99Tcm-HL91 SPECT探测缺血存活心肌的初步应用研究

目的 研究99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(99Tcm-HL91)在缺血心肌中的显像表现,探讨99Tcm-HL91探测缺血但存活心肌的价值.方法 18例已确诊为心肌缺血或心肌梗死的患者均行99Tcm-甲氧基异丁基异腈(99Tcm-MIBI)与99Tcm-HL91心肌灌注显像.在心脏短轴图像上通过感兴趣区技术获取缺血区与正常心肌组织的平均放射性计数,获得99Tcm-MIBI与99Tcm-HL91在局部缺血区与正常心肌组织的放射性比值.结果 10例患者在99Tcm-MIBI显像的放射性稀疏或缺损区而在99Tcm-HL91 SPECT可见到明显的放射性充填;其余8例患者99Tcm-HL91显像心肌摄取不高.结论 99Tcm-HL91可选择性地被存活乏氧心肌摄取,与99Tcm-MIBI SPECT联合应用,可望有效提高检测存活心肌的效能.     

99Tcm-HL91在心肌活性检测中的应用

目的探讨乏氧显像剂99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)检测心肌活性的可能性.方法急性心肌梗死患者25例(病史≤6周)和陈旧性心肌梗死患者5例(病史＞6周)分别行硝酸甘油介入和静息99Tcm-甲氧基异丁基异腈(MIBI)显像、99Tcm-HL91显像,根据99Tcm-MIBI显像结果将心肌分为正常心肌组、缺血心肌组(硝酸甘油介入后99Tcm-MIBI聚集量上升＞20%)和梗死心肌组(硝酸甘油介入后99Tcm-MIBI聚集量上升≤20%),比较三组间99Tcm-HL91聚集量有无差别.结果①急性心肌梗死患者正常心肌组99Tcm-HL91聚集量为95%,缺血心肌组为157%,梗死心肌组为93%,99Tcm-HL91在缺血心肌组聚集量明显高于正常心肌组和梗死心肌组.②陈旧性心肌梗死患者三组间99Tcm-HL91聚集量无差别.结论Tcm-HL91可用于探测缺血但存活的心肌.     

用201Tl与99Tcm-HL91双核素显像评价心脏病患者心肌灌注与乏氧

目的用201Tl与99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)同时评价心脏病患者心肌灌注与乏氧.方法22例心脏病患者及9例临床诊断正常者行10 min、3和24 h延迟201Tl与99Tcm-HL91双核素心肌显像,用5分法评价图像质量,用17节段法分析201Tl显像缺损与乏氧显影心肌节段.结果双核素显像中99Tcm-HL91显像图质量不如201Tl(P＜0.01);80.85%(38/47个节段)的急性心肌梗死患者201Tl灌注缺损心肌节段在99Tcm-HL91显像中显影,乏氧显影心肌节段数明显多于201Tl灌注缺损节段数;陈旧性心肌梗死201Tl、99Tcm-HL91均不显影的符合率为85.71%.结论201Tl与99Tcm-HL91双核素心肌显像能同时提供判断心肌血流灌注与乏氧的信息.     

99Tcm-HL91显像用于骨转移瘤的诊断

目的 探讨乏氧显像剂99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)在骨转移瘤诊断中的应用价值.方法 27例骨痛患者,其中19例经病理检查证实为骨转移瘤(未行放化治疗),8例为骨良性病变.所有患者均行99Tcm-亚甲基二膦酸盐(MDP)显像,2 d后注射99Tcm-HL91740 MBq,注射4 h后依据99Tcm-MDP显示的病灶进行断层显像,利用感兴趣区(ROI)技术,计算肿瘤与对侧正常组织的放射性(T/N)比值.采用SPSS 11.0软件进行t检验.结果 19例骨转移患者99Tcm-MDP显像提示的85处病灶,有79处99Tcm-HL91显像呈异常放射性浓聚;经病理检查或临床证实的8例骨良性疾病中,99Tcm-MDP显像提示的12处病灶99Tcm-HL91显像全部呈阴性.HL91断层显像骨转移组和骨良性疾病组的T/N比值分别为1.877±0.288和0.735±0.236,差异有统计学意义(t=13.065,P＜0.05).肺癌、前列腺癌骨转移病灶的T/N比值分别为1.915±0.344和1.825±0.175,2种病理类型间差异无统计学意义(t=1.378,P＞0.05).结论 99Tcm-HL91显像在骨骼良恶性病变的鉴别中可能有一定价值.     

