Susceptibility of C5b-9(m) to postmortem changes

Summary C5b-9_(m) is a specific and sensitive marker for myocardial cell necrosis. The diagnostic value of this marker would be considerably limited in forensic practice if its immuno-histochemical demonstration were hampered by putrefaction or autolysis. We could demonstrate C5b-9_(m) immunohistochemically in necrotic myocardium due to infarction up to the 11th day of experimentally induced putrefaction and autolysis, when reliable demonstration of myocardial infarction with hematoxylin-eosin was no longer possible. Under the experimental conditions of this study, no false positive immunohistochemical staining occurred.     

The application of selected histochemical and immunohistochemical markers and procedures to the diagnosis of early myocardial damage

Summary Histochemical (= HIS) methods (haematoxylin-eosin, luxol fast blue, chromotrope aniline blue) and various immunohistochemical (= IH) markers (myoglobin, desmin, fibrinogen, complement C5b-9) were applied in parallel to test the efficiency, specificity and sensitivity for the recognition of early ischemic myocardial damage. The whole series was subgrouped into cardiac deaths (N= 35) and controls (N= 13). Cardiac deaths were sub-divided into 3 groups: l. infarction visible in gross examination (N = 15), 2. coronary thrombosis without infarction (N = 11), 3. stenosing coronary athero-sclerosis without infarction (N = 9). The control group (group 4) consisted of unnatural deaths with presumed short agonal periods (N = 13). Group 1 cases usually exhibited extended coagulation necrosis of the diffuse type and the contraction type in combination (1 exception). Group 2 showed mainly a patchy type of coagulation necrosis and contained 1 case where all methods failed to react and 3 more cases where only the HIS methods failed to react. Group 3 and 4 were associated with a disseminated type of single and/or grouped fibre necrosis. — In addition, the average reaction strengths showed a decrease from group 1 to group 4 which was more pronounced in the HIS reactions compared with the IH reactions. One case in group 1 showing negative IH reactions cannot be explained. Positive IH reactions observed in a few cases in group 2 contrasting with negative HIS reactions would indicate a greater sensitivity of this methodology and this interpretation also applies to groups 3 and 4. From pathophysiological considerations, the positive cases in groups 3 and 4 can be well explained. — The results show that selected application of a single criterion to the diagnosis of early myocardial infarction and/or ischemic fibre damage cannot resolve the diagnostic problem. However, a selected set of HIS/IH methods and the synoptic interpretation of all findings will improve the detection of early myocardial infarction/ischemic damage.     

Dystrophin and metalloproteinase 9 in myocardial ischemia: A post-mortem immunohistochemical study

The presented study evaluated the expression of dystrophin and MMP-9 in cases of sudden cardiac death (SCD) due to coronary atherosclerotic disease (CAD) in order to analyze the characteristics and the chronology of their expression, providing evidence on the possible role in post-mortem diagnosis of myocardial ischemia. The expression of these proteins was also compared to C5b-9 complex and fibronectin expression to evaluate any differences. Two groups of CAD-related SCD, respectively group 1 with gross and/or histological evidence and group 2 with no specific histological signs of myocardial ischemia, were used. A third group formed by cases of acute mechanical asphyxiation was used as a control. The immunohistochemical staining by dystrophin, MMP-9, C5b-9, and fibronectin antibodies was performed. The study revealed that dystrophin and MMP-9 showed different expression in group 1 and group 2 as, respectively, different degree of sarcolemmal staining depletion and increasing of interstitial and granulocytes immunopositivity. Moreover, loss of dystrophin staining and C5b-9 immunopositivity were more significant when compared to MMP-9 increasing. Dystrophin and MMP-9 seemed to be useful immunohistochemical markers for the detection of myocardial ischemic damage. However, the comparison of the four markers suggested that loss of dystrophin could be considered as an earlier marker.     

