99Tcm-MIBI心肌灌注断层显像评价通心络对急性心肌梗死后心肌无再流的影响

目的 应用99Tcm-MIBI MPI评价通心络(超微粉剂)对AMI患者接受急诊PCI治疗后心肌无再流的效果.方法 38例急诊入院AMI患者,按随机数字表法分为常规组18例和通心络组(常规治疗+通心络)20例.2组患者均分别于急诊PCI治疗后7d及180 d行99Tcm-MIBI MPI.将左室心肌分为17个节段,对心肌摄取99Tcm-MIBI的程度进行评分,分别统计2组第7天及第180天心肌稀疏缺损节段数及两者相减的节段数,并分别计算2组第7天和第180天心肌显像的总积分及两者相减的积分.使用SPSS 11.5软件,对数据行t检验和x2检验.结果 通心络组急诊PCI治疗后7dMPI稀疏缺损节段数共59个,180 d时显像示改善的节段数为37个(62.7％,37/59);常规组急诊PCI治疗后7 d MPI稀疏缺损节段数共64个,180 d时显像示改善的节段数为26个(40.6％,26/64);2组改善节段数差异有统计学意义(x2=5.994,P＜0.05).通心络组与常规组急诊PCI治疗后7d心肌显像的总积分分别为6.2±8.4和7.4 ±6.9(t =0.5,P＞0.05);180 d心肌显像的总积分分别为3.4±4.6和6.8±5.9(t=2.1,P＜0.05);2组2次心肌显像总积分的差值(即患者心肌血流灌注改善情况的积分)分别为2.9±5.7和0.6±3.3(t =1.5,P＞0.05).结论 通心络(超微粉剂)能够缩小AMI再灌注治疗后心肌无再流面积,对心肌无再流现象有一定疗效.     

超声心动图定量犬冬眠心肌的方法学研究

目的:建立经胸小剂量多巴酚丁胺超声心动图激发试验(Dobu-UCG)评价犬冬眠心肌定量的方法学。材料和方法:成功建立冬眠心肌犬7条3～6个月后进行DoBu-UCG试验,测量Dobu-UCG后的心肌梗死区运动幅度(wall motion amplitude of area with myocardium infarction,MMI)和非梗死区心内膜运动幅度(wall mo-tion amplititude of areas with non myocardium infarction,MNMI)的比值(MMI/MNMI),以及试验后MMI/MNMI与试验前MMI/MNMI的差值(D值);并与实验后测量组织切片的冬眠心肌面积(the area oftotal alive myocardium,ATAM)和梗死区总面积(the area of total infarction myocardium,ATIM)的比值(ATAM/ATIM)进行比较。结果:Dobu-UCG激发试验后MMI/MNMI比值、D值分别与ATAM/ATIM进行对比分析,显示两者均高度相关(r=0.83～0.90,P分别为<0.05和<0.001)。结论:测量Dobu-UCG激发试验后MMI/MNMI比值,以及试验后、前MMI/MNMI差值(D)是定量梗死区内冬眠心肌的较好方法。     

