激光心肌血运重建联合基因转染治疗急性心肌缺血后血管密度的变化

目的 观察激光心肌血运重建联合血管内皮生长因子基因（VEGF165cDNA)治疗急性缺血心肌后心肌血管密度的变化。方法 健康杂种犬48只，随机分为对照，激光打孔，激光打孔 VEGF165cDNA和激光打孔 空质粒4组，每组12只，所有犬均结扎冠状动脉，造成急性心肌缺血后，立即按预定组别行CO2激光心肌打孔及心肌基因转染，并于6周后处死动物，取心肌实验区标本，光镜下观察血管密度，数据采用SPSS统计软件处理。结果 激光打孔 VEGF165cDNA组心外膜，心内膜和心肌中层血管密度显著高于激光心肌打孔组。结论 激光打孔联合VEGF基因治疗后，缺血心肌血管生成显著增加。     

高压喷射载VEGF165、bFGF凝胶促缺血心肌血管新生的实验研究

目的探讨高压喷射心肌内给药的可行性以及载VEGF165、bFGF温敏型壳聚糖水凝胶对缺血心肌的促血管新生和心肌保护作用。方法健康杂种犬32只,随机均分为单纯心肌梗死(SMI)组,高压喷射生理盐水(NS)组,高压喷射温敏型壳聚糖水凝胶(Chitosan)组,高压喷射载VEGF165、bFGF温敏型壳聚糖水凝胶(Chitosan+VEGF165+bFGF)组。结扎左冠状动脉前降支制备急性心肌梗死模型后,SMI组直接关胸,NS组、Chitosan组和Chitosan+VEGF165+bFGF组在结扎线以下左室前壁行高压喷射心肌内给药8～10次,1次/cm2。术后6周取材行组织学、免疫组化检查并计算心肌梗死面积,处死动物前行血流动力学检测。结果术后6周心肌内仅有少量壳聚糖水凝胶样物质残留,其周围无明显的炎性细胞浸润;与SMI组比较,Chitosan组和Chitosan+VEGF165+bF-GF组梗死区新生血管数量增加(P<0.05),梗死面积缩小(P<0.05),左室舒张末压和左室内压最大下降速率明显改善(P<0.05)。结论高压喷射心肌内给药安全、可行;载VEGF165、bFGF温敏型壳聚糖水凝胶心肌内注射能促进...     

双核素心肌灌注-代谢显像评价存活心肌对心肌梗死患者择期血运重建术后左心功能的影响

目的采用^99Tc^m-MIBI加^18F-FDG双核素心肌灌注-代谢显像（DISA）评价冠心病心肌梗死患者有无存活心肌,以判断择期血运重建后存活心肌对左心功能的影响。方法选择确诊心肌梗死患者91例,行DISA。根据超声心动图（UCG）结果将患者分为心功能不全（A组）和心功能正常（B组）2组,在行PCI术后1,3和6个月观察UCG结果。采用SPSS13．0软件进行统计学处理,2组间均值比较采用t检验,率的比较采用,检验。结果A组灌注平均缺损（9．8±3．5）个节段,B组灌注平均缺损（5．4±2．6）个节段;2组相比,t=6．87,P〈0．01。A组代谢平均缺损（7．5±3．4）个节段,B组代谢平均缺损（4．6±2．8）个节段,2组相比,t=4．46,P〈0．01。A组检出存活心肌173个节段,占37．8％（173／458）,B组检出188个节段,占61．2％（188／307）,2组相比,x2=40．61,P〈0．001。A组灌注显像总评分（SPS）为（Z8．43±11．86）分,代谢显像总评分（SMS）为（20.17±8．52）分,（代谢-灌注）总评分之差（SDS）为（0．39±3．17）分;B组SPS为（21．36±9．54）分,SMS为（15．19±5．74）分,SDS为（-12．72±4．55）分,2组相比,t=3．15,3．32和15．59,P均〈0．01。A组存活心肌≥4个节段的LVEF升高差值（ALVEF）为（12．81±2．62）％,明显高于B组的（5．90±1．91）％,t=16．33,P〈0．001;左心室舒张末期内径回缩差值（△LVEDd）为（-13．13±4．20）mm,也明显高于B组（-7．75±2．31）mm,t=6．86,P〈0．001;A组存活心肌〈4个节段的△LVEF和△LVEDd则明显低于B组,t=3．25和4．92,P均〈0．01。结论心肌梗死区是否有存活心肌及存活心肌节段数可能是择期血运重建后左心功能改善程度的重要影响因素。     