Demonstration of myocardial necrosis in the presence of advanced putrefaction

Samples of heart tissue were investigated in two series for the detectability of myocardial necrosis after artificial and natural putrefaction, respectively. In the first series heart tissue with and without infarction was artificially subjected to humid and dry autolysis and putrefaction. In the second investigation heart tissue was obtained from exhumed bodies after periods of burial ranging between 10 and 929 days. Besides histology a variety of immunohistochemical markers were applied and C5b-9 gave positive results even after long periods of artificial and natural putrefaction. From the methods tested, this was by far the most sensitive method with a high robustness against putrefaction. NP57, which indicates neutrophilic leucocytes could be demonstrated considerably longer after humid putrefaction than after dry putrefaction. The time limits of detection were considerably longer than for H & E. These two methods are the methods of choice for the detection of myocardial infarction and leucocyte infiltration in advanced stages of putrefaction. Received: 5 November 1999 / Accepted: 26 January 2000     

The sudden and unexpected death of a female-to-male transsexual patient

A 32-year-old woman, who was intramuscularly injected with testosterone enanthate (125 mg) once or twice a month over a two-year period for female-to-male transsexualism, died suddenly. A forensic autopsy was performed to investigate the cause of death. Concentric cardiac hypertrophy was macroscopically observed. In the left and right coronary arteries, atherosclerosis was generally observed within the endothelium. In particular, there was severe stenosis (>90%) at the start of the left descending branch. In the myocardium, both coagulation necrosis and contraction band necrosis were microscopically observed. Moreover, myocardial fibrosis and myocardial calcification were diffusely detected, respectively. The cause of death was diagnosed as ischemic heart disease due to coronary stenosis. There is some debate as to whether cross-hormone replacement is related to the occurrence of coronary artery disease or not, however, it is possible that the development of ischemic heart disease was aggravated by the administration of testosterone enanthate in the current case.     

Detection of Helicobacter pylori in gastric biopsy and resection specimens

AIM: To compare the sensitivity of detecting H. pylori in gastric biopsy and resection specimens using modified Giemsa stain and immunohistochemistry, using a commercially available anti-H. pylori antibody (Dako, Denmark). METHODS: Gastric antral biopsy specimens showing chronic gastritis (28 cases) together with tissue blocks from gastrectomy specimens for duodenal ulcer (2 cases) were stained with modified Giemsa and immunoenzymatic alkaline phosphatase - anti-alkaline phosphatase (APAAP) method, and were carefully examined for the presence of H. pylori. RESULTS: Using a modified Giemsa stain, the spiral shaped bacteria of H. pylori stained blue, were attached to the brush border of the gastric foveolar epithelial cells. However, the specificity of modified Giemsa stain depended on the morphological appearance of H. pylori. The specificity of immunostaining permitted detection of low numbers or even single organisms. In all cases bacteria were more prominent and easier to detect in immunostained preparations. H. pylori was identified in 22 (73.3%) of 30 sections stained with modified Giemsa stain, but it could be identified with greater frequency in sections stained with APAAP, in 27 (90%) of 30 sections. CONCLUSION: Immunohistochemical identification of H. pylori was better than Giemsa stain for detecting that organism.     

Myocardial necrosis and cocaine

A quantification of different forms of acute myocardial necrosis, myocardial leukocytic infiltrates and myocardial fibrosis was accomplished in 26 chronic cocaine abusers who died of cocaine intoxication and compared to 45 normal subjects who died from head trauma and 38 who died of acquired immunodeficiency syndrome. The findings were: absence of infarct necrosis, a similar frequency and extent of coagulative myocytolysis (contraction band necrosis) and leukocytic infiltrates in cocaine abusers and normal controls, and an absence of myocardial fibrosis in cocaine abusers. These findings question both the acute and chronic cardiotoxicity of cocaine. The infarct-like pattern in some predisposed subjects may be due to an excess of catecholamine release induced by the drug resulting in coagulative myocytolysis and platelet thrombi. Received: 5 August 1996 / Received in revised form: 3 February 1997     

中性粒细胞碱性磷酸酶染色实验条件探讨

目的探讨中性粒细胞碱性磷酸酶染色的实验条件。方法用40％、60％、80％的丙酮-枸缘酸固定液对中性粒细胞碱性磷酸酶染色固定条件进行测定。同时用2-氨基-2-甲基-1．3-丙二醇（pH9．4—9．6）缓冲液、巴比妥（pH9．2）缓冲液、Tris（pH9．2）缓冲液配制的基质液分别在10、15、20分钟的染色条件进行测定。结果是选择60％的丙酮-枸缘酸固定30秒染色结果最好。三种不同的缓冲液和三个不同的孵育时间的染色结果经多因素方差分析,P〈0．05,结果有统计学意义。结论最佳染色条件为60％的丙酮-枸缘酸固定30秒,用Tris（pH9．2）缓冲液配制的基质液,孵育时间为15分钟。本方法帮助鉴别慢性粒细胞性白血病和类白血病有较大的实用价值。     

