抗心肌肌凝蛋白轻链单克隆抗体亲大鼠梗死心肌放射免疫显像 …

目的　探讨抗心肌肌凝蛋白轻链单克隆抗体 ( AMLCA)亲梗死心肌显像的可行性。　方法　大鼠静脉注射99m Tc标记 AMLCA,观察梗死心肌摄取99m Tc-AMLCA的特异性及摄取与注射时间和梗死时间的关系。　结果　 99m Tc-AMLCA在大鼠血中的清除呈双相 :注射后 ,99m Tc-AMLCA血浓度由 2 h的 ( 4.0 7± 0 .90 ) ID% / g组织迅速降至 4 h的 ( 2 .70± 0 .54) ID% / g组织 ;此后缓慢下降。注射后 6h、8h、2 4 h,肝脏均较梗死心肌摄取强。梗死心肌在注射后 2 h就开始摄取99m Tc-AMLCA,4～ 8h渐趋平衡 ,2 4 h达到高峰。梗死 6h至 1 4 d的不同梗死时间 99m Tc-AMLCA摄取差异无显著性( P>0 .0 5)。注射后相同时间 ,梗死心肌与正常心肌放射比 ,99m Tc-AMLCA明显大于 99m Tc-N-Ig G( P<0 .0 1 )。　结论　大鼠梗死心肌能特异地摄取 99m Tc-AMLCA,并且具有摄取时间早 ,持续时间长 ,受梗死时间影响较小的特点 ,为99m Tc-AMLCA亲梗死心肌显像的研究提供了初步的实验依据。     

抗心肌肌凝蛋白抗体亲梗死心肌显像的研究进展

本文介绍了抗心肌肌凝蛋白单克隆抗体及抗肌凝蛋白重链单克隆抗体亲梗死心肌显像的研究进展,存在的缺点和对其所做的技术改进以及通过基因工程制备之单链抗体的优点,对利用噬菌体抗体库技术所生产的单链抗体及其抗肌凝蛋白显像在心脏病学中的应用前景进行了展望。     

99mTc标记抗心肌肌钙蛋白T单抗在急性心肌损伤大鼠模型中的生物学分布

目的研究99mTc标记抗心肌肌钙蛋白T单抗在急性心肌损伤大鼠模型中的生物学分布。方法先制备99mTc标记抗心肌肌钙蛋白T单抗和建立急性心肌损伤大鼠模型。本研究分3组:实验组、对照组和空白组,各组20只大鼠。实验组急性心肌损伤大鼠静脉注射99mTc标记抗心肌肌钙蛋白T单抗0.3 mCi,分别于注射后2、4、8、12h时处死(每时间点5只),取血液、肝、脾、肾、肌肉、结肠、肺、心脏,以计算每克组织放射性计数占总注入计数的百分比(ID%/g)及心/肺比值。对照组(急性心肌损伤大鼠)和空白组(正常心肌大鼠)分别静脉注射99mTc-N-IgG和99mTc标记抗心肌肌钙蛋白T单抗0.3 mCi,其它处理方法同实验组。结果实验组的ID%/g和心/肺比值均较对照组和空白组显著为高,提示急性损伤心肌对99mTc标记抗心肌肌钙蛋白T单抗是特异性摄取,且摄取高峰时间为4 h。结论99mTc标记抗心肌肌钙蛋白T单抗有望作为亲心肌损伤显像剂用于诊断急性心肌损伤。     