MRI评价骨髓问质干细胞治疗猪急性心肌梗死效果的实验研究

目的 应用MRI评价经冠状动脉途径移植猪自体骨髓间质干细胞(BM-MSCs)治疗急性心肌梗死(AMI)的治疗效果.方法 8月龄中华小型猪14只[(27±3)kg],平均分成移植组与对照组.胶圈套扎左前降支第一对角支分叉以远90 min后松开,建成AMI模型.心肌梗死后1周进行细胞移植,将干细胞悬液(移植组:1×106/ml × 10 ml)或无血清培养液(DMEM)(对照组10 ml)经微导管注入前降支.AMI术后1周(基线)和MSCs移植后6周(终点)各行1次MR扫描,评价移植前后心脏形态、功能、心肌灌注及延迟增强.第2次MR扫描后立即处死动物,分别行冰冻切片、石蜡切片和电镜观察.结果 与对照组比较,移植组在移植6周后左心室整体功能较前明显改善,实验组与对照组比较,左心室平均射血分数(EF)值从(42.7±7.5)%升至(50.1±10.1)%(P＜0.01),左心室节段运动异常数平均减少4个(P＜0.01)、梗死面积减少3.2 cm2(P＜0.01),心脏重量指数增加4.1 g/m2(P＜0.05).病理证实移植组梗死区和梗死周边的病变情况显著轻于对照组,有大量存活心肌,纤维化程度显著减轻;并且可见核大、边集,胞质丰富的幼稚细胞;在梗死区和梗死周边区组织的冰冻切片上可见4-6-二脒基二苯基吲哚(DAPI)阳性的移植细胞存活.免疫荧光检测进一步表明大部分DAPI阳性细胞表达心肌特异性肌钙蛋白T(troponin T),并且表达间隙连接蛋白43(connexin 43).部分DAPI阳性细胞表达平滑肌肌动蛋白(smooth muscle actin)和血管性血友病因子(Von Willebrand),移植组梗死周边区毛细血管密度显著高于对照组[分别为(8.7±2.0)、(4.9±1.3)个/高倍镜](P＜0.01).结论 MRI可作为猪BM-MSCs在体移植前后评价其治疗效果的可靠影像检查方法 .     

用18 F-FDG和99 TCm-MIBI显像评估冷冻心肌骨髓CD34+细胞移植后代谢和灌注的变化

目的用18F-脱氧葡萄糖(FDG)、99Tcm-甲氧基异丁基异腈(MIBI)评价犬冷冻心肌骨髓CD34+细胞移植后心肌代谢和灌注的变化.方法12只杂种犬分为细胞移植组和对照组.用免疫磁珠法从犬肋骨骨髓分离CD34+细胞并注射到用CO2冷冻建立的慢性心肌梗死模型区,对照组注射伊思考夫改良杜尔贝可培养基(IMDM)培养液.分别于建立模型前、后4周和干细胞移植后8周行18F-FDG和99Tcm-MIBI心肌显像,评价细胞移植结果,计算冷冻心肌代谢与灌注显像的F值.干细胞移植后8周取心肌做第8因子免疫组织化学和病理检查.结果正常心肌代谢与灌注显像清晰,F值接近0,干细胞移植前、后8周冷冻心肌18F-FDG与99Tcm-MIBI显像的F值分别为5.50±1.31,5.44±0.70与1.17±0.41,1.50±0.55(P＜0.01);对照组为5.53±0.80,5.54±1.29与5.00±1.55,5.08±1.46(P＞0.05),骨髓CD34+细胞移植使冷冻心肌的代谢与灌注明显得到恢复.干细胞移植后8周冷冻区血管密度高于对照组(P＜0.01).结论骨髓CD34+细胞移植后冷冻区存在大量活的心肌细胞.     