肺部良性疾病摄取99Tcm-HL91特点临床研究

目的探讨肺部良性疾病对乏氧组织显像剂99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)的摄取特点,以提高对肺癌诊断的特异性。方法32例肺部良性疾病患者在静脉注射99Tcm-HL91 1110 MBq后1h(早期相)及4 h(延迟相)进行平面显像,根据显像进行目测和半定量分析[计算病灶与对侧正常肺组织摄取99Tcm-HL91的放射性计数比值(T/N)],并同时获得4 h T/N与1 h T/N之相对比值(RR)。结果肺部良性疾病对99Tcm-HL91摄取表现为3种类型:(1)早期相及延迟相显像均未见异常放射性摄取,前后T/N值相比无统计学差异(1.10±0.01与1.09±0.01,n=14,t=1.87,P(0.05)。(2)病灶对99Tcm-HL91表现为早期相明显摄取及延迟相无明显清除,前后T/N值相比无统计学差异(1.46±0.33与1.50±0.37,n=13,t=0.29,P(0.05)。(3)病灶对99Tcm-HL91表现为早期相明显摄取及延迟相明显清除,前后T/N值相比有统计学差异(1.43±0.22与1.11±0.19,n=5,t=2.46,P<0.05)。3种类型的RR值分别为1.01±0.01、1.12±0.10、0.90±0.11,均<1.25。结论肺部良性疾病对99Tcm-HL91的摄取具有多样性,熟悉这些多样性,并结合半定量分析技术,尤其是RR值,有助于提高对肺癌诊断的特异性。     

有机介质中99TcmO4-非胶体还原产物的制备及其性质研究

目的 研究能在肿瘤中浓聚的99TcmO4-非胶体还原产物(99Tcm-Rs)的物理化学特性和生物学表现.方法 采用乙腈与Na99TcmO4洗脱液混合蒸发除去水,在各种有机溶剂中,用氯化亚锡还原Na99TcmO4.对99Tcm-Rs进行薄层层析(TLC)、纸电泳、液相分配系数、滤膜通过特性研究,对类似物非胶体还原铼(Re-Rs)做元素分析.并对H460细胞摄取99Tcm-Rs和99Tcm-Rs在SD大鼠体内分布、在肿瘤内分布及在缺血心肌内分布进行研究.结果 在乙腈中还原Na99TcmO4可以获得高产率的99Tcm-Rs(＞90%).99Tcm-Rs的物理、化学性质和生物学特征与99TcmO4-不同,而且不是有机化学反应产品.99Tcm-Rs对乏氧细胞和缺血组织有亲和作用.静脉注射99Tcm-Rs后2和18 h,在H460肿瘤中,肿癯/血液放射性比值分别为3.05±0.34和8.07±1.19,肿瘤/骨骼肌放射性比值分别为10.38±1.21和20.55±2.80.缺血心肌也明显摄取99Tcm-Rs.乏氧、pH值降低和钙离子累积浓度增加,H460细胞摄取99Tcm-Rs随之增加,乏氧和钙离子浓度增加能提高99Tcm-Rs对二巯丙磺酸钠的标记率.以乙腈为展开剂,硅胶TLC结果显示99Tcm-Rs有2种成分,Rf值分别为1.0和0.78,后者在正常和肿瘤组织中分布与99Tcm-O4-无差异.结论 99Tcm-Rs是99TcmO4-在有机溶剂中还原或歧化反应产生的无机化合物,其制备简便,是前景较好的乏氧显像剂.     