99mTc标记抗心肌肌钙蛋白T单抗Fab片段在SD大鼠急性心肌梗死模型中的生物学分布

目的 研究^99mTc标记抗心肌肌钙蛋白T单抗片段（^99mTc-AcTnTMA-Fab）在急性心肌梗死大鼠模型中的生物学分布规律。方法 先制备^99mTc-AcTnTMA-Fab和^99mTc-AcTnTMA,并建立急性心肌梗死大鼠模型。本研究分为实验组、对照组和空白组,每组20只大鼠。实验组急性心肌梗死大鼠静脉注射^99mTc-AcTnTMA-Fab 0.3 mCi,分别于注射后2 h、4 h、8 h、12 h时处死（每时间点5只）,取血液、肝、脾、肾、肌肉、结肠、肺、心脏,以计算每克组织放射性计数占总注射计数的百分比（ID%/g）及梗死心肌ID%/g/肺ID%/g比（HLR）。对照组急性心肌梗死大鼠和空白组正常心肌大鼠分别静脉注射 ^99mTc-AcTnTMA和^99mTc-AcTnTMA-Fab 0.3mCi,其它处理方法同实验组。结果 实验组和对照组的ID%/g和HLR均较空白组显著为高,提示急性梗死心肌对^99mTc-AcTnTMA-Fab和 ^99mTc-AcTnTMA的摄取均是特异的,且实验组的ID%/g和HLR较对照组显著为高,提示^99mTc-AcTnTMA-Fab摄取能力更强。结论 ^99mTc-AcTnTMA-Fab有望作为亲心肌梗死显像剂用于诊断急性心肌梗死。     

急性心肌梗塞心肌肌凝蛋白轻链1测定的临床意义

本文采用抗人心肌肌凝蛋白轻链1(M-LC_1) 单克隆抗体和免疫酶联夹心法测定了急性心肌梗塞(AMI)病人血清M-LC_1峰值和梗塞后不同时间过程中M-LC_1变化。结果示:(1) 33例AMI 的M-LC_1峰值均高于正常值高限;(2) 5例AMI 发病后0-12h M-LC_1水平均高于正常值;(3) AMI 后M-LC_1有意义升高持续8天以上,并有37. 5%病例呈双相型改变。表明M-LC_1是心肌严重损伤的特异指标,可用于AMI早期和晚期诊断。     

大鼠心肌梗死后的原癌基因表达

目的本实验旨在探讨心肌梗死后左心室重构的分子生物学机制。方法用地高辛标记的原位杂交方法观察了大面积心肌梗死后存活心肌细胞的原癌基因c-myc。c-fos及c-jun的mRNA水平的动态变化，并用巯甲丙脯酸进行干涉。大鼠随机分为三组：（1）单纯心肌梗死组；（2）梗塞给药组；（3）假手术组。梗塞给药组于手术前3d开始饲以巯甲丙脯酸（2g／L）。结果左室非梗塞区心肌的c-myc，c-fos及c-jun的mRNA水平手术后24h达峰值，c-myc于手术后10d，c-jun于手术后7d恢复到假手术组水平，但c-fos于术后持续高表达。在梗塞给药组，c-myc，c-fos于手术后7d、10d，c-jun于手术后各时间点其mRNA水平达假手术组程度。结论上述基因在非梗塞区心肌均有过量表达，持续时间较长，转换酶抑制剂对其有所抑制。     

二氧化硫通过调控MMP-3/TIMP-1表达改善急性心肌梗死大鼠心肌纤维化

目的探讨气体信号分子二氧化硫(SO2)对急性心肌梗死大鼠心肌纤维化的作用及其对基质金属蛋白酶(MMP)-3/MMPs抑制剂(TIMP)-1蛋白表达的影响。方法将40只健康雄性成年SD大鼠随机分为正常对照(Control)组、模型[异丙肾上腺素(Iso)]组、SO2干预(Iso+SO2)组、SO2对照(SO2)组。首先构建急性心肌梗死大鼠模型组,Iso组和Iso+SO2组予以持续2 d腹腔注射Iso 50 mg/(kg·d),Control组及SO2组大鼠则腹腔注射等量生理盐水,行心电图及肌钙蛋白检测,确定造模成功后,Iso+SO2组和SO2组大鼠腹腔注射亚硫酸钠(Na 2SO 3)/亚硫酸氢钠(NaHSO 3)溶液(0.54±0.18)mmol/(kg·d),Control组及Iso组则腹腔注射等量生理盐水;持续4 w后,将大鼠处死,通过Masson染色检测心肌胶原沉积情况,用Western印迹对大鼠心肌组织MMP-3和TIMP-1蛋白表达水平变化进行检测。结果与Control组相比,Iso组心肌组织间可见明显胶原纤维沉积,MMP-3蛋白表达显著上升(P<0.05),TIMP-1蛋白表达显著下降(P<0.05)。Iso+SO2组与Iso组相比,大鼠心肌组织可见胶原纤维沉积减少,MMP-3蛋白表达水平下降(P<0.05),TIMP-1表达水平明显上升(P<0.05)。结论SO2可能通过调控MMP-3/TIMP-1改善Iso诱导的急性心肌梗死大鼠的心肌纤维化。     

