Acute myocardial infarct imaging with indium-111-labeled monoclonal antimyosin Fab

Indium-111 monoclonal antimyosin Fab scintigraphy was used to detect myocardial necrosis in 52 of 54 patients (96.3%) with acute myocardial infarction. Infarcts were visualized when coronary arteries were persistently occluded (n = 10), became patent after thrombolysis (n = 33), or became patent after spontaneous reperfusion (n = 7). Posteroinferolateral visualizations were obtained in two patients with clinical and enzymatic evidence of infarction but normal electrocardiograms. Of the two patients in whom no infarcts were visualized, one had an anterior myocardial infarct. This patient underwent successful thrombolytic therapy, with attendant minimization of creatine kinase release. The other patient had a small, nonreperfused inferior myocardial infarct. Five patients with a history of remote infarction and acute necrosis showed antimyosin uptake only in regions concordant with the acute episodes of infarction, and radiolabeled antimyosin Fab localized in neither old infarcts nor normal, noninfarcted myocardium. Antimyosin Fab scintigraphy, thus, appears to be a highly specific means of delineating necrotic myocardium, at least in this limited and selected group of patients.     

Clinical trial of 111In-antimyosin antibody imaging: (2). Imaging of myocardial infarction and myocarditis

A new scintigraphic method to detect myocardial necrosis has been developed using antimyosin monoclonal antibody F ab labeled with indium-111 (111In-antimyosin). We investigated 111In-antimyosin scintigraphy in 35 patients with myocardial infarction, 5 patients with myocarditis and 3 patients with angina pectoris. 111In-antimyosin F ab was administered iv and antimyosin images were recorded by planar and single photon emission computed tomography (SPECT) 48-72 hrs after injection. Planar images showed discrete localization of 111In-antimyosin in 26 of 27 patients within 16 days after the onset of acute myocardial infarction in 14 of whom creatine kinase, glutamic oxaloacetic transaminase and lactic dehydrogenase had already normalized. In addition, positive scans were also obtained in 4 of 8 patients 1 to 9 months after the onset of the disease. Three patients with acute myocarditis (two of whom were biopsy-proven) had positive scans 2 and 4 weeks after the onset of the disease. Although mechanism of persistent positive anti-myosin images in the chronic stage remains to be clarified, 111In-antimyosin scintigraphy holds potential promise as a noninvasive method for the detection of myocardial injury.     

Role of noninvasive antimyosin imaging in infants and children with clinically suspected myocarditis.

Endomyocardial biopsy is an invasive procedure, often performed on children for the diagnosis of myocarditis, and is not without risk. Therefore, a noninvasive test of adequate diagnostic accuracy is highly desirable. We evaluated the role of antimyosin scintigraphy in infants and children with clinically suspected myocarditis. METHODS: Forty patients (age range, 2 mo to 14 y) with suspected myocarditis underwent (111)In-antimyosin scintigraphy. All patients were clinically followed for 29 +/- 17 mo; 21 patients underwent serial antimyosin scans (3.8 +/- 1.7 per patient). The antimyosin uptake was assessed by heart-to-lung ratio (HLR). The scan results were compared with endomyocardial biopsy results in 22 patients. RESULTS: Thirty-five of the 40 patients showed abnormal antimyosin findings; 17 patients showed intense myocardial antimyosin uptake (HLR > 2). The HLR was higher in patients presenting within the first 2 mo of illness (2.09 +/- 0.43 vs. 1.74 +/- 0.34, P = 0.01). Of 22 patients with endomyocardial biopsy, 17 demonstrated myocarditis. All 9 patients who had an HLR > 2 and underwent endomyocardial biopsy had histologic evidence of myocarditis. Of the remaining 13 patients with HLR < 2, 8 had biopsy-verified myocarditis (62%). The intensity of antimyosin uptake was the major determinant of survival in children, with a relative risk of 18 (confidence interval, 1.34-242; P = 0.027). High antimyosin uptake (HLR > 2) seen within 2 mo of the onset of symptoms was associated with a higher mortality rate. The survivors with an HLR > 2 and those with an HLR < 2 showed a high likelihood of complete functional recovery. Furthermore, the patients with serial antimyosin scans having persistently positive findings showed a poor clinical outcome. CONCLUSION: Intense myocardial uptake of antimyosin antibody is a reliable indicator of myocarditis in infants and children. Severe myocardial damage detected in the early phase of disease is associated with a higher mortality rate. The persistence of antimyosin uptake is associated with poor clinical outcomes.     