MRI对自体骨髓间质干细胞移植于缺血心肌后动态监测价值的实验研究

目的 评价MRI对干细胞移植于缺血心肌后的动态监测价值.方法 中华小型猪6头,抽取髂骨骨髓并制备自体骨髓间质干细胞(mesenchymal stem cells,MSCs),以注射用超顺磁性氧化铁颗粒(SPIO)及4',6.二脒基-2.苯基吲哚(DAPI)标记细胞并进行标记率检测.开胸结扎冠状动脉左前降支制备小型猪心肌梗死模型.模型建立后14 d,MR延迟增强成像(DE-MRI)检测梗死面积,之后行第2次开胸,于每只动物心肌梗死周边区和正常心肌区直视下经心外膜各注射标记的MSCs 2个点,同时分别于各区注射培养基2个点作为对照点.细胞移植后24 h及21 d,快速梯度回波序列(F'GRE)T2*像检测十细胞移植点低信号区的面积及信号强度.T2*信号减低区范围的测量由FGRE面积法实现,其信号减低的程度以正常心肌区和该区的T2*值之差与正常心肌区T2*值的百分比表示.病理组织学检查心肌细胞形态、瘢痕形成、毛细血管密度及干细胞分布情况.不同时间点MSCs注射点低信号区面积及T2*信号强度的比较采用重复测量方差分析及配对t检验.干细胞注射点与对照点毛细血管密度的比较、梗死周边区及正常心肌区MSCs注射点信号衰减幅度和DAPI阳性细胞密度的比较采用成组资料t检验.结果 DAPI及SPIO对MSCs的标记率均达100%.心肌梗死模型建立后第14天,小型猪心肌梗死面积为(33.6±8.9)%.细胞移植后24 h,标记MSCs注射点于MRI显示为边界清晰的卵圆形T2*低信号区,梗死周边区与正常心肌区MSCs注射点T2*低信号区的信号强度[分别为(67.00±5.48)%、(61.92±7.76)%,t=1.65,P=0.1158)]及面积[分别为(0.56±0.24)、(0.52±0.25)cm2,t=0.39,P=0.7044.)]差异均无统计学意义.移植后3周,T2*低信号区与正常心肌区的对比程度均较前下降,梗死周边区减低至(40.12±5.93)%(t=9.53,P＜0.01);正常心肌区减低为(46.92±6.25)%(t=11.03,P＜0.01).梗死边缘区T2*减低的程度大于正常心肌区MSCs注射点,且2组间信号强度减弱幅度分别为(26.88±7.27)%和(15.00±4.51)%,差异有统计学意义(F:20.08,P=0.0003).正常心肌区MSCs注射点心肌组织中荧光标记的细胞核分布密度高于梗死边缘区.MSCs注射点[分别为(106±25)和(143±31)个/高倍镜(f=-2.47,P=0.0293)].梗死边缘区MSCs注射点组织中毛细血管分布密度高于该区对照点[分别为(13.4±4.0)和(9.4±3.1)个/高倍镜,f=2.49,P=0.0229].MSCs移植于心肌组织中3周后,普鲁十蓝染色阳性的铁颗粒仅位于部分移植MSCs细胞核周围.结论 MRI可在一定时间内实现对移植干细胞的示踪并反映移植MSCs在心肌局部的数量变化趋势,但是对于移植细胞的半定量监测存在局限性.移植干细胞所在的微环境是影响其牛存时间的重要因素之一.     

贫铀吸入性肺损伤犬模型的建立

目的建立适用于亚急性贫铀吸入性肺损伤研究的犬模型。方法将26只犬随机分为对照组(n=6)、低剂量组(n=10)和高剂量组(n=10)。3组犬麻醉后经气管插管,行左侧肺灌注,对照组给予0.2ml/kg生理盐水,低、高剂量组分别给予低浓度(10mg/ml)和高浓度(100mg/ml)贫铀混悬液。记录贫铀灌注后各组犬的生存时间,观察时间截止为贫铀灌注后30d。在灌注后31d,对存活犬行胸部CT检查,处死后取肺组织行病理检查。结果在30d的观察期内,对照组动物无死亡,低剂量组中1只犬在贫铀灌注后22d死亡,其余犬存活均超过30d;高剂量组所有犬均在30d内死亡,存活时间11.2±8.9(中位值12)d。高剂量组与低剂量组和对照组比较,差异有统计学意义(P=0.000),但后两组比较差异无统计学意义(P=0.439)。低剂量组肺组织的病理学改变主要为肺泡腔内炎细胞渗出、出血及透明膜形成,肺泡壁毛细血管扩张、充血,肺间质炎细胞浸润;胸部CT显示左肺片状渗出和实变影。结论采用贫铀混悬液以2mg/kg剂量行单侧肺灌注所建立的犬模型,适合用于进行1个月内亚急性贫铀毒性的实验研究。     

心肌SPECT显像观察卡托普利对犬心肌梗死后左心室重构的作用

目的 应用心肌SPECT显像观察卡托普利对实验犬急性心肌梗死后早期左心室重构的预防作用.材料与方法 34只杂种犬采用完全随机分组方法分为对照组(n=23)和治疗组(n=11).开胸结扎所有犬的左前降支制作心肌梗死模型.治疗组术前3d 口服卡托普利20mg,每天2次.术后6h行SPECT心肌显像,观察两组术前与术后左心室舒张末期容积( EDV)、收缩末期容积(ESV)、射血分数(EF)的变化.结果 ①对照组与治疗组分别有16只犬和6只犬成功建立模型并纳入实验.②对照组术前左心室EDV、ESV与术后比较,差异有统计学意义(t =2.81、2.83,P＜0.05);术前EF与术后比较,差异无统计学意义(t=0.06,P＞ 0.05).治疗组术前EDV、ESV、EF与术后比较,差异均无统计学意义(t=0.76、0.56、1.20,P＜0.05);两组术前EDV、ESV差异无统计学意义(t=0.08、0.94,P＞ 0.05),术后EDV、ESV差异有统计学意义(t=6.12、9.91,P＜0.05),EF差异无统计学意义(t=0.79,P＞0.05).结论 急性心肌梗死前预防性使用卡托普利可阻止早期左心室重构;心肌SPECT显像对评价预防性使用卡托普利控制急性心肌梗死后早期左心室重构有重要价值.     