心肌梗死大鼠心肌组织中AQP1、HIF-1α的表达变化及其与心肌水肿的关系

目的观察大鼠心肌梗死模型中心肌梗死组织中水通道蛋白1(AQP1)和缺氧诱导因子-1α(HIF-1α)的表达水平,并探讨其与心肌水肿的相关性。方法将48只SD大鼠随机分为心肌梗死组和假手术组,每组24只。采用结扎左冠状动脉前降支法建立大鼠心肌梗死模型,假手术组仅开胸不结扎。于造模后12、24、48、72 h分批处死大鼠,取左心室心肌组织,采用酶联免疫法检测AQP1、HIF-1α的蛋白表达水平,采用Real-time PCR检测AQP1、HIF-1αmRNA表达,采用干湿重法检测心肌组织含水量。结果心肌梗死组大鼠心肌组织中AQP1、HIF-1αmRNA以及蛋白水平较假手术组明显升高,差异有统计学意义(P均0.05)。心肌梗死组大鼠心肌组织AQP1、HIF-1αmRNA以及蛋白水平在术后72 h内呈时间梯度升高,各时间点差异具有统计学意义(P均0.05)。心肌梗死组大鼠术后12、24、48、72 h心肌组织含水量逐渐升高,与假手术组比较也升高,差异有统计学意义(P均0.05)。心肌梗死大鼠心肌组织中AQP1 mRNA以及蛋白水平与心肌含水量呈正相关(r=0.507,P=0.010;r=0.585,P=0.008),HIF-1αmRNA以及蛋白水平与心肌含水量呈正相关(r=0.408,P=0.025;r=0.486,P=0.017)。结论心肌梗死大鼠心肌组织中AQP1、HIF-1α呈高表达,且与心肌水肿严重程度明显相关。     

胞浆型磷脂酶A2在急性心肌梗死大鼠心肌组织中的表达

目的 观察急性心肌梗死早期心肌组织胞浆型磷脂酶A2(cPLA2)mRNA及蛋白表达,探讨cPLA2在心肌细胞损伤中的作用.方法 雄性SD大鼠随机分为假手术组,心肌梗死组(AMI组,按时间不同分5组,每组10只),建立大鼠急性心肌梗死模型,按照心肌梗死不同时间(0、1、2、3、6和12 h)处死动物.免疫组化检测心肌cPLA2蛋白表达情况.采用RT-PCR检测心肌cPLA2mRNA表达水平.通过透射电镜观察心肌细胞超微结构的改变.结果 ①与假手术组比较,AMI组心肌cPLA2mRNA水平均出现不同程度上调,以梗死后2 h达到峰值(0.655±0.035,P＜0.01).②假手术组与AMI组cPLA2蛋白都有阳性表达,AMI组cPLA2表达增加,且以梗死后2 h最为显著(0.207±0.018,P＜0.01).③假手术组心肌组织形态及超微结构改变不明显;AMI组心肌损伤较重,缺血心肌在急性心肌缺血后12 h内,其病理学变化未见显著改变.结论 心肌梗死后心肌组织cPLA2激活导致了心肌细胞及细胞器膜完整性破坏、能量代谢及收缩功能的障碍.     