树突状细胞的补体攻膜复合物C5b-9模型的建立

目的建立树突状细胞（DC）的补体攻膜复合物C5b-9模型,为研究补体攻膜复合物对DC的影响奠定基础。方法诱导人外周血单核细胞分化成为不成熟DC,C5b-9体外组装,激光共聚焦检测C5b-9在DC表面组装情况。结果成功诱导出不成熟DC,激光共聚焦显示C5b-9完整组装于DC表面。结论本研究成功建立了DC的补体攻膜复合物C5b-9模型,为将来进一步探讨C5b-9对DC的功能影响奠定了基础。     

A comparative study on the immunohistochemical detection of early myocardial damage

The study was undertaken to evaluate the kinetics and distribution patterns of several immunohistochemical markers in ischemically and hypoxically damaged myocardium. The myocardium of 8 cases of acute myocardial infarction (AMI), 8 cases of diagnosed acute cardiac death (ACD) and 12 cases of acute exogenic hypoxia (AEH) due to CO poisoning or hanging were analysed for depletion of the cardiac antigens FABP, troponin C and T, desmin and myoglobin, loss of CD59 and deposition of the plasma antigens fibrinogen, fibronectin and the terminal complement complex C5b-9. The visualisation of the terminal complement complex was positive as early as 30 min after onset of symptoms of AMI. Depletion of cellular antigens started earlier than the deposition of plasma antigens. The deposition of fibronectin and fibrinogen began earlier than the detection of C5b-9 but later than the depletion of the cellular antigens. Our findings indicate that for the immunohistochemical detection of very early myocardial damage, the depletion of myoglobin is at least of the same rank or better than depletion of FABP and troponin. Received: 19 November 1998 / Received in revised form: 18 February 1999     

Burden of myocardial damage in cardiac allograft rejection: Scintigraphic evidence of myocardial injury and histologic evidence of myocyte necrosis and apoptosis

BACKGROUND: Because myocardial damage determines morbidity and outcomes in heart transplant rejection, assessment of total burden of myocardial damage is highly desirable. In addition to myocyte necrosis, programmed cell death, or apoptosis, has recently been shown to contribute to cardiac allograft rejection. In the present study, we noninvasively determined myocardial damage by antimyosin scintigraphy and compared it with necrotic and apoptotic myocardial damage in endomyocardial biopsy (EMB) specimens. METHODS AND RESULTS: Forty scintigraphic and histologic studies were simultaneously performed. Of these, 19 patients had no EMB evidence of allograft rejection (group I, International Society of Heart and Lung Transplantation [ISHLT] grade 0/4), 12 had mild rejection (group II, ISHLT grades 1A and 1B), and 9 had evidence of moderate allograft rejection (group III, ISHLT grades 2, 3A, and 3B). None of the biopsies demonstrated severe allograft rejection (ISHLT grade 4/4). The severity of global myocyte damage in 40 patients was assessed by antimyosin scintigraphy. Endomyocardial biopsies were performed in these patients within 48 hours of imaging study; biopsy specimens were characterized for presence of myocyte necrosis and apoptosis. Evidence of myocyte necrosis was observed in 9 (23%) of 40 EMB specimens. Nineteen EMB specimens of group I had no inflammation and no myocyte necrosis, 12 of group II specimens showed interstitial mononuclear cell infiltration (only) but no myocyte necrosis, and all 9 of group III specimens had evidence of cellular infiltration and myocyte damage. Myocyte necrosis was assessed by hematoxylin-eosin and trichrome staining of EMB specimens. On the other hand, apoptosis of myocytes, as assessed by TUNEL staining of DNA fragments, was seen in 22 (55%) of the 40 biopsy specimens: 47%, 58%, and 67% in groups I, II and III, respectively. Abnormal antimyosin scan findings, indicating presence of myocardial damage, were observed in 9 of the 19 patients in group I and in all patients in groups II and III. Although positive antimyosin scan results in group III patients are concordant with the presence of histologic myocardial necrosis, myocardial uptake of antimyosin antibodies in groups I and II (no apparent myocyte damage at light microscopic examination) could reflect either sampling error of the biopsy or ongoing apoptotic myocyte damage. CONCLUSIONS: Apoptosis of myocytes is frequently observed during cardiac allograft rejection. The presence of apoptotic myocytes in the absence of histologic rejection activity in patients with antimyosin uptake suggests that apoptosis could be an additional mechanism of transplant-associated myocardial damage.     