用双核素心肌断层显像评价Q波和非Q波心肌梗死存活心肌

目的利用^99Tc^m-甲氧基异丁基异腈(MIBI)/^18F-脱氧葡萄糖(FDG)双核素心肌断层显像评价Q波和非Q波心肌梗死(MI)患中存活心肌的情况。方法45例MI患分为无Q波MI(NQMI，n=17)和有Q波MI(QMI，n=28)2组。均行^99Tc^m-MIBI SPECT门控心肌灌注显像、^18F-FDG SPECT心肌代谢显像和冠状动脉造影。根据心肌血流灌注、代谢和门控信息等比较2组患存活心肌的情况。结果NQMI组的缺血存活心肌节段数明显高于QMI组，非存活心肌节段数明显低于QMI组(P值分别为0．001和0．005)；左室射血分数(LVEF)明显高于QMI组(t=4．603，P：0．000)。门控分析所得室壁增厚率和缺血存活心肌间存在良好相关性(r=0．671，P=0．000)，NQMI组室壁增厚率降低的节段数明显低于QMI组(t=4．183，P=0．000)。结论对NQMI患采取更积极的治疗策略有助于挽救更多的缺血存活心肌，改善其预后。     

骨髓间质干细胞治疗家猪急性心肌梗死的SPECT显像

目的评价心肌 SPECT 显像对自体骨髓间质干细胞治疗家猪心肌梗死的价值。方法选择21头中国小型家猪,应用闭胸经股动脉介入的方法制作心肌梗死模型。10余天后实验组(11头)在心肌梗死区移植培养的骨髓间质干细胞,对照组(10头)在梗死区植入培养液。移植前及移植后8周对2组进行(99)~Tc~m-甲氧基异丁基异腈(MIBI)心肌显像及图像半定量分析;同时进行超声心动图及免疫组织化学检查。结果心肌显像示实验组在移植后心肌异常节段数从46个下降至26个,心肌梗死的面积从(34±12)%缩小至(21±10)%,心肌缺血总分值(SS)从20.0±4.3下降至12.1±3.6,与对照组相比差异均有显著性(P<0.05)。与同期进行的超声心动图及免疫组织化学检查结果一致。结论骨髓间质于细胞移植可改善心肌缺血区血流灌注及心肌活力。心肌 SPECT 显像可准确观察骨髓间质干细胞在心肌梗死部位的存活情况。     

孤立性左心室心肌致密化不全患者的心肌灌注显像研究

目的 分析孤立性左心室心肌致密化不全（ILVNC）患者的心肌灌注受损情况,及其与心脏MRI结果之间的关系.方法 前瞻性入选19例（男14例,女5例,年龄15 ～ 76岁）经心脏MRI确诊的ILVNC患者,同期行99Tcm-MIBI SPECT MPI.采用标准的17节段法分析MRI及SPECT图像.计算MRI所示各节段心肌非致密层（NC）与致密层（C）厚度比值（NC/C）,NC/C＞2.3者诊断为心肌致密化不全.计算并比较致密不全节段和致密化节段延迟强化（DE）出现率及心肌灌注异常的出现率.两样本率的比较采用χ^2检验;lgLVEF（LVEF由MRI测定）和心肌灌注受损节段数、致密化不全节段数和DE节段数的关系采用Pearson或Spearman法分析.结果 19例患者中16例（84.2％） MPI出现灌注受损;MRI示19例共有致密化不全节段107个和致密化节段216个,灌注异常出现率分别为33.6％（36/107）和31.9％（69/216）,差异无统计学意义（χ^2=0.09,P＞0.05）.共31个节段出现DE,致密化不全节段和致密化节段DE出现率分别为5.6％（6/107）和11.6％ （25/216）,差异也没有统计学意义（χ^2=2.94,P＞0.05）.DE节段灌注异常出现率高于非DE节段[54.8％（17/31）与30.1％（88/292）;χ^2=7.80,P＜0.01].lgLVEF与致密化不全节段数、DE节段数、灌注受累节段数间相关系数均无统计学意义（r=-0.35、0.15和-0.34,均P＞0.05）.结论 大部分ILVNC患者存在不同程度的心肌血流灌注受损,MRI所示致密化不全和非致密化不全心肌均可出现;心肌灌注受损在该病的发生及进展中的作用尚需进一步研究.     