急性心肌梗死大鼠心脏一氧化氮合酶表达的改变

目的 通过建立大鼠心肌梗死模型，观察急性心肌梗死对大鼠心脏内皮型一氧化氮合酶mRNA和诱导型一氧化氮合酶蛋白表达的影响。方法48只健康成年SD大鼠（体重200～250g）随机分为假手术组和缺血组，取1、2、8和24h四个不同时间点观察。采用开胸结扎冠状动脉左前降支建立心肌缺血模型，逆转录聚合酶链反应检测大鼠心肌梗死后1、2及24h三个时段缺血心肌内皮型一氧化氮合酶mRNA的表达；免疫组织化学染色检测冠状动脉结扎后8h缺血心肌诱导型一氧化氮合酶蛋白的表达。结果冠状动脉结扎后2h，缺血组大鼠缺血心肌组织内皮型一氧化氮合酶mRNA表达下降（P〈0．05），并持续至结扎后24h；结扎后24h组内皮型一氧化氮mRNA的表达与结扎后2h组相比无显著性差异（P〉0．05）。冠状动脉结扎后8h，梗死区存活心肌组织细胞诱导型一氧化氮合酶蛋白大量表达，而假手术组未见诱导型一氧化氮合酶蛋白表达。结论正常大鼠心肌组织有内皮型一氧化氮合酶基因表达，无诱导型一氧化氮合酶蛋白表达。在心肌梗死早期缺血心肌内皮型一氧化氮合酶mRNA表达减少。心肌急性缺血刺激早期诱导大鼠缺血心肌组织诱导型一氧化氮合酶蛋白大量表达。     

What factors determine indium-111 antimyosin monoclonal antibody uptake in patients with myocardial infarction?

The intensity of indium-111 antimyosin monoclonal antibody uptake for visualization of myocardial infarction seems partially dependent on the state of the infarct related coronary artery. The aim of this study is to determine the factors which could account for the monoclonal antibody uptake variability. For this purpose, we investigated 27 patients (mean age 52.7 ± 9.6 years) with a first proven myocardial infarction, by monoclonal antibody scintigraphy and coronary arteriography within the same period of time (7.12 ± 6 days). The monoclonal antibody uptake was quantified by the heart/lung ratio on images recorded 24 h after injection. The infarct size was quantitatively estimated on wall motion analysis of twelve segments in 30° right anterior-oblique view with a radial method. The infarct related coronary artery state was assessed by the Thrombosis in Myocardial Infarction grade and the functional characteristics of collateral vessels by Rentrop's classification. These three variables as well as location of myocardial infarction, left ventricular ejection fraction, administration of a thrombolytic therapy, delay between myocardial infarction and monoclonal antibody scintigraphy were studied using non parametric test, or by linear regression method in order to determine whether these factors would influence the heart/lung ratio. None of these parameters except infarct size was related to heart/lung ratio. Consequently, monoclonal antibody uptake is only dependent on the extent of infarcted myocardium and the intensity of uptake cannot predict the patency of an infarct related coronary artery.     

Scintigraphic assessment of sympathetic innervation after transmural versus nontransmural myocardial infarction

To evaluate the feasibility of detecting denervated myocardium in the infarcted canine heart, the distribution of sympathetic nerve endings using I-123 metaiodobenzylguanidine (MIBG) was compared with the distribution of perfusion using thallium-201, with the aid of color-coded computer functional map in 16 dogs. Twelve dogs underwent myocardial infarction by injection of vinyl latex into the left anterior descending coronary artery (transmural myocardial infarction, n = 6), or ligation of the left anterior descending coronary artery (nontransmural myocardial infarction, n = 6). Four dogs served as sham-operated controls. Image patterns were compared with tissue norepinephrine content and with histofluorescence microscopic findings in biopsy specimens. Hearts with transmural infarction showed zones of absent MIBG and thallium, indicating scar. Adjacent and distal regions showed reduced MIBG but normal thallium uptake, indicating viable but denervated myocardium. Denervation distal to infarction was confirmed by reduced norepinephrine content and absence of nerve fluorescence. Nontransmural myocardial infarction showed zones of wall thinning with decreased thallium uptake and a greater reduction or absence of MIBG localized to the region of the infarct, with minimal extension of denervation beyond the infarct. Norepinephrine content was significantly reduced in the infarct zone, and nerve fluorescence was absent. These findings suggest that 1) MIBG imaging can detect viable and perfused but denervated myocardium after infarction; and 2) as opposed to the distal denervation produced by transmural infarction, nontransmural infarction may lead to regional ischemic damage of sympathetic nerves, but may spare subepicardial nerve trunks that course through the region of infarction to provide a source of innervation to distal areas of myocardium.     