用99Tcm标记突触结合蛋白I-C2A片段评价缺血预处理对心肌缺血再灌注损伤的保护作用

目的 应用99TcmO-4标记突触结合蛋白I-C2A片段(99Tcm-Syt I-C2A)评价缺血预处理对心肌缺血再灌注损伤的保护作用.方法 (1)采用2-亚氨基噻吩盐酸盐(2-IT)方法标记Syt I-C2A片段,纸层析法测定99Tcm-Syt I-C2A放化纯,用喜树碱处理的Jurket细胞测定标记蛋白质活性.(2)制备心肌缺血再灌注大鼠模型(A组)和心肌缺血预处理大鼠模型(B组)各6只,分别由尾静脉注射99Tcm-syt I-C2A 7.4 MBq,注射后1h处死动物,取出心脏,用生理盐水将心肌冲洗干净,并进行氯化三苯基四氮唑(TTC)染色,根据染色结果,分别取2组缺血损伤心肌和正常心肌,测量质量及放射性计数,比较2组缺血损伤心肌和正常心肌的每克组织百分注射剂量率(%ID/g).采用SPSS 12.0软件行统计分析,数据间比较用t检验.结果 (1)标记后的99Tcm-Syt I-C2A放化纯为(98.90±o.43)%,标记蛋白质与喜树碱处理组细胞结合测定的放射性计数是未处理组细胞的(10.99±O.55)倍.(2)A组缺血损伤心肌摄取99Tcm-Syt I-C2A(2.41±0.32)%ID/g,正常心肌为(O.16±O.02)%ID/g;而B组缺血损伤心肌和正常心肌的放射性摄取则分别为(0.46±0.05)和(0.20±0.05)%ID/g.B组缺血损伤心肌的99Tcm-Syt I.C2A摄取量明显低于A组(t=8.52,P相似文献   

小鼠恶性淋巴瘤99Tcm-HL91显像实验研究

目的验证乏氧显像剂99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)对IRM-2小鼠IRM-2-ML恶性淋巴瘤的探测作用.方法测定不同时间99Tcm-HL91在正常及荷瘤小鼠体内的分布,并进行平面显像.结果 99Tcm-HL91能选择性地浓集于肿瘤组织,且清除较慢.肿瘤/血液比值和肿瘤/肌肉比值均随时间延长而增加,2 h时分别为2.63±0.25和3.37±0.22,6 h时分别为3.51±0.17和6.44±0.29.平面显像中,肿瘤灶清晰可见.结论肯定了IRM-2-ML恶性淋巴瘤为实体肿瘤的结论,确证了99Tcm-HL91探测乏氧组织的作用.     

99Tcm-HL91乏氧显像在鼻咽癌治疗中的应用

目的探讨99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)SPECT/CT乏氧断层显像在鼻咽癌(NPC)治疗中的临床应用价值.方法38例NPC患者按常规进行鼻咽、颈部99Tcm-HL91断层显像;并对病灶的靶/非靶组织放射性比值(T/N)进行半定量分析;其中16例NPC患者在放疗前、后均行99Tcm-HL91乏氧显像;同时对16例患者按乏氧靶区调整放疗剂量,行后程三维适形放疗(3DCRT).结果NPC患者乏氧断层显像检查阳性率约为82%;99Tcm-HL91乏氧显像对NPC诊断的灵敏度、特异性、准确性分别为82%、78%、87%;放疗前鼻咽、颈部乏氧病灶的T/N分别为2.37±1.13、2.17±1.08,两者比较差异无显著性(P＞0.05).16例NPC患者在放疗前、后NPC病灶的T/N平均值分别为2.21±1.05、1.29±0.39,两者比较差异有显著性(P＜0.001);NPC病灶的乏氧状态与其对放疗的响应密切相关,相关系数r为0.532,P＜0.01.NPC 3DCRT的近期疗效优于常规放疗,肿瘤局部控制率较高,急性放射毒性较轻.结论99Tcm-HL91乏氧显像可监测NPC病灶的乏氧状态,指导NPC的3DCRT;NPC乏氧靶区3DCRT可提高其放疗疗效,减轻急性放射毒性.     

