾阳虚证”下心肌梗死模型与单纯心肌梗死模型在MIS,血清AST、CK及LDH活性,PAR、PAG、ESR及HCT增加程度差异无统计学意义（P>0.05）;肾阳虚模型组、单纯心肌梗死模型组及“肾阳虚证”下心肌梗死模型组大鼠体外血栓干重及长度均明显增加（P<0.05或P<0.01）,“肾阳虚证”下心肌梗死模型组的增加程度大于单纯心肌梗死模型组及肾阳虚模型组,但三者之间差异无统计学意义（P>0.05）;尽管“肾阳虚证”下心肌梗死模型组大鼠血栓弹力图r、k值的缩短程度及ma值的增大程度高于单纯心肌梗死模型组,但2组之间差异无统计学意义（P>0.05）。结论：大鼠“肾阳虚证”下心肌梗死模型与单纯心肌梗死模型心肌梗死面积、血清心肌酶学、红细胞压积、血沉、血小板功能、体外血栓重量及血栓弹力图等指标均无明显差异。     

超声心肌造影技术对心肌梗塞患者心肌微循环的定量评价

目的：探讨超声心肌造影技术在心肌梗塞(简称心梗)患者心肌微循环灌注改变中的应用价值。方法：对30例急性心梗患者进行超声心动图及心肌造影检查,观察患者梗塞区域(AMI组,同时以患者非梗塞区域为自身对照组)心肌微循环灌注并以CPS造影软件进行分析。结果：心肌梗塞患者梗塞区域心肌微循环灌注开始时间(AT)、达峰时间(APT)较同一切面内的非梗塞区域明显延长（P<0.05）,梗塞区域造影剂灌注的峰值强度(PI)及灌注速度(β)均明显低于同一切面内的非梗塞区域（P<0.05）。结论：超声心肌造影技术可以定量评价心梗患者心肌微循环灌注,具有重要的临床应用价值。     

Factors affecting thrombolysis in myocardial infarction myocardial perfusion frame count: insights of myocardial tissue-level reperfusion from a novel index for assessing myocardial perfusion

Background  Myocardial tissue-level perfusion failure is associated with adverse outcomes following ST-elevation myocardial infarction (STEMI) despite successful epicardial recanalization. We have developed a new quantitative index—thrombolysis in myocardial infarction (TIMI) myocardial perfusion frame count (TMPFC)—for assessing myocardial tissue level perfusion. However, factors affecting this novel index of myocardial perfusion are currently unknown.

Methods  A total of 255 consecutive STEMI patients undergoing primary angioplasty were enrolled. Myocardial tissue level perfusion was assessed by TMPFC, which measures the filling and clearance of contrast in the myocardium using cine-angiographic frame counting. We differentiate three groups with two cut off values for TMPFC: a TMPFC of 90 frames was the upper boundary of the 95% confidence interval (CI) for the TMPFC observed in normal arteries, and a TMPFC of 130 was the 75th percentile of TMPFC.

Results  STEMI patients with TMPFC >130 frames (68 patients, 26.7%) had higher clinical and angiographic risk factor profiles as well as a higher 30-day MACE rate compared with those with TMPFC ≤90 frames and those with TMPFC >90 and ≤130 frames. Multivariable analysis identified that the independent predictors of TMPFC >130 frames were age ≥75 years (OR 2.08, 95% CI 1.21 to 3.58, P=0.007), diabetes (OR 1.37, 95% CI 1.01 to 1.86, P=0.042), Killip class ≥2 (OR 1.52, 95% CI 1.05 to 2.21, P=0.027), and prolonged pain-to-balloon time (OR 1.73, 95% CI 1.07 to 2.79, P=0.013). TMPFC >130 frames was identified as the strongest independent predictor of 30-day major adverse cardiac event (MACE) (OR 2.77, 95% CI 1.21 to 6.31, P=0.008), along with age ≥75 years (OR 2.19, 95% CI 1.11 to 4.33, P=0.016), female gender (OR 1.67, 95% CI 1.03 to 2.70, P=0.038), and Killip class ≥2 (OR 1.83, 95% CI 1.07 to 3.14, P=0.021).

Conclusions  STEMI patients with poor myocardial perfusion assessed by TMPFC had higher risk factor profiles. Advanced age, diabetes, higher Killip class, and longer ischemia time were independent predictors of impaired TMPFC after primary percutaneous coronary intervention. These results emphasize that particular attention should be paid on myocardial microvascular reperfusion in STEMI patients with these risk factors.

     

Relation of myocardial bridge to myocardial infarction: a meta-analysis

Background Small case series have suggested an association of coronary myocardial bridge （MB） with myocardial infarction （MI）.However,the relationship between MB and major adverse cardiac events （MACE） remains largely unknown.The aim of this study was to assess the relationship between MB and MACE involving MI.Methods We performed a systematic search of MEDLINE,PreMEDLINE,and all EMB Reviews as well as a reference list of relevant articles according to the SPICO （Study design,Patient,Intervention,Control-intervention,and Outcome） criteria using the following keywords：myocardial bridging,myocardial bridge,intramural coronary artery,mural coronary artery,tunneled coronary artery,coronary artery overbridging,etc.Bibliographies of the retrieved publications were additionally hand searched.Studies were included for the meta-analysis if they satisfied the following criteria：（1） they evaluate the association of MB with cardiovascular endpoint event; （2） they included individuals with MB and those without MB; 3） they excluded individuals with obstructive coronary artery disease （CAD）.Studies were reviewed by a predetermined protocol including quality assessment.Dates were pooled using a random effect model.Results Seven observational studies that followed 5 486 patients eligible for the enrolled criteria were included from 7 136 initially identified articles.The prevalence of MB was 24.8％ （1 363/5 486）.During 0.5-7.0 years of follow-up of this cohort of population,crude outcome rates were 8.0％ in the MB group and 7.7％ in the non-MB group.The odds ratio of overall MACE and MI were 1.34 （95％ confidence interval （CI）：0.57-3.17,P=0.51,n=7 studies） and 2.75 （95％ CI：1.08-7.02,P ＜0.03,n=5 studies） respectively for subjects of MB compared to non-MB.Conclusion Relationship between MB and MI appears to be a real one,although the study did not reveal a connection of MB to MACE,suggesting whether the necessity of antiplatelet therapy needs to be further studied in a larger cohort of patients with MB prospectively.