心肌代谢-灌注半定量评分在冠状动脉旁路移植术中的应用

目的评估放射性核素心肌显像代谢-灌注半定量评分在冠状动脉旁路移植术（CABG）中的应用价值。方法选择21例多支冠状动脉病变的冠心病患者进行前瞻性研究。所有患者术前均进行^99Tc^m-甲氧基异丁基异腈（MIBI）门控心肌灌注显像（G—MH）与^18F-脱氧葡萄糖（FDG）PET心肌代谢显像，评估心肌缺血的范围、程度及心肌活力。检查后2周内行CABG。所有患者术后第3个月随访行G—MH。结果G—MH和PET图像的定性和半定量分析均根据美国核心脏病学会（ASNC）提出的阅片指南，分别计算每一心肌节段的静息灌注评分（RS）、代谢-灌注差值（DS）及静息灌注总分（SRS）和代谢-灌注总差值（SDS）。心肌节段的DS〈0分即认为该部位心肌存活，反之则认为心肌活力丧失。在共420个心肌节段中，G—MH共检出164个缺血节段，其中93个节段活力丧失，71个节段存活。根据术前SDS结果，将患者分为3组：A组SDS≥0分，5例；B组-5分≤SDS〈0分，8例；C组SDS〈-5分，8例。随访G—MH发现上述3组术后左室射血分数绝对值较术前分别提高-3．60％，3．38％和6．88％。结论心肌代谢-灌注半定量评分可准确评价患者CABG后疗效，并可预测术后左室功能恢复程度。     

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.     

特发性扩张型心肌病合并甲状腺功能减退加重心肌损伤的影像学评价

目的通过^99Tcm-MIBI心肌灌注SPECT／^18F—FDG心肌代谢PET显像和心脏MRI延迟增强成像（cMRI—LGE）,探讨特发性扩张型心肌病（IDC）合并甲状腺功能减退（简称甲减）与心肌损伤的关系。方法2010年10月至2012年12月诊断为IDC的连续病例63例[男42例,女21例,平均年龄（52±11）岁]入选,患者均进行血浆TT3、TT4、FT3、FT4和TSH全自动化学发光免疫法测定、^99Tcm-MIBI心肌灌注SPECT／^18F—FDG心肌代谢PET显像和cMRI—LGE。利用标准17节段模型进行心肌节段分析,灌注／代谢图像分成4种类型：正常灌注／代谢、灌注／代谢不匹配、灌注／代谢轻中度匹配、灌注／代谢完全匹配;cMRI-LGE图像分为无延迟强化、壁间强化和透壁强化。通过x^2检验进行分组数据的比较。结果根据所测血浆激素水平,患者被分成甲状腺功能（简称甲功）正常组（53例）和甲减组（10例）。甲功正常组正常灌注／代谢的心肌节段数所占的比例明显高于甲减组：71.8％（647／901）和57．6％（98／170）,x^2=13．50,P〈0．001;而灌注／代谢不匹配的心肌节段比例则低于甲减组：17．8％（160／901）和31．2％（53／170）x^2=16．20,P〈0．001。甲功正常组cMRI—LGE无延迟强化的心肌节段比例明显高于甲减组,分别为88．0％（793／901）和69．4％（118／170）,x^2=35．70,P〈0．001;但壁间强化的心肌节段比例则低于甲减组,分别为4．8％（43／901）和24．1％（41／170）,x^2=74．70,P〈0．001。结论^99Tc^m-MIBI心肌灌注SPECT／^18F—FDG心肌代谢PET显像和cMRI—LGE证实甲减能够加重IDC患者的心肌损伤。SPECT／PET可以检测出更多的慢性缺血／存活心肌,而cMRI-LGE可以检测出更多的心肌纤维化病变,两者结合能提供更全面的心肌损伤信息。     