Myocardial scintigraphy by infarct-avid radiotracers

Specific radioindicators are sequestered by acute myocardial infarctions, and their uptake is detectable by external detection systems, such as the Anger scintillation camera. The resultant scintigraphic image may be used to estimate infarct size, although inferior and subendocardial infarcts may pose difficulties. Infarct localization as to anatomic area of the heart is also reasonably accurate.The majority of the clinical experience has been with technetium chelates, particularly ^99mTc-tetracycline and ^99mTc-pyrophosphate. Optimal imaging with ^99mTc-tetracycline is within the first 3 days after infarction, with gradual return to normal of the scintigraphic appearance after this time. While larger infarcts remain positive for longer periods of time, significant uptake or reappearance of uptake after the initial period may be helpful in the identification of reinfarction or extension after an initial infarct. Tetracycline appears to be sequestered only by acutely infarcted myocardium, and therefore is a sensitive agent for distinguishing normal, previously infarcted, and ischemic myocardium from acutely infarcted myocardium.The major clinical experience has been with ^99mTc-pyrophosphate, a bone-seeking radionuclide. The major advantage of ^99mTc-pyrophosphate over ^99mTc-tetracycline is the earlier imaging interval. Optimal scans are obtained at 1–2 days after infarction and only 90 min after the administration of ^99mTc-pyrophosphate (as opposed to 24 hr with ^99mTc-tetracycline). While ^99mTc-pyrophosphate is a quite sensitive indicator of infarction, there is suggestive evidence that ischemic as well as infarcted myocardium sequesters the agent. In addition, various other conditions, including cardioversion, rib fractures, left ventricular aneurysms, and breast tumors may cause uptake of ^99mTc-pyrophosphate and lead to false positive myocardial infarct scintigrams. Thus, while only a few patients with negative scans who have been imaged at the appropriate time will turn out to have clinically detectable infarcts, a somewhat larger number without infarction will have positive scans, particularly those patients with unstable angina pectoris but without clinical infarction.While the final role of acute myocardial scintigraphy remains to be determined, its contribution to the further understanding of the pathogenesis of ischemia and infarction, as well as its clinical utility, has been significant.     

Delineation of acute myocardial infarction with dysprosium DTPA-BMA: influence of dose of magnetic susceptibility contrast medium.

OBJECTIVES. The contrast enhancement of acutely infarcted myocardium produced by the nonionic magnetic susceptibility-enhancing agent dysprosium diethylenetriamine pentaacetic acid-bis-methylamide (DyDTPA-BMA [S-043 Injection]) was assessed in the current study to establish the lowest dose that would yield optimal contrast between normal and acutely infarcted myocardium. BACKGROUND. Magnetic susceptibility contrast agents enhance differences between normal and ischemic tissue by reducing the signal of the normally perfused tissue to which they distribute. METHODS. Acute myocardial infarctions were produced by ligation of the left coronary artery. At 3 to 4 h after occlusion, a dose of 0.1, 0.3 or 0.5 mmol/kg of DyDTPA-BMA was injected intravenously into eight rats each in group 1, 2 or 3, respectively; a fourth group of seven rats served as a control group. Nuclear magnetic resonance (NMR) transverse relaxation time (T2)-weighted images (electrocardiographically gated to every 5th beat, echo delay time [TE] = 60 ms) were acquired before and for 1 h after administration of contrast agent. RESULTS. Images obtained before the injection of contrast agent showed moderate differences in signal intensity between normal and infarcted myocardium (p < 0.05). The contrast enhancement and the duration of delineation between infarcted and normal myocardium produced by this agent were dose dependent. At doses of 0.1, 0.3 and 0.5 mmol/kg, DyDTPA-BMA produced signal loss in normal myocardium: 63 +/- 5%, 41 +/- 4% and 28 +/- 4% of the baseline values, respectively, without any significant reduction in signal intensity of the infarcted region. The reduction in signal of normal myocardium and delineation of the infarct persisted for 5 min at a dose of 0.1 mmol/kg, for 20 min at a dose of 0.3 mmol/kg and for 40 min at a dose of 0.5 mmol/kg. No change in signal intensity or signal intensity ratio between normal and infarcted myocardium was observed in the control group during the same observation period. CONCLUSIONS. These results suggest that low doses of this agent, comparable to those of longitudinal relaxation time (T1)-enhancing agents, can delineate acutely infarcted myocardium. A dose of 0.3 mmol/kg of DyDTPA-BMA (S-043 Injection) provides reasonably persistent demarcation of acute myocardial infarction. Because this dose dramatically suppresses the NMR signal of normal myocardium, it shows the infarcted region as a region of high intensity (bright spot) on NMR images.     