用99Tcm-HL91显像预测脑肿瘤放疗敏感性

目的应用99Tcm-4,9-二氮-3,3,10,10-四甲基十二烷-2,11-二酮肟(HL91)乏氧显像预测脑肿瘤放疗疗效.方法经临床确诊的30例未治疗的脑肿瘤患者,肘静脉注射99Tcm-HL91 740 MBq后进行早期(10 min)、中期(2 h)和晚期(4 h)显像.应用感兴趣区(ROI)技术勾画并分别测定早、中、晚期肿瘤部位放射性计数(T),以及对侧相应部位放射性计数(N),求出相应T/N比值.检查后患者接受放射治疗,4周后按WHO标准,在放疗科医师协助下进行放疗疗效评价,分为完全缓解(CR),部分缓解(PR),无变化(NC)和进展加重(PD),并与99Tcm-HL91显像结果比较.结果①30例脑肿瘤患者99Tcm-HL91显像早、中、晚各时相的T/N比值分别为1.453±0.292,1.532±0.299和1.607±0.305,各时相间差异均有显著性(P=0.000,双侧).②30例脑肿瘤患者中CR 0例,PR 15例,NC 6例,PD 1例,死亡或失访共8例;放疗有效组(CR+PR)与放疗无效组(NC+PD)99Tcm-HL91显像早、中和晚期相T/N比值分别为1.333±0.277与1.779±0.183,1.409 ±0.274与1.856±0.185和1.484±0.278与1.937±0.191,差异均有显著性(P=0.001,双侧).③受检者均未发现主观性不适和毒副作用.④99Tcm-HL91在鼻、口咽部有明显放射性摄取.结论99Tcm-HL91脑肿瘤显像可预测脑肿瘤的放疗敏感性,对鼻、口咽部肿瘤应用价值较低.     

磁共振多技术联合应用检测存活心肌的实验研究

目的　评估磁共振多技术联合应用检测心肌存活的价值。材料与方法　选择慢性心肌缺血模型猪 2 0只 ,分别于制作模型前、后 1～ 2个月行磁共振多技术联合应用扫描 (形态、电影扫描、心肌灌注和心肌活性扫描 ) ,判断心肌缺血区和坏死区的大小 ,并与病理结果对照了解其准确性。结果　MRI检查发现 2 0只猪中有 3只形态扫描见左室侧壁变薄 ;负荷电影扫描见 11(11/2 0 )只猪左心室收缩功能正常 ,有 9(9/2 0 )只静息时左室节段不同程度运动减弱 (n =7)或丧失 (n =2 )。多巴酚丁胺负荷电影扫描检测到 7只猪左室节段功能改善 ,但有 2只猪无明显改善。心肌灌注扫描有 13只猪共 4 7.8个节段缺血 ,心肌活性扫描有 8只猪共 2 3.6个节段坏死 ,病理检查发现共有 7只猪 2 3个节段坏死。与MRI延迟强化区所显示的梗死区一致 ,差异无统计学意义 (t=0 .0 4 5 ,P >0 .0 5 )。结论　磁共振多技术联合应用可有效检出缺血、坏死心肌 ,并准确判断其程度和范围     

磁共振多技术成像对心肌存活性的实验研究

目的:评估磁共振多技术成像对判断心肌存活性的价值。材料和方法:冬眠心肌模型猪6只,于术前、术后2周及5周行MR多技术成像(包括:形态扫描、电影扫描、心肌灌注及心肌活性扫描),判断心肌缺血区及坏死区大小,与病理对照评价其诊断的准确性。结果:术后2周模型猪左室平均4.2±0.8个节段心肌缺血、平均0.5±0.8个节段心肌变性坏死;术后5周模型猪左室平均3.4±0.9个节段心肌缺血、平均0.3±0.4个节段心肌变性坏死;术后5周的病理提示左室平均3.3±0.5个节段缺血,0.2±0.4个节段坏死。结论:术后5周时左室心肌缺血及变性坏死的范围较2周时缩小,MR多技术成像对判断心肌存活性敏感,但轻度高估了心肌缺血及变性坏死的程度。     

激光心肌血管重建术对犬缺血心肌血流量和氧代谢的影响

目的　探讨激光心肌血管重建术（TMLR）对急性缺血心肌血流量和氧代谢的作用与机制。 方法　18只犬随机等分为正常对照组、心肌缺血组、激光治疗组。采用连续型Nd∶YAG激光行TMLR。测左前降支冠状动脉（LAD）结扎前、结扎后30min和60min的心肌血流量（MBF）,动脉血氧含量（C     