99Tcm-NOET门控心肌灌注SPECT评价冠心病的价值

目的评价99Tcm--双（N-乙氧基,N-乙基-二硫代氨基甲酸酯）氮化锝（99Tcm-NOET）静息门控断层心肌灌注显像对冠心病患者的诊断价值。方法疑诊为冠心病的45例患者注射925MBq 99Tcm-NOET后1h用SPECT行静息门控心肌灌注显像,获得舒张未期容积（EDV）、收缩未期容积（ESV）、左室射血分数（LVEF）等心功能参数和舒张末期容积灌注、局部射血分数、局部室壁活动和室壁增厚度4个靶心图。所有患者在1周内行冠状动脉造影,将冠状动脉狭窄≥50％定为病变血管。根据冠状动脉造影结果将其分为心肌梗死组、心肌缺血组和对照组三组。结果99Tcm-NOET静息门控SPECT诊断冠心病的灵敏度和特异度分别为68．42％和83．33％。心肌梗死组的心功能参数[EDV=（129．32±9．14）ml,ESV=（80．97±9．49）ml,LVEF=（40．15±3．28）％】与对照组【EDV=（80．91±3．12）ml,ESV=（30．12±1．79）ml,LVEF=（63．51±1．04）％]相比,统计学差异有显著性（EDV：F=22．103,ESV：F=32．277,LVEF：F=42．60：4,均为P〈0．01）,心肌缺血组的心功能参数[（EDV=（70．83±3．46）ml,ESV=（25．13±2．85）ml,LVEF=（65．55±2．62）％1与对照组相比,统计学差异无显著性意义。心肌梗死组左室心肌共分为460个节段,其中209个节段局部灌注、局部射血分数、局部室壁活动和室壁增厚度4个靶心图均异常。局部灌注异常的节段共328个节段,伴有局部射血分数、局部室壁活动和室壁增厚度异常分别有250个、240个和276个节段。局部灌注异常的节段与局部射血分数、局部室壁活动和室壁增厚度异常的节段不完全匹配。结论99Tcm-NOET静息门控心肌灌注显像对冠心病的诊断有较大临床应用价值,所获得的整体心室功能参数在心肌梗死的评价中有优越性,但对心肌缺血的诊断价值不大。心肌梗死中存在有不少的局部灌注与心肌?     

心脏磁共振在冠状动脉非阻塞性心肌梗死中的应用价值

【摘要】目的：探讨心脏磁共振（CMR）多序列成像在冠状动脉非阻塞性心肌梗死（MINOCA）中的应用价值。方法：筛选出临床拟诊为急性心肌梗死（AMI）并接受冠状动脉造影（CAG）或冠状动脉CTA检查,同时符合欧洲心脏病协会（ESC）诊断标准的21例MINOCA患者,所有患者在冠状动脉检查后一周内完成CMR检查。CMR检查包括心脏形态、首过心肌灌注、磁共振延迟增强（LGE）扫描。根据LGE结果分析心肌梗死节段的分布;冠状动脉狭窄程度与心肌梗死节段数的相关性。根据心肌首过灌注结果,将MINOCA患者左心室节段分为灌注缺损、灌注降低、灌注正常节段,并与LGE检测的心梗透壁程度进行对照,分析不同透壁程度与不同灌注类型间的相关性。结果：21例MINOCA患者共84个心肌节段发生心肌梗死,61.9%的心肌梗死发生于前壁、前间壁和下间壁。相对于无明显狭窄的冠状动脉,冠状动脉轻度狭窄者所支配的心肌发生MINOCA的概率更大（OR=1.924,95%CI=1.165~3.177,P=0.012）。不同灌注类型与心梗透壁程度的Kendall等级相关分析结果显示,心肌首过灌注量越低,心肌梗死透壁程度越高（等级相关系数τb=－0.819,P=0.025）。结论：MINOCA多发生于前壁及间壁;轻度狭窄的冠状动脉所支配的心肌发生MINOCA的概率更大;MINOCA患者不同的心肌灌注状态与心梗透壁程度具有显著的相关性。     

SPECT心肌灌注显像评价激光心肌血管重建术

目的 观察激光心肌血管重建术（ＴＭＬＲ）对实验性急性心肌梗死的近期效果。方法 将１６只羊随机分为实验组和对照组,结扎冠状动脉左前降支（ＬＡＤ）,建立急性心肌梗死模型。实验组于结扎后１ｈ用功率为６Ｗ的钬激光,在前壁缺血区打孔;对照组结扎后不打孔。结扎之后４ｈ行＾９９Ｔｃ＾ｍ－甲氧基异丁基异腈（ＭＩＢＩ）ＳＰＥＣＴ心肌灌注显像,采用半定量法,计算左室心肌短轴,垂直长轴,水平长轴前壁感兴趣区内象素的平均     