Usefulness of ultrafast magnetic resonance imaging in healed myocardial infarction.

The value of ultrafast magnetic resonance imaging (MRI) in the assessment of dynamic contrast enhancement and myocardial perfusion abnormalities was evaluated in 20 patients with healed myocardial infarction, who also underwent 2-dimensional echocardiography. At baseline and after bolus injection of the paramagnetic contrast agent gadolinium-diethylenetriaminepentaacetic acid (DTPA) (0.04 mmol/kg body weight), single-level short-axis MRI was performed every third RR interval with an acquisition time of 500 ms. Myocardial signal intensities were measured in transmural myocardial regions of interest. After gadolinium-DTPA injection, infarcted and normal myocardium demonstrated a signal intensity enhancement of 50 and 134%, respectively (p < 0.001). A signal intensity of normal relative to infarcted myocardium increased from 1.25 +/- 0.22 (SD) before to 1.91 +/- 0.41 after gadolinium-DTPA (p < 0.001). The rate of signal increase in the infarcted and normal myocardium was 5.17 +/- 2.22 and 18.99 +/- 9.96 s-1 (p < 0.001), respectively. Ultrafast MRI using gadolinium-DTPA bolus administration clearly identifies myocardial perfusion abnormalities in patients with healed myocardial infarction. The infarct site on MRI corresponded with the location of wall motion asynergy determined by echocardiography. It is concluded that gadolinium-DTPA-enhanced ultrafast MRI provides noninvasive assessment of myocardial perfusion in patients with proven coronary artery disease.     

Correlation of acute myocardial infarct scintigraphy with postmortem studies.

Acute myocardial infarct scintigraphy with technetium-99m-pyrophosphate was performed in a patient with an acute massive transmural infarct. The patient died 12 hours later, and postmortem tracer studies demonstrated a tracer concentration ratio of 13:1 between acutely infarcted myocardium and normal myocardium remote from the infarct. The concentration of tracer in tissue bordering on the infarct but without histologic evidence of acute infarction was 1.5 times that in normal tissue remote from the infarct. In vitro scintigraphy of the excised heart revealed a pattern of tracer distribution similar to that of scintiscans obtained before death. The biologic distribution of 99mTc-pyrophosphate, with large tracer concentrations only within the acutely infarcted tissue, suggests that acute myocardial infarct scintigraphy can be used to estimate the extent of an acute myocardial infarct.     

Monoclonal antibodies specific for human cardiac myosin: selection, characterization and experimental myocardial infarct imaging

Radiolabelled anti-myosin antibodies (AM Ab) specifically accumulatein necrotizing myocytes and, therefore, allow the scintigraphicdetection of myocardial infarction. In order to provide a constantsupply of myosin-specific antibodies, the somatic cell fusiontechnique was used for the selection and propagation of A MAb. Out of 126 antibody producing cell lines, nine were selectedfor further subcloning, due to their high affinity for purifiedmyosin. For the in vivo imaging, two IgG-antibody moleculesappeared particularly useful based on their antigenic specificityas assessed by immunoblotting and indirect immunofluorescencetechnique. After radiolabelling with iodine-123, undigestedantibody molecules or their Fab fragments were injected into10 dogs with experimental myocardial infarction. The accumulationof radioactivity in myocardial infarction was assessed by invivo imaging and in vitro scintigraphy of ventricular slicesstained by tetrazolium. The use of undigested AM Ab resultedin a high uptake ratio of radioactivity in the infarcted ascompared to normal myocardium (20: 1). In vivo infarct imaging,however, was not possible due to sustained labelling of theblood pool. The uptake ratio of iodine-123 labelled Fab fragmentswas only 9 1, but due to a faster plasma clearance of the Fabfragments, uptake in the heart could be visualized 5 h afterintravenous injection. Clear differentiation between infarctedand noninfarcted myocardium, however, was limited by accumulationof radioactivity in the thoracotomy wound, in the liver, andin the stomach.     