Acute, subacute, and chronic myocardial infarction: quantitative analysis of gadolinium-enhanced MR images

The value of gadolinium enhancement to enable detection of infarcted myocardium at T1-weighted magnetic resonance (MR) imaging was assessed in 84 patients after acute myocardial infarction (AMI). Five healthy subjects served as controls. All patients underwent MR imaging before and 20 minutes after administration of gadopentetate dimeglumine. Contrast enhancement of normal myocardium varied 7% +/- 4 after administration of gadopentetate dimeglumine. Mean intensity ratio after gadolinium enhancement in group 1 (imaging less than 1 week after AMI), group 2 (imaging 1-3 weeks after AMI), and group 3 (imaging 3-6 weeks after AMI) was significantly higher than before gadolinium enhancement. In group 4 (imaging more than 6 weeks after AMI), no significant difference was observed. After gadolinium enhancement, the intensity ratio was abnormally increased in 82% of the MR examinations in group 1, in 62% of group 2, in 58% of group 3, and in 12% of group 4. Gadolinium enhancement improved visualization of myocardial infarction at MR imaging up to 6 weeks after onset of symptoms and had a maximal effect within 1 week after AMI.     

Blood pool contrast agent CMD-A2-Gd-DOTA-enhanced MR imaging of infarcted myocardium in pigs.

The purpose of this study was to assess the ability of the new blood pool contrast agent meglumine-carboxymethyldextran-ethylenediamino-gadoterate (CMD-A2-Gd-DOTA) to depict acute occlusive myocardial infarction (AMI). First-pass gradient-echo and delayed spin-echo magnetic resonance imaging (MRI) was performed 5 days after induction of AMI in a pig model. MRI was correlated with pathology. First-pass imaging with CMD-A2-Gd-DOTA allowed detection of infarcted myocardium in all pigs (n = 7). The infarction was recognized as a black spot on MRI as well as on a parametric image. The signal intensity (SI) amplitudes of normal versus infarcted myocardium were 80.55 +/- 18.61 versus 8.48 +/- 15.50 on MRI and 81.62 +/- 18.50 versus 1.61 +/- 3.73 on the parametric image (both P values < 0.001. The contrast ratio between normal and infarcted myocardium was not significantly improved on spin-echo MRI, suggesting largely intact vascular integrity outside the occluded area. CMD-A2-Gd-DOTA is useful for depicting occlusive myocardial infarction by first-pass MRI. Spin-echo imaging is promising in assessing vascular integrity. J. Magn. Reson. Imaging 1999;10:170-177.     