静息门控心肌显像评价冠心病患者CABG术后早期疗效

目的应用^99Tc^m-甲氧基异丁基异腈（MIBI）心肌灌注及心室显像评价冠状动脉旁路移植（CABG）术的近期疗效。方法对52例接受CABG术的患者于手术前1周、术后3～5周分别行静息心肌灌注及心室显像，采用QGSPECT专用软件程序定量分析整体及局部心室功能，并与超声心动图检查结果进行比较。结果①术后^99Tc^m-MIBI显像示左室射血分数（LVEF）提高（P〈0．05），左室舒张末期容积（EDV）、收缩末期容积（ESV）均明显减小（P〈0．001），与超声心动图检查示EDV、ESV变化结果符合。②手术前后LVEF改变值与整体室壁运动（WM）改变值（r=0．75，P〈0．01）及整体室壁收缩增厚率（WT）改变值（r=0．51，P〈0．01）均有良好相关性；手术前后整体-12,肌血流灌注值与整体WM值（r=0．54、0．36，P均〈0．01）及整体WT值（r=0．63、0．65，P均〈0．01）均有较好的相关性。③术后心肌显像剂相对摄取值提示前壁、间隔、下壁多节段心肌灌注明显改善（P〈0．05）。④术后显像提示前壁、间隔的WM降低（P〈0．05），下壁、前侧壁、下侧壁WM明显改善（P〈0．05），并与超声心动图结果基本符合；WT仅下侧壁明显改善（P〈0．05），在间隔无变化（P〉0．05）。结论CABG术后心肌显像的WM低估间隔室壁运动，高估侧壁运动；WT与心肌血流灌注在手术前后均有较好的相关性，可能更适用于评价CABG术后心功能。     

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     

猪缺血心肌内膜注射VEGF基因的长期疗效观察

目的探讨经心内膜心肌内直接注射血管内皮生长因子(VEGF)基因治疗猪心肌缺血后的远期心脏电机械活动及心功能改善情况。方法30只实验用小香猪随机均分为对照组(n=15)和治疗组(n=15)。建立心肌缺血模型后,通过NOGA系统经心内膜分别将空载质粒pIRES2-EGFP及质粒pIRES2-EGFP-hVEGF165直接注射至对照组或治疗组缺血部位心肌内。在注射前及注射后1年,分别应用左心室电机械标测(LVEMM)监测局段线性缩短率(LLS)和单极电压(UpV),并用超声监测M型局部室壁运动幅度和背向散射积分的心动周期变异(CVIB)、左心室射血分数(LVEF)。1年后处死动物,组织学切片观察心肌组织中毛细血管生成情况。结果LVEMM监测显示,注射后1年治疗组LLS显著高于注射前及对照组(P<0.05),而UpV与注射前及对照组比较无显著差异(P>0.05);超声监测显示,治疗组注射后1年的局部室壁运动幅度和CVIB、LVEF均显著高于对照组(P<0.05)。组织学检查显示,治疗组心肌内毛细血管数目(38.1±4.8/HP)显著高于对照组(13.2±5.1/HP,P<0.01)。结论经心内膜直接注射pIRES2-...     

外源性碱性成纤维生长因子对犬急性心肌梗塞后血管生成作用

目的　探讨外源性碱性成纤维生长因子 (basicfibroblastgrowthfactor ,bFGF)对心肌梗塞血管生成的作用。方法　 2 4只犬随机分成对照组 (心梗区注射生理盐水 )和实验组 (心梗区注射bFGF)。每组观察 4个不同的时间点 (1d、3d、10d、17d)。各组分别在术后 3h内及处死前行MR心肌灌注成像。免疫组织化学方法检测各组心肌细胞中血管内皮生长因子 (vascularendothelialgrowthfactor ,VEGF)的表达及微血管数量。结果　微血管的数量除第 1天外各个时间点实验组比对照组明显增多 ;VEGF的表达除第 17天外各时间点实验组比对照组明显增强 ;TTC染色和MR心肌灌注成像 2种方法显示心梗范围对照组和实验组各个时间点之间无显著性差异。结论　局部心肌内注射bFGF有促进心梗区域新生血管形成、减小心梗范围的作用 ;VEGF的表达与组织中微血管的密度密切相关 ;MR心肌灌注成像可有效评价心肌血流灌注和定量评价心肌梗死的范围。     

PET for evaluation of differential myocardial perfusion dynamics after VEGF gene therapy and laser therapy in end-stage coronary artery disease.