Clinical application of Indium-111 antimyosin antibody and Thallium-201 dual nuclide single photon emission computed tomography in acute myocardial infarction

The significance of indium-111 antimyosin antibody and thallium-201 dual nuclide single photon emission computed tomography (SPECT) was evaluated in 7 patients with acute myocardial infarction (AMI) who underwent emergency coronary angiography with successful revascularization by intracoronary thrombolysis. Indium-111 antimyosin antibody and thallium-201 dual nuclide SPECT was performed 11 to 36 days after the onset of AMI. Antimyosin SPECT images delineated areas of myocardial necrosis in all 7 patients (100%), but planar images detected necrotic areas in only 4 of 7 patients (57%). Peak CPK-MBs of the 3 patients in which no necrotic area was detected by indium-111 planar image showed a tendency to be smaller. Indium-111 antimyosin antibody/thallium-201 overlap was observed in all patients. The area of overlap was at the center of necrosis in 4 patients (2 anterior infarction, 1 inferior infarction, 1 inferolateral infarction) and at the peripheral portion in 3 patients (all 3 had inferior infarction). Indium-111 antimyosin antibody and thallium-201 dual nuclide SPECT is useful in identifying the localization of myocardial infarction and the overlap of these tracers might reflect the presence of salvaged myocardium adjacent to the necrotic myocardium.     

Fluorine-18-antimyosin monoclonal antibody fragments: preliminary investigations in a canine myocardial infarct model.

The purpose of this study was to determine in a canine model whether selective myocardial infarct uptake of 18F-labeled antimyosin monoclonal antibody fragments could be achieved in a time frame compatible with the short half-life of this nuclide. Antimyosin monoclonal antibody fragments were labeled with 18F using a succinimidyl [18F]fluorobenzylamine ester acylation agent. Six dogs had myocardial infarction induced by coronary artery occlusion and were reperfused prior to the intravenous administration of 0.6-4.7 mCi of 18F-labeled F(ab')2 (two dogs) or Fab (four dogs). Analysis of tissues obtained 2-4 hr after antibody administration revealed infarct:normal myocardium uptake ratios as high as 14-21:1 for F(ab')2 and 9-12:1 for Fab. Even with Fab, however, prolonged 18F activity in the blood pool interfered with delineation of infarcts by PET imaging. In one dog, perfusion imaging with [13N]ammonia before antimyosin administration was performed, and regions of normal and ischemic myocardium were determined. With these regions of interest, infarct:normal myocardium uptake ratios calculated from the 18F-labeled Fab images increased from 1.5:1 at 1 hr to 4.0:1 at 5 hr. We conclude that 18F-labeled antimyosin fragments may be of value for hot-spot imaging of damaged myocardium with PET; however, blood-pool subtraction techniques will probably be required.     

Indium-111-antimyosin images compared with triphenyl tetrazolium chloride staining in a patient six days after myocardial infarction.

The results of indium-111 (111In) antimyosin imaging during life and the findings on postmortem imaging and triphenyl tetrazolium chloride (TTC) staining of the heart are reported from a patient who received 111In-antimyosin on the sixth day following myocardial infarction and died after imaging the next day. The planar images obtained during life showed abnormal 111In-antimyosin uptake in the posterior, lateral, and apical walls of the left ventricle. Autopsy revealed extensive infarction of the left ventricular lateral and posterior walls with cardiac rupture, which was the cause of sudden death. Direct imaging of the sliced specimen of heart revealed abnormal tracer uptake in the lateral and posterior walls of the left ventricle, which correlated closely with the area of necrosis outlined by TTC staining. Our results confirm the experimental findings that antimyosin antibody binds specifically to the acute irreversibly damaged myocardial cells. A high degree of tracer uptake can be seen even when 111In-antimyosin is injected six days postinfarction.     