18F-FDG／99Tcm—MIBI双核素心肌断层显像检测急性心肌梗死患者存活心肌

目的探讨18F-FDG／99Tcm-MIBI双核素心肌断层显像检测AMI患者存活心肌,评价该方法对心功能改善及预后判断的价值。方法98例[男87例,女11例,年龄（58±11）岁]确诊为AMI患者,均行18F-FDG／99Tcm-MIBI双核素心肌断层显像,采用半定量方法将心肌分成9个节段,并评分,放射性轻度减低=1分,明显减低=2分,缺损=3分。根据灌注和代谢显像情况,两者不匹配视为存活心肌,两者匹配为心肌无存活。治疗前后行超声心动图检查观察LVEF变化;所有患者进行随访,统计心脏事件发生率,比较再血管化治疗和药物治疗患者的心脏事件发生率差别。频数的比较采用x2检验。结果心肌存活组患者27例,接受冠状动脉再血管化和药物治疗者分别为27和10例;心肌无存活组61例,接受冠状动脉再血管化治疗和药物治疗者分别为35和26例。无论是心肌存活组还是心肌无存活组,再血管化治疗和药物治疗相比较,心功能明显改善（LVEF提高≥10％）的患者比例差异均无统计学意义（心肌存活组：矿=0．509,P〉0．05;心肌无存活组：x2=0．035,P〉0．05）。平均随访时间为（234-11）个月,心肌存活组接受药物治疗患者的心脏事件发生率明显高于接受再血管化治疗的患者（50．0％和14．8％,X2=4．91,P〈0．05）;在心肌无存活组,药物治疗患者的心脏事件发生率也同样明显高于再血管化治疗（30．7％和5．7％,x2=6．83,P〈0．05）。结论利用18F-FDG／99Tcm-MIBI双核素心肌断层显像检测AMI患者存活心肌,以判断心功能改善和预后,具有一定价值,同时也有局限性,还需要大规模前瞻性研究进一步证实。     

彩色室壁动力技术小剂量多巴酚丁胺负荷试验检测冬眠心肌与病理学检查对比的实验研究

目的: 探讨彩色室壁动力技术(CK)小剂量多巴酚丁胺超声心动图负荷试验(CK-DSE) 检测冬眠心肌(HM)的价值.材料和方法: 22只犬结扎冠状动脉造成实验性心肌缺血损伤的动物模型.应用CK-DSE检测动物模型的心肌梗塞区心内膜运动幅度/非梗塞区心内膜运动幅度比值(AMI/ANMI),与病理组织切片显示冬眠心肌面积/梗塞区总面积的比值(ATAM/ATIM)进行对比分析.结果: 本实验成功地建立11只实验性心肌缺血损伤的动物模型,CK-DSE检测冬眠心肌的敏感性、特异性和准确性分别为90%、80%和83%.CK-DSE检测AMI/ANMI比值,与ATAM/ATIM具有较好的相关关系(r=0.75).结论: CK-DSE能准确地检出心肌梗死后存活的冬眠心肌,是定量检测梗塞区内冬眠心肌的较好方法.     

Magnetic resonance imaging of acute myocardial infarction using a nitroxyl spin label (PCA)

The effects of an intravenously administered nitroxyl spin label (PCA) on the magnetic resonance imaging (MRI) appearance and relaxation times of acute canine myocardial infarctions were studied. Twenty-four hours after ligation of the left anterior descending coronary artery (LAD), animals were either sacrificed immediately (three dogs) or injected with 3.0 mmol/kg of PCA prior to sacrifice (six dogs). The PCA group dogs were sacrificed at either 5 minutes postinjection (three dogs) or 15 minutes postinjection (three dogs). Magnetic resonance imaging (0.35 T) using spin-echo techniques demonstrated high signal intensity in the infarct relative to normal myocardium in all three groups. In the control group, the T1 and T2 relaxation times were longer in infarcted compared with normal myocardium, but only the measure in T2 reached statistical significance (P less than .05). PCA produced infarct-avid T1 shortening in the six dogs that received it. Contrast in the group sacrificed at 15 minutes postcontrast administration was greater than that in the control group due to T1 shortening in the infarct. Thus, PCA produces differential effects on normal and infarcted myocardium. Between 5 and 15 minutes after IV administration, it causes greater changes in the infarct due to prolonged retention in this region.     