The purpose of this study was to appraise the value of PET in the assessment of the effect of supposedly proangiogenic new therapies such as gene therapy with vascular endothelial growth factor (VEGF) gene and endomyocardial laser therapy. METHODS: Thirty-five patients with end-stage coronary artery disease and class III (Canadian Cardiovascular Society) angina were included. Myocardial ischemia was evaluated with dipyridamole PET scanning and exercise tolerance with bicycle ergometry. Ten patients were treated with naked plasmid DNA encoding for human VEGF165 (VEGF) and 12 patients were treated with laser therapy (direct myocardial revascularization [DMR]) using an electromechanical mapping system. Thirteen patients were treated with standard medical therapy (control). RESULTS: In both active treatment groups, angina was reduced in most subjects, except in 2 VEGF and 5 DMR patients. In the control group, no improvement in anginal classification was found, except in 3 subjects. On the PET scan, solely in the VEGF group, the stress perfusion was significantly improved (from 57 +/- 33 to 81 +/- 55 mL/min/100 g; P = 0.031). Furthermore, in the VEGF group, the number of ischemic segments was reduced from 274 +/- 41 to 234 +/- 48 segments (P = 0.004) but not in the DMR group (from 209 +/- 43 to 215 +/- 52 segments) or in the control group (from 218 +/- 18 to 213 +/- 28 segments). Bicycle exercise duration showed slight nonsignificant changes in the VEGF group (from 3.6 +/- 2.0 to 4.6 +/- 2.1 min), in the DMR group (from 5.1 +/- 1.5 to 4.7 +/- 1.3 min), and in the control group (from 3.3 +/- 1.8 to 3.5 +/- 2.3 min). CONCLUSION: PET showed that intramyocardial gene therapy with the human VEGF165 gene in contrast to laser DMR treatment effectively reduces myocardial ischemia.     

Exercise training increases myocardial perfusion in residual viable myocardium within infarct zone

Purpose:

To study the effect of exercise training on the myocardial perfusion in the postinfarct myocardium.

Materials and Methods:

Twenty‐nine patients with stable chronic myocardial infarction were randomly assigned to either a training group (N = 17) or a control group (N = 12). The training group received a 3‐month exercise program. Cardiovascular MR was first performed before the training to establish a baseline, and subsequently performed once again upon conclusion of the program. Late gadolinium enhancement was used both to define the infarct and remote zones and to quantify the ratio of the residual viable myocardium (VMR) within the infarct zone. The myocardium was divided into subendocardial and subepicardial layers with equal thickness. The interval change of myocardial perfusion reserve (MPR) was computed for each zone and layer. The association between the exercise‐induced perfusion change and VMR was analyzed for layers of the infarct zone.

Results:

In the training group, the remote zone showed significantly increased MPR. The infarct zone showed no perfusion change in the subendocardial layer, but it demonstrated significantly increased MPR in the subepicardial layer. In the infarct zone, the change in MPR was associated with VMR.

Conclusion:

In chronic myocardial infarction, the exercise‐induced perfusion change in the infarct zone is proportional to the amount of residual viable myocardium. J. Magn. Reson. Imaging 2011;. © 2011 Wiley‐Liss, Inc.     

^13N—NH3 PET及冠状动脉造影评价CD151基因转染对小型猪心肌梗死后血流灌注的影响

目的用^13N—NH,PET及冠状动脉造影共同评价CD151基因转染促小型猪心肌梗死后血运重建。方法结扎20头小型猪冠状动脉左前降支（LAD）,建立心肌梗死模型。对梗死区及梗死周围心肌直接注射CD151及绿色荧光蛋白（GFP）重组腺相关病毒（rAAV）进行基因转染。8周后用免疫组织化学方法分析心肌组织CD151蛋白的表达和心肌组织微血管密度,用^13N—NH,PET显像评价心肌血流灌注,用LAD造影评价侧枝循环的建立。采用SPSS11．0软件行配对t检验或方差分析（ANOVA）。结果CD151基因转染促进局部心肌组织CD151高表达并增加缺血区心肌组织微血管密度。rAAV—CD151组心肌血流灌注明显增加,心肌缺血总分值为10．82±2．36,明显小于rAAV—GFP组（19．33±1．67,t=5．86,P=0．002）。冠状动脉造影显示rAAV—CD151组缺血心肌的侧枝循环建立明显较rAAV—GFP组增加。结论CD151基因转染可以明显促进心肌梗死后血运重建、增加血流灌注。^13N—NH,PET及冠状动脉造影能直观地评价心肌血运重建。     