Imaging and characterization of acute myocardial infarction in vivo by gated nuclear magnetic resonance

Imaging by nuclear magnetic resonance (NMR) techniques has been shown to provide high-contrast resolution between soft tissues and characterization of normal and pathologic tissues by differences in magnetic relaxation times. The current study was designed to determine whether electrocardiogram (ECG)-gated NMR imaging of the canine heart in vivo could distinguish normal from infarcted myocardium without the use of intravenous paramagnetic contrast agents. Seven dogs were studied by ECG-gated NMR imaging in vivo (spin-echo technique) with a 0.35 Tesla superconducting magnet at 2 to 7 days after ligation of the left anterior descending coronary artery. In six of the seven dogs, signal intensity was increased in the anterior wall compared with the remainder of the left ventricle; this region of high signal intensity corresponded to the area of myocardial infarction demonstrated at postmortem examination. The signal intensity of the infarcted region was 66 +/- 27% greater than that of normal myocardium (p less than .01). The T2 (spin-spin) relaxation time was 69 +/- 3% longer in the infarcted myocardium as compared with normal myocardium (p less than .01). The NMR images from the seventh dog had uniform signal intensity throughout the myocardium of the left ventricle. An infarct was not evident on postmortem examination in this dog. Thus gated NMR imaging in vivo by the spin-echo technique displays acute myocardial infarctions as regions of high signal intensity without the use of contrast media. The infarct is characterized by a prolonged T2 relaxation time.     

Uptake of radioiodinated cardiac specific troponin-I antibodies in myocardial infarction

STUDY OBJECTIVE--To examine the potential diagnostic value of the cardiac myofibrillar protein troponin-I as a target for radiolabelled antibodies in detecting heart damage, the uptake of 131I labelled polyclonal cardiac troponin-I Fab was investigated in necrotic myocardial cells in canine myocardial infarction. DESIGN--Cardiac specific troponin-I Fab was prepared by immunoaffinity chromatography and injected 5 h after coronary artery ligation. Whole body gamma camera scintigraphic images were taken after the injection, and heart slices were examined for the presence of labelled antibody. SUBJECTS--Adult dogs of either sex (n = 6) were used. MEASUREMENTS and MAIN RESULTS--Scintigraphic whole body images at 24 and 40 h after troponin-I Fab injection showed increased 131I-localisation over the apical region of the heart which corresponded to the infarcted areas. Localisation in infarcted tissue was confirmed in isolated heart and histochemically stained heart slice images. Uptake of 131I Fab was up to 24 times greater in necrotic than in normal myocardium and was inversely related to regional blood flow as determined by 141cerium microsphere distribution. Confirmation that 131I Fab uptake was due to direct binding to troponin-I in necrotic cells was obtained by coinjection of non-immune 125I labelled Fab. CONCLUSIONS--Results indicate that troponin-I could act as a suitable target for detecting myocardial necrosis.     

Differential accumulation of radiopaque contrast material in acute myocardial infarction

The differential accumulation of radiographic contrast materials in ischemically damaged and normal myocardium was assessed with direct measurement (fluorescent excitation analysis) of the iodine content of tissue samples from dogs with 48 hour old myocardial infarctions. Tissue samples were obtained 10, 30, 60 and 180 minutes after the intraveneus administration of 2 ml/kg body weight of diatrizoate meglumine and sodium (Renografin-76). At all time intervals, the iodine concentration of infarcted tissue was at least threefold greater than that of normal myocardium. At 180 minutes the ratio between iodine concentration in infarcted myocardium and that in normal myocardium was 8.5 and between that in infarcted myocardium and that in blood was 2.6. The iodine concentration in the liver was similar to or greater than that in the infarcted area at time intervals after 10 minutes. These results suggest that the intraveneus administration of contrast material may facilitate the identification of acutely infarcted myocardium with computerized X-ray transmission tomography.