心脏MR延迟强化在急性心肌梗死的应用及研究现状

急性心肌梗死（AMI）梗死心肌、心肌活性和微血管梗阻（MVO）的定量评价对于AMI病人的危险程度分级、治疗决策的制定、治疗效果的评价以及预后评估具有重要意义。心脏MR延迟强化（LGE-CMR）具有较高的时间及空间分辨力,可用于AMI梗死心肌、心肌活性和MVO的定量评价,并且具有较好的可重复性和较高的准确性。就LGE-CMR在AMI的应用及研究现状进行综述。     

缺血心肌应用bFGF后心肌中VEGF的表达

目的　探讨心肌内注射碱性成纤维生长因子 (basicfibroblastgrowthfactor ,bFGF)对急性心肌梗死 (myocardialinfarction ,MI)血管内皮生长因子 (vascularendothelialgrowthfactor ,VEGF)的表达作用。方法　 2 4只犬建立急性MI模型后随机分成对照组 (MI区注射生理盐水 15ml)和实验组 (MI区注射 5 0mgbFGF与生理盐水的混合液 15ml) ;每组观察 4个不同的时间点 (术后第 1、3、10、17天 )。各组动物分别在处死前应用敏感编码技术 (sensitivityencodedtechnique ,SENSE)行磁共振电影成像 (cinemagneticresonanceimag ing ,cine -MRI)。免疫组织化学方法检测VEGF的表达。结果　心肌缺血区对照组VEGF的表达增多 ;实验组左心室射血分数 (leftventricularejectionfraction ,LVEF)自第 10天明显增加 (第 10天 :对照组 2 4.0 9± 3 .3 2、实验组 45 .71± 6.2 7;第 17天 :对照组 3 1.46± 4.60、实验组 5 3 .46± 5 .2 4;单位 :%)。结论　局部心肌内注射bFGF有促进MI区域VEGF的表达及提高左心室功能的作用     

Myocardial BOLD imaging at 3 T using quantitative T2: Application in a myocardial infarct model

Left ventricular remodeling as a result of acute myocardial infarction (AMI) is associated with significant morbidity, leading to cardiovascular dysfunction, disability, and death. Despite successful revascularization, coronary vasodilatory dysfunction has been shown in infarcted and remote myocardium of patients following AMI. Our study explored the utility of a T₂‐based blood‐oxygen‐level‐dependent approach in probing regional and longitudinal fluctuations in vasodilatory function in a porcine model of AMI at 3 T. Ten pigs underwent MRI in control state and at day 2, weeks 1–6 following 90 min occlusion followed by reperfusion. The remote myocardium exhibited vasodilatory dysfunction at weeks 1 and 2 that gradually recovered, whereas the infarct zone showed no vasodilatory alterations. Our study suggests that microvascular alterations occurring in infarcted and remote myocardium after AMI might serve as an indicator of adverse left ventricular remodeling. The blood‐oxygen‐level‐dependent technique using quantitative T₂ could potentially be a useful noninvasive tool to evaluate novel therapeutic strategies aimed at limiting vasoconstriction and improving coronary flow reserve after AMI. Magn Reson Med, 2011. © 2011 Wiley Periodicals, Inc.     

Prognostic value of adenosine Tl-201 myocardial perfusion imaging after acute myocardial infarction: Results of a prospective clinical trial

BACKGROUND: We have previously shown in retrospective studies that adenosine myocardial perfusion imaging (MPI) done after acute myocardial infarction (AMI) can effectively predict the risk of future cardiac events in these patients. The objective of this study was to validate these observations in a prospective clinical trial. METHODS AND RESULTS: One hundred twenty-six stable patients underwent quantitative adenosine MPI at a mean of 4.5 +/- 2.9 days after AMI. On the basis of the MPI results, they were divided into 3 risk groups: low risk (< 20% perfusion defect), intermediate risk (> or = 20% perfusion defect with < 10% ischemia), and high risk (> or = 20% perfusion defect with > 10% ischemia). The patients were followed up for 11 +/- 5 months for the occurrence of cardiac events: death, myocardial infarction, unstable angina, or congestive heart failure. The actual event rates correlated very well with the prespecified risk groups (19% for the low-risk group, 28% for the intermediate-risk group, and 78% for the high-risk group; P < .001). The significant multivariate predictors for events were female gender (relative risk [RR], 2.90; P = .002), left ventricular ejection fraction (RR, 1.34; P = .04), and ischemic defect size (RR, 1.46; P = .001), with a global chi2 value of 26.7. CONCLUSION: This study demonstrates, in a prospectively designed clinical trial, that quantitative adenosine MPI performed soon after AMI can effectively predict the risk of future cardiac events. These findings are currently being validated in an ongoing, large, multicenter, international clinical trial.