Teboroxime is a marker of reperfusion after myocardial infarction

Background  

It has been shown that serial teboroxime imaging can rapidly assess coronary perfusion in viable myocardial distributions. However, the myocardial uptake of teboroxime after reperfusion of acutely infarcted myocardium has not been critically evaluated. The study object was to assess whether teboroxime uptake in acutely infarcted myocardium is linearly related to blood flow.     

Selective intracoronary injection of sestamibi to detect myocardial viability: Prediction of perfusion and contractile recovery after percutaneous transluminal coronary angioplasty

BACKGROUND: The main limitation of myocardial single photon emission computed tomography (SPECT) in detecting hibernating myocardium is the poor delivery of radiotracers in hypoperfused areas supplied by severely stenotic coronary arteries. Increasing local availability of radiotracers by intracoronary injection might represent an attractive solution. The hypothesis that the intracoronary administration of sestamibi could improve myocardial SPECT accuracy in detecting hibernating myocardium was addressed in this pilot study. METHODS AND RESULTS: Seven patients with prior myocardial infarction and severe stenosis of the infarct-related artery underwent myocardial SPECT after intracoronary injection of technetium 99m sestamibi immediately before percutaneous transluminal coronary angioplasty (PTCA). Wall motion and perfusion were evaluated, before and 1 month after PTCA, by 2-dimensional echocardiography and rest-redistribution thallium 201 SPECT. A "low-flow area" was identified on the pre-PTCA Tl-201 SPECT image as the area with less than 50% of maximum radiotracer uptake. Changes in wall motion and perfusion in the low-flow area were compared with results of intracoronary sestamibi imaging. On a pixel-by-pixel analysis, intracoronary sestamibi predicted perfusion recovery within the low-flow area with a 91% sensitivity, a 78% specificity, and an 82% overall accuracy. Only in the 5 patients with an extent of sestamibi uptake greater than one third of the low-flow area was an improved regional and global left ventricular wall motion observed after PTCA (wall motion score index decreased from 1.95 +/- 0.28 to 1.60 +/- 0.34, P =.007; left ventricular ejection fraction increased from 42% +/- 7% to 49% +/- 7%, P =.001; asynergic segments in the low-flow area decreased from 3.6 +/- 0.9 to 1.8 +/- 1.5, P =.021). CONCLUSIONS: In patients with prior myocardial infarction and severe stenosis of the infarct-related artery, sestamibi uptake after intracoronary administration identified viable myocardium that was undetected after rest-redistribution thallium SPECT but capable of clinically significant contractile improvement after revascularization.     

Chronic hibernation and chronic stunning: A continuum

Identification of myocardial viability is of increasing clinical importance in managing patients with coronary artery disease and advanced left ventricular dysfunction. Although viable chronically dysfunctional myocardium is always the result of repetitive episodes of reversible ischemia, there may be multiple mechanisms responsible for the contractile dysfunction. Many patients have contractile dysfunction with normal resting perfusion, as determined by imaging, that is related to chronic myocardial stunning. Viability studies are generally unnecessary because normal resting perfusion would preclude significant fibrosis. The clinical problem arises in evaluating patients with depressed resting flow that can be due to hibernating myocardium or nontransmural infarction. In this circumstance viability studies are required to assess the likelihood of functional recovery after revascularization. Although hibernating myocardium was originally posited to develop in response to prolonged episodes of myocardial ischemia (experimentally termed "short-term hibernation"), subsequent studies have shown that this tenuous balance can only be maintained for a period of several hours before resulting in some degree of subendocardial infarction. More recent experimental studies have demonstrated that there is a progression from chronic stunning with normal flow to hibernating myocardium with reduced resting flow. This presumably arises from repetitive episodes of spontaneous ischemia that increase in frequency as the physiologic significance of a coronary stenosis progresses. Thus in this new paradigm reduced flow is a result, rather than the cause, of the contractile dysfunction. This review summarizes basic and clinical pathophysiologic studies supporting the claim that chronic stunning and hibernation are distinct entities that may represent opposite ends of a continuum of mechanisms in viable chronically dysfunctional myocardium.