Accumulation of 111In-antimyosin antibody at the focal site of inflammation

An p6-year-old man with anterior acute myocardial infarction was administered antimyosin antibody labeled with 74 MBq (2 mCi) 111In, and abnormal hot activity was observed in the left lung by immunoscintigraphy. 67Ga-citrate scintigraphy also showed abnormal uptake in this lesion. At this time, this patient complained of fever and cough with sputum, and roentgenography showed a coin lesion-like shadow at the same location of the lung. By treatment with antibiotics, his symptom was improved and coin lesion-like shadow disappeared. So we thought the RI uptake area in the left lung was inflammatory lesion. This case suggests that 111In-antimyosin antibody can be trapped to the focal site of inflammation.     

Scintigraphic quantification of myocardial necrosis using "hot spot" imaging agents in acute myocardial infarction]

Both technetium-99m pyrophosphate/thallium-201 dual nuclide SPECT and indium-111 antimyosin antibody/thallium-201 dual nuclide SPECT were performed in identical 11 patients with acute myocardial infarction. Infarct size was calculated by both hot spot imaging agents on dual nuclide SPECT. Antimyosin accurately accumulated in the infarcted area in all 11 patients on SPECT images corresponding with the electrocardiography, but pyrophosphate accumulated at the site of infarct in 10 of 11 patients. The mean volume obtained from pyrophosphate was 32.5 ml and that from antimyosin was 21.9 ml. The relationship between infarct volume calculated by pyrophosphate and that by antimyosin was linear and correlated well (r = 0.98, p less than 0.001). However the volume of infarction determined with pyrophosphate exceeded that with antimyosin SPECT by 1.64 (p less than 0.001). The reason for this difference is not yet known, but may relate to pyrophosphate uptake in border zones that may or may not be irreversibly injured.     

In-111 antimyosin-Fab uptake in contractile myocardium of old myocardial infarction]

As In-111 monoclonal antimyosin antibody (AM) has been thought to bind with human myosin exposed in myocytes irreversibly damaged by an ischemic event. The AM uptake in contractile myocardium after acute myocardial infarction was studied. AM planar images were obtained 48 hours later after injection of 74 MBq of AM in 6 patients 2-10 months later after acute myocardial infarction. Mean ejection fraction was 66% (75-58). Myocardial AM uptake was definite in comparison with mediastinum uptake in all 6 patients and mean heart lung ratio was 2.3 +/- 0.5. AM SPECT images and T1-201 SPECT images were obtained with dual mode. Mean T1-201 uptake at the region of maximal AM uptake was 77% (90-63). Echocardiography showed contractility of the region. Mean maximal AM uptake in the anterior wall region was 83% (100-75) and mean T1-201 uptake at the region was 81% (90-75) and shortening rate of the region was 34% (52-25). The region with AM uptake has been shown to correlate with the region salvaged from necrosis by reperfusion. It has been shown that AM was uptaken in contractile myocardium in chronic phase of acute myocardial infarction. It was suspected that myocardium under severe ischemic event may be salvaged by reperfusion therapy and retain contractility in chronic phase, however irreversible damage, which permit AM uptake, may remain in myocardium.     

Indium-111 antimyosin monoclonal antibody uptake in patients with cardiomyopathy and myocarditis

Prognostic significance of myocardial uptake of indium-111 antimyosin antibody was evaluated in 17 patients with idiopathic cardiomyopathy; 10 patients with dilated cardiomyopathy and 7 patients with hypertrophic cardiomyopathy. Seven of 10 patients with dilated cardiomyopathy showed positive images. Three of these 7 patients with strongly positive scans died after scintigraphic examination. Six of 7 patients with hypertrophic cardiomyopathy showed positive images. Three of the patients with dilated left ventricle had prominent positive scans and higher heart to lung ratio. The heart to lung ratio of antimyosin uptake in total patients was correlated with left ventricular end-diastolic dimension and ejection fraction measured by echocardiography. In patients with myocarditis, all three patients showed positive scintigrams within 4 weeks after the onset of the disease and 1 of 6 patients was positive thereafter, who had dilated ventricle and decreased cardiac function. Thus, indium-111 antimyosin antibody imaging may be useful to evaluate prognosis of patients with cardiomyopathy and myocarditis.     

Visualization of myocardial infarction 6 h after injection of 111In-antimyosin antibodies using a blood pool subtraction technique.