~(201)Tl再注射心肌显像和再注射后延迟显像检测心肌存活的对比研究

为了解２０１Ｔｌ再注射及再注射后延迟显像对心肌存活的检测能力，对６２例心肌梗塞患者进行了２０１Ｔｌ运动、３～５小时再分布、２０１Ｔｌ再注射后１６～３５分钟及再注射后１２～１９小时延迟心肌断层显像。１５例患者于显像后行经皮冠状动脉腔内成形术（ＰＴＣＡ），并于ＰＴＣＡ后重复运动再分布心肌显像。结果：６２例患者运动再分布显像共有１２６个不可逆缺损节段，其中４８个节段再注射后１６～３５分钟出现放射性填充，心肌存活检出率为３８１％（４８／１２６）；５１个节段再注射后延迟显像出现再分布，心肌存活检出率为４０５％（５１／１２６）。两种显像方案的检出率差异无显著性（χ２＝０１６，Ｐ＞００５），但两者结合６２个节段示有放射性填充，心肌存活检出率可提高到４９２％（６２／１２６）。１５例患者ＰＴＣＡ前共检出１７个心肌存活节段，术后１２个节段２０１Ｔｌ灌注改善，阳性预测率为７０６％；ＰＴＣＡ前检出１１个梗塞节段，术后９个节段２０１Ｔｌ摄取无改善，阴性预测率为８１８％。结果表明：２０１Ｔｌ再注射与延迟显像心肌存活检出率无明显差别，但两者联合应用可提高检出率。     

Contrast agents and cardiac MR imaging of myocardial ischemia: from bench to bedside

This review paper presents, in the first part, the different classes of contrast media that are already used or are in development for cardiac magnetic resonance imaging. A classification of the different types of contrast media is proposed based on the distribution of the compounds in the body, their type of relaxivity and their potential affinity to particular molecules. In the second part, the different uses of the extracellular type of T1-enhancing contrast agent for myocardial imaging is covered from the detection of stable coronary artery disease to the detection and characterization of chronic infarction. A particular emphasis is placed on the clinical use of gadolinium-chelates, which are the universally used type of MRI contrast agent in the clinical routine. Both approaches, first-pass magnetic resonance imaging (FP-MRI) as well as delayed-enhanced magnetic resonance imaging (DE-MRI), are covered in the different situations of acute and chronic myocardial infarction.     

Assessment of myocardial perfusion and viability from routine contrast-enhanced 16-detector-row computed tomography of the heart: preliminary results

To assess the diagnostic accuracy of 16-detector-row computed tomography (16DCT) of the heart in the assessment of myocardial perfusion and viability in comparison to stress perfusion magnetic resonance imaging (SP-MRI) and delayed-enhancement magnetic resonance imaging (DE-MRI). A number of 30 patients underwent both 16DCT and MRI of the heart. Contrast-enhanced 16DCT data sets were reviewed for areas of myocardium with reduced attenuation. Both CT and MRI data were examined by independent reviewers for the presence of myocardial perfusion defects or myocardial infarctions (MI). Volumetric analysis of the hypoperfusion areas in CT and the infarct sizes in DE-MRI were performed. According to MRI, myocardial infarctions were detected in 11 of 30 cases, and perfusion defects not corresponding to an MI were detected in six of 30 patients. CTA was able to detect ten of 11 MI correctly (sensitivity 91%, specificity 79%, accuracy 83%), and detected three of six hypoperfusions correctly (sensitivity 50%, specificity 92%, accuracy 79%). Assessing the volume of perfusion defects correlating to history of MI on the CT images, a systematic underestimation of the true infarct size as compared to the results of DE-MRI was found (P<0.01). Routine, contrast-enhanced 16-detector row CT of the heart can detect chronic myocardial infarctions in the majority of cases, but ischemic perfusion defects are not reliably detected under resting conditions.Dr. Sanzs work is supported in part by a Research Grant (Beca para la Formación en Investigación Post-Residencia) from the Spanish Society of Cardiology.     

Acute oedema in the evaluation of microvascular reperfusion and myocardial salvage in reperfused myocardial infarction with cardiac magnetic resonance imaging

The accurate measurement of myocardial salvage is critical to the ongoing refinement of reperfusion strategies in acute myocardial infarction (AMI). Cardiac magnetic resonance imaging (CMR) can define the area at risk in AMI by the presence of myocardial oedema, identified by high signal intensity on T₂-weighted imaging with a short inversion time inversion-recovery (STIR) sequence. In addition, myocardial necrosis can be identified with CMR delayed contrast enhanced imaging. In this prospective study we examined the relationship of acute oedema and necrosis with impaired microvascular reperfusion. We also evaluated acute oedema as a marker of the area at risk in AMI, for the purposes of documenting myocardial salvage. CMR was performed on 15 patients with (AMI), within 24 h of successful percutaneous coronary intervention (PCI). Left ventricular (LV) systolic dysfunction was defined by a systolic thickening <40% (severe <20%). Microvascular reperfusion was evaluated during the acute phase of contrast wash-in. CMR was repeated 3 months post-PCI to evaluate recovery of LV function and final infarct size. Myocardial salvage was defined as the percentage of the area at risk that was not infarcted on follow up CMR. There was a significant correlation between impaired microvascular reperfusion and the extent of segmental oedema (R = 0.363, P < 0.01), but not myocardial necrosis (R = 0.110, P > 0.5). The extent of myocardial salvage correlated with recovery of systolic function (R = 0.241, P < 0.05), which was strongest in LV segments with severely reduced systolic function (R = 0.422, P < 0.01). Conclusions: In acutely reperfused AMI, oedema can be used to identify the area at risk for the purpose of calculating myocardial salvage. The correlation between myocardial oedema and reperfusion status suggests a pathological role of acute oedema in the impairment of microvascular reperfusion.     