Dityrosine,a protein product of oxidative stress,as a possible marker of acute myocardial infarctions

The verification of acute and lethal myocardial infarctions remains a crucial problem in the daily routine work of legal medicine. In order to enhance the possibilities in micromorphologic diagnostics, we investigated if dityrosine as a protein product of oxidative stress can be detected in myocardial tissue after an infarction and, if so, if it occurs early enough to be used in the diagnosis of infarctions with a short survival time. We examined tissue samples from 61 autopsy cases (37 male, 24 female) with verified or suspected infarctions as well as 11 control cases (7 male, 4 female). Immunohistochemical staining was performed for dityrosine and the established markers fibronectin and C_5b-9. Positive staining for dityrosine was obtained in nearly all cases with infarctions aged 4 h to 2 weeks. Single positive results were obtained in cases with older (up to 2 months) or assumedly very fresh (up to 4 h) infarctions. Furthermore, single positive results with a different staining pattern were obtained in the control group. We concluded that dityrosine as a marker of oxidative stress can be detected after infarctions and might occur early enough to be helpful in the diagnosis of infarctions with a short survival time. Though dityrosine does not seem to be specific for infarctions, the different staining patterns enable a differentiation.     

骨形态发生蛋白9促进小鼠颅骨间充质祖细胞成骨分化的实验研究

目的：研究腺病毒载体介导的骨形态发生蛋白9（BMP-9）对小鼠永生化颅骨间充质祖细胞（iCAL）成骨分化的诱导作用。方法以iCAL为模型,设置绿色荧光蛋白（ GFP）对照组和BMP-9诱导组,于诱导后的3、5、7 d对早期成骨分化指标碱性磷酸酶（ ALP）活性进行定性和定量检测;于诱导后的14 d通过茜素红染色检测骨钙结节形成;荧光定量PCR法和Western印迹检测成骨细胞分化标志基因Runx2、OCN表达情况。结果 BMP-9诱导组细胞内ALP活性高于GFP对照组,差异具有统计学意义（P＜0．05）;BMP-9诱导组形成较多的钙盐结节沉积;荧光定量PCR检测结果显示诱导组中Runx2、OCN的mRNA表达量明显上调,差异具有统计学意义（P＜0．05）,Western印迹检测3 d Runx2蛋白表达上调,5 d OCN蛋白表达上调。结论 BMP-9促进小鼠永生化iCAL成骨分化。     

人脐血源基质细胞分离培养条件的优化

目的探索人脐血源基质细胞(hUCBOSCs)的分离扩增条件,并观察其生物学特性。方法取产科胎儿脐带血,比较不同的分离方法、首次换液时间及培养体系对人脐血源基质细胞原代培养的影响。倒置显微镜动态观察细胞生长情况,瑞氏染色观察细胞形态特征,并采用细胞化学和免疫细胞化学方法对获得的细胞进行鉴定。结果明胶沉淀法优于其他分离方法,首次换液时间为第4天、改良Dexter培养体系培养效果最好。原代培养9~14d(平均12.1d)时贴壁细胞开始形成集落,15~21d(平均19.4d)时集落数量最多,培养28d贴壁细胞铺满培养皿底,细胞类型以"成纤维样"细胞、"巨噬样"细胞、"小圆"类细胞为主。细胞化学染色显示非特异性酯酶(NSE)染色阳性率100%,糖原染色(PAS)阳性率为100%,碱性磷酸酶(ALP)染色阳性率26%,过氧化物酶(POX)染色阴性;免疫细胞化学染色显示CD31阳性率96%,CD68阳性率95%,Fn阳性率94%,CD45阴性。结论在体外可以成功培养人脐血源基质细胞,为进一步的基础及临床研究提供了基础。     

人脐带间充质干细胞来源的外泌体促进小鼠成骨前体细胞增殖与分化

 