111In-antimyosin antibodies are capable of visualizing myocardial infarction (MI). Because of slow blood clearance, images are usually recorded 24 or 48 h postinjection. In this pilot study, a blood pool subtraction technique, which makes it possible to visualize MI 6 h postinjection, is validated. Twenty-five patients with proven MI (16 anterior, 9 inferior) were imaged a few minutes, 6 and 24 h after an injection of 111 MBq 111In-labelled antimyosin antibodies. Three planar views are obtained each time. Using software which performs the geometric registration, the grey level normalization and the subtraction of images, the blood pool image (obtained a few minutes postinjection) is subtracted from the 6 h image. The resulting image is the blood pool corrected 6 h image. The 24 h images and the blood pool corrected 6 h images were interpreted blindly and the number of correct, incorrect and impossible MI localizations was counted. The number of correct localizations is 19/25 for the standard 24 h images and 22/25 for the blood pool corrected 6 h images. Then, with this blood pool subtraction method, it is possible to visualize MI 6 h postinjection. This has to be taken into account when discussing the role of antimyosin scintigraphy in the management of patients with MI.     

Myocardial damage assessed by indium-1 11-antimyosin: correlation with persistent enteroviral ribonucleic acid in dilated cardiomyopathy

The persistence of enteroviral ribonucleic acid (RNA) in the myocardium has been implicated as a pathogenetic factor in idiopathic dilated cardiomyopathy. Enteroviral persistence may lead to myocardial cell membrane damage, resulting in increased uptake of antimyosin antibodies. To further evaluate this hypothesis, a direct comparison of myocardial antimyosin uptake with the presence of enteroviral RNA was performed in ten patients (one female, nine male; 53±8 years) with chronic dilated cardiomyopathy. Planar antimyosin images were obtained 48 h after the injection of indium-111-labelled antimyosin Fab. Using a region of interest technique, the heart to lung uptake ratio (HLR) was calculated as a semiquantitative parameter of myocardial tracer uptake. Cardiac catheterization was performed to assess left ventricular function and to obtain myocardial biopsy samples. In the biopsy samples, gene amplification by polymerase chain reaction (PCR) was used to specifically detect enteroviral RNA. In the ten patients, the left ventricular ejection fraction was 39%±11% and the end-diastolic volume 131±46 ml/m². The HLR was 1.72±0.21 and showed no correlation with functional parameters. In two patients with a positive PCR consistent with persisting enteroviral RNA, the HLR was not higher than that in eight patients with a negative PCR (1.46±0.18 vs 1.78±0.18, respectively). These results suggest that increased uptake of¹¹¹In-antimyosin in chronic idiopathic dilated cardiomyopathy cannot be explained by pure persistence of enteroviral RNA. Other pathogenetic factors such as myocardial autoantibodies or microvascular spasm may be responsible for myocyte membrane damage detected by antimyosin.     

Antimyosin uptake and myofibrillarlysis in dilated cardiomyopathy

Background

Although antimyosin scintigraphy detects myocyte necrosis associated with myocarditis, it has also been reported to yield positive results in a large number of patients with clinical dilated cardiomyopathy without histologic evidence of myocarditis. The question to be resolved is whether this discordance represents false-positive results of antimyosin scans or whether antimyosin scintigraphy more accurately identifies the presence of myocyte necrosis than does endomyocardial biopsy testing.

Methods and Results

Forty patients with the acute onset of dilated cardiomyopathy (left ventricular ejection fraction <45%; mean 27%±11%) but no endomyocardial biopsy evidence of myocarditis, were identified from a consecutive series of 50 patients who had undergone indium 111 antimyosin antibody scintigraphy and endomyocardial biopsy for suspected myocarditis. The endomyocardial biopsy specimens were analyzed to identify features correlating with antimyosin uptake or improvement in left ventricular ejection fraction (LVEF) over time. Twenty-five patients showed left ventricular myocardial uptake of radiolabeled antimyosin antibody by both planar and tomographic imaging. The remaining 15 patients had no antimyosin uptake. Of the 25, 22 (88%) patients with positive findings on antimyosin scans had degenerated, myofibrillarlytic myocytes in their biopsy specimens. Of the 15 patients with negative findings on antimyosin scans, only 6 (40%) had similar myofibrillarlytic myocytes (χ²; p<0.0047). No other histological feature correlated with the antimyosin positivity. Stepwise multiple regression analysis was performed for identification of predictors of short-term improvement in LVEF. Patients with positive findings on antimyosin scans showed a trend toward improvement with time (F=3.97; p>0.05). None of the histologic features predicted improvement in the LVEF. However, the combination of positive findings on an antimyosin scan and myofibrillarlysis did correlate significantly with spontaneous improvement in ejection fraction (F=4.53; 0.01; <p<0.05).