Diagnostic value of late gadolinium-enhanced MRI and first-pass dynamic MRI for predicting functional recovery in patients after acute myocardial infarction

Purpose The aim of this study was to determine the comparative diagnostic values of late gadolinium-enhanced magnetic resonance imaging (MRI) and first-pass dynamic MRI for predicting functional recovery of regional myocardial contraction in patients early after acute myocardial infarction. Materials and methods First-pass and late-enhanced MRI were performed in 18 patients 5.5 ± 2.5 days after the onset of myocardial infarction. Images analysis was performed using a 12-segment model. Regional systolic wall thickening (SWT) was measured on cine-MRI obtained 273 ± 130 days later. Results Late-enhanced MRI revealed hyperenhancement in all patients, whereas hypoenhancement on first-pass MRI was observed in 67% (12/18) of the patients. The area under the receiver operating characteristics curve was 0.86 for late-enhanced MRI and 0.74 for first-pass MRI (P = 0.27). First-pass MRI was useful for predicting functional recovery of the segments that showed hyperenhancement of >50% of tissue on late-enhanced MRI. In these segments, preserved SWT was observed in 15 of 33 segments (45%) with first-pass hypoenhancement of ≤50% of tissue, but in only 2 of 22 segments (9%) with first-pass hypoenhancement of >50% of tissue. Conclusion Whereas the diagnostic capability of first-pass MRI alone is limited, complementary use of first-pass MRI can enhance the diagnostic performance of late-enhanced MRI because hypoenhancement during first-pass imaging is more specific to nonviable myocardium. An abstract of this article was presented at the Japan Radiological Society spring meeting in 2002     

Cardiac adrenergic denervation in patients with non-Q-wave versus Q-wave myocardial infarction

In spite of smaller infarct size and better preserved left ventricular function the long-term prognosis after a non-Q-wave infarction is not better than after a Q-wave infarction. In fact, the risk of sudden cardiac death is higher in patients with a non-Q-wave infarction than in patients with a Q-wave infarction. One possible reason for postinfarction arrhythmias is cardiac adrenergic denervation resulting from myocardial infarction. In this study we compared cardiac adrenergic innervation after non-Q-wave and Q-wave infarctions. Single-photon emission tomography using iodine-123 metaiodobentzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) tracers were conducted in order to compare cardiac adrenergic denervation and myocardial perfusion in 12 patients with a non-Q-wave infarction and 15 patients with a Q-wave infarction. MIBG and MIBI defects were determined as regional uptake ≤30% of maximal myocardial activity. The size of MIBI defects calculated as a percentage of left ventricular mass was significantly smaller in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (4%±3% vs 9%±7%, P<0.05, respectively). According to the maximal serum creatine kinase activity, less myocardium was damaged in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (502±436 IU/l vs 1878± 1265 IU/l, P<0.001). In spite of this, the extent of MIBG defects was similar in patients with a non-Q-wave and patients with a Q-wave infarction (21%±18% vs 23%± 12%, respectively). In addition, the size of MIBG defect correlated with the infarct size (maximal creatine kinase activity) (r=0.52, P<0.05) after a Q-wave infarction but not after a non-Q-wave infarction. In conclusion, despite a smaller infarct size in non-Q-wave infarct patients, the extent of cardiac adrenergic denervation was similar in patients with a non-Q-wave and patients with a Q-wave infarction. In addition, the extent of cardiac adrenergic denervation was related to the infarct size in patients with a Q-wave infarction but not in patients with a non-Q-wave infarction. Received 19 January 2000 and in revised form 24 March 2000