目的 提取人脐带间充质干细胞(human umbilical cord mesenchymal stem cells, hucMSCs)来源的外泌体(hucMSC-exo),观察其对小鼠成骨前体细胞(mouse osteoblast progenitor cells, mOPCs)的作用。方法 体外分离培养hucMSCs,超速离心法收集外泌体;采用CCK8试剂盒检测不同浓度梯度hucMSC-exo对mOPCs增殖的影响,碱性磷酸酶活性检测以及茜素红染色观察不同浓度梯度hucMSC-exo对mOPCs矿化的影响。结果 成功提取hucMSCs,呈现旋涡状贴壁式生长,形态呈长梭形,具有多向诱导分化潜能。HucMSCs来源的外泌体呈圆形、椭圆形,大小在80 nm左右最多,阳性表达CD9,CD63。CCK8法结果显示5、10 μg/ml的hucMSC-exo可以显著地促进mOPCs在体外的增殖(P<0.05),碱性磷酸酶和茜素红染色结果发现5、10 μg/ml的hucMSC-exo组可以明显提高mOPCs碱性磷酸酶活性及钙化结节的形成,且10 μg/ml的外泌体浓度作用强于5 μg/ml,差异有统计学意义(P<0.05)。结论 成功提取了hucMSCs及hucMSC-exo,hucMSC-exo可以以浓度依赖的方式促进mOPCs的增殖与成骨分化。

     

MR心肌延遲期強化與CTA冠狀動脈狹窄程度的對照分析

目的:探討MR心肌延遲期強化(Delayed-Enhancement,DE)所檢出的心肌壞死與CTA供血冠狀動脈狹窄程度的相關性。方法:對臨床提示心肌壞死的70例患者成功進行了3T DE-MR檢查,通過觀察患者的心肌壞死程度及心肌運動狀況,對照其同期完成的冠狀動脈CTA結果,分析二者之間的相關性。結果:70例患者共發現心肌壞死54處,83%的心肌壞死發生在狹窄程度≥75%的42支血管中。在冠狀動脈狹窄75%~84%的13支血管中,發生心肌壞死7處(13%);85%~94%的9支血管中,發生心肌壞死12處(22%);≥95%的20支血管,發生心肌壞死26處(48%)。隨著CTA評價冠狀動脈狹窄的嚴重程度增加,DE-MR檢出相應供血區心肌壞死的陽性率也逐漸增加,二者呈顯著性相關(P<0.01)。結論:DE-MR檢測的心肌壞死及其程度與冠狀動脈狹窄的CTA結果互為印證,具有較高的一致性。     

Immunohistochemical expression of fibronectin and C5b-9 in the myocardium in cases of carbon monoxide poisoning

Even if there is clinical evidence that carbon monoxide poisoning determines cardiac damage, the literature on the cardiac pathomorphology in such cases is scarce. We investigated the immunohistochemical expression of two known markers of fresh cardiac damage, fibronectin and the terminal complement complex C5b-9, in both cardiac ventricles in 26 cases of CO intoxication (study group, 15 ??, 11 ??, mean age 47?years, mean COHb level 65.9%, min. 51%, max. 85%) compared to a group of 23 cases of hanging (n?=?23, 4??, 19??, mean age 42?years) as well as to 25 cases of myocardial infarction (n?=?25, 13??, 12??, mean age 64?years). Fresh cardiac damage was detected with the antibody fibronectin in cases of CO poisoning and was prevalently localised at the right ventricle.     

Percutaneous tumor ablation: increased coagulation by combining radio-frequency ablation and ethanol instillation in a rat breast tumor model

PURPOSE: To determine if percutaneously applied radio frequency (RF) combined with percutaneous ethanol instillation (PEI) can increase the extent of ablation in rat breast tumors. MATERIALS AND METHODS: R3230 mammary adenocarcinoma was implanted bilaterally in the mammary fat pads of 18 female rats. The tumor nodules measured 1. 2-1.5 cm. Eight tumors each were treated with (a) conventional, monopolar RF (96 mA +/- 28; 70 degrees C for 5 minutes); (b) PEI (250 microL of ethanol infused over 1 minute); (c) combined therapy of PEI immediately followed by RF ablation; or (d) combined therapy of RF ablation immediately followed by PEI. Four tumors were not treated and served as controls. Histopathologic examination included staining for mitochondrial enzyme activity. Resultant coagulation necrosis was compared between treatment groups. RESULTS: Coagulation necrosis was observed only within treated tumors. Tumors treated with RF alone had 6.7 mm +/- 0.6 of coagulation surrounding the electrode, and those treated with PEI alone had 6.4 mm +/- 0.6 of coagulation around the instillation needle (not significant). Significantly increased coagulation of 10.1 mm +/- 0.9 (P: <.001) was observed with the combined therapy of PEI followed by RF. RF followed by PEI did not increase coagulation (6.4 mm +/- 0.8 around the needle; not significant). CONCLUSION: PEI followed by RF ablation therapy increases the extent of induced coagulation necrosis in rat breast tumors, as compared with either therapy alone.     

Lethal case of myocardial ischemia following overdose of the synthetic cannabinoid ADB-FUBINACA

The serious adverse effects of synthetic cannabinoids (SCB), the lack of human pharmacological data on SCBs, and the increasing number of SCBs with diverse structures are growing public health concerns. A fatal case of myocardial ischemia after ADB-FUBINACA overdose is reported. A 41-year-old male died after consuming a brown, powder-like drug. Autopsy revealed pallor in the left ventricle of the subendocardial two-third of the myocardium, and histological examination revealed early signs of myocardial ischemia: few wavy myocardial fibers, contraction band necrosis in the subendocardial region, and patchy subendocardial complement component 9 (C9) positivity. Toxicological analysis detected a high concentration of the indazole carboxamide derivative SCB ADB-FUBINACA (peripheral blood: 105 ng/mL) and a low concentration of the synthetic cathinone (SC) derivative stimulant N-ethylpentylone (NEP).The literature concerning ADB-FUBINCA overdoses is reviewed, and the possible mechanism of death and the cardiac effects of SCBs are discussed. Effects of SCBs are unpredictable, but they are potentially cardiotoxic, capable causing arrhythmias, cardiac hypertrophies, and myocardial ischemia. The cardiotoxicity of SCBs can be attributed to vasospasms, decreased myocardial contractility, and increased cardiac workload and oxygen demand.Based on the autopsy, histology, and toxicology, it could be reasonably suggested, that ADB-FUBINACA have been a significant contributor to the myocardial ischemia seen in histology. The mechanism of death was likely fatal arrhythmia induced by the patchy myocardial ischemia. Due to the low concentration of NEP, it’s role in the fatal outcome is improbable.     

MR多技术扫描检测活性心肌及其影像学对比的实验研究

目的 评估各种影像学方法检测活性心肌的价值。材料与方法 建立慢性心肌缺血模型猪10头,分别于制作模型前和后1～2月进行磁共振多技术扫描及小剂量多巴酚丁胺负荷超声心动图（LDDSE）、^201TI单光子发射计算机体层显像（^201TI SPECT）、正电子发射体层显像（^18F-PET）检查,判断心肌缺血区和坏死区的大小,并与病理结果对照了解各种方法的敏感性、特异性。结果 7头动物顺利完成所有检查,负荷磁共振电影扫描见10个（8．93％）节段为梗死心肌,6个（5．36％）节段为缺血心肌;心肌灌注扫描见34个（30．35％）节段缺血,心肌活性扫描见12个（10．71％）节段坏死。LDDSE检查见8个（7．14％）节段为梗死心肌,9个（8．04％）节段为缺血心肌。SPECT检查见9个（8．04％）节段为梗死心肌。PET检查见17个（15．18％）节段为梗死心肌。TTC染色见14个（12．50％）节段为梗死区。MR电影检出的坏死节段比TTC染色显示的节段少并有统计学意义（P=0．0455,Kappa=0．8100）;MR活性扫描检出的坏死节段比TTC染色显示的坏死节段略少但无统计学意义（P=0．1573,Kappa=0．9130）。LDDSE检出的坏死节段较TTC染色显示的节段少并有统计学意义（P=0．0140,Kappa=0．7000）;PET检出的坏死节段多于磁共振活性扫描（P=0．0253,Kappa=0．8028）和MR电影扫描（P=0．0082,Kappa=0．7079）并有统计学意义;亦多于TTC染色显示的坏死节段（P=0．0833,Kappa=0．8879）,但无统计学意义;SPECT检出的坏死节段比TTC染色显示的节段少并有统计学意义（P=0．0253,Kappa=0．7590）。以TTC染色结果为金标准,MRI电影、MRI活性扫描、LDDSE、SPECT、PET检出无活性心肌的敏感性、特异性分别为71．43％、100％;85．71％、100％;57．10％、100％;64．29％、100％;100％、96．94％。结论 MR多技术扫描可结合形态、功能及灌注多种方法检测活性心肌．清晰显示心肌梗死的位置、程度,并可对左窒室壁运动进行直观显示,且价格相对PET便宜;磁共振和PET、病理结果均有较高一致性。PET高估心肌坏死范围,且不能判断心肌梗死的透壁程度。SPECT和LDDSE低估心肌活性。而且亦不能显示心肌梗死的透壁程度。