Conclusions

This study identifies myofibrillarlysis as a common pathologic alteration in patients with recent onset of dilated cardiomyopathy and positive findings on antimyosin scan, who lack right ventricular biopsy evidence of myocarditis. Because myofibrillarlytic cell population may represent a histologic spectrum of viable to necrotic myocytes, it appears that antimyosin uptake detects necrotic myofibrillarlytic myocytes that are not identified by light microscopy.     

111In-antimyosin scintigraphy on acute myocardial infarction]

Indium-111 antimyosin (InAM) scintigraphy was performed in 17 patients with acute myocardial infarction (on 15 +/- 6 days from the onset). The degree of myocardial uptake was classified into 3 groups. They were ranged from low intensity as in bone marrow to high intensity as in liver. All of 17 cases showed positive myocardial uptake including low intensity. The locations of infarction judged by InAM were in agreement with those by electrocardiography, coronary angiography (CAG), and 99mTc-pyrophosphate scintigraphy (PYP, performed on 5 +/- 2 days from the onset). In 5 cases, the uptake of InAM showed doughnuts or diffuse pattern which was occasionally observed on PYP. These cases showed myocardial uptake of 4th degree of Parkey's classification with doughnuts-like pattern on PYP, and showed involvement of left anterior descending artery on CAG. In some cases, the extent of myocardial uptake on InAM did not agree with those on PYP.     

Immunoscintigraphy with 111In antimyosin Fab

Monoclonal 111In antimyosin Fab is a marker for myocytes which have lost their membrane integrity. Because of the slow blood pool clearance of the radiopharmaceutical, imaging is usually started 24-48 h after intravenous injection of 74 MBq of the tracer. This long postinjection interval restricts its utilization in the primary diagnosis of acute myocardial infarction. However, antimyosin may help to differentiate between necrotic and viable myocardium in the subacute stage of incomplete myocardial infarction. Serial endomyocardial biopsy for early detection of transplant rejection after heart transplantation may be partially replaced or supplemented by antimyosin scintigraphy. The compound may facilitate the diagnosis of myocarditis. Other potential indications may be prognostic assessment of dilated cardiomyopathy, monitoring cardiotoxic side-effects of chemotherapeutics, recognition of cardiac contusion as well as diagnosis of rhabdo- and leiomyosarcoma. In specific clinical situations 111In antimyosin Fab immunoscintigraphy may provide valuable diagnostic information.     

Assessment of myocardial necrosis by 111In-antimyosin F ab scintigraphy

111In-antimyosin F ab (AM) myocardial scintigraphy was carried out in (A) 13 patients with acute myocardial infarction (9.9 +/- 2.2 days from the onset) and (B) 9 with myocarditis and/or dilated cardiomyopathy. Forty eight hours after injection of AM, the patients were injected with 74 MBq (2 mCi) of thallium-201 (TL). The two sets of Planar and SPECT image were obtained simultaneously using dual energy window sets. In group A, positive focal AM uptake was demonstrated in 12 (92%) patients. Higher AM uptake was observed in patients who had PTCR/PTCA. By combination with TL, it is useful to detect inferior infarction and to differentiate old from acute infarction. Dual SPECT images gave precise information about the infarcted area. In group B, positive diffuse AM uptake was demonstrated in 7 (77%) patients. In conclusion, AM myocardial scintigraphy was proven to be useful for the assessment of acute necrosis after myocardial infarction but also on-going necrosis of myocarditis and/or myopathy.     

Assessment of myocardial damage in dilated-phase hypertrophic cardiomyopathy by using indium-111-antimyosin Fab myocardial scintigraphy

For the detection of myocardial cell damage, an 111In-antimyosin Fab study was carried out on seven patients (Group A) in the dilated phase of hypertrophic cardiomyopathy, seven patients (Group B) with dilated cardiomyopathy, and eight control patients (Group C). Imaging was done 48 hr after intravenous injection of 74 MBq of 111In-antimyosin Fab. Myocardial antimyosin uptake was visually graded as 0, +1, +2 or +3. A score of +2 or +3 was considered positive. The heart/lung ratio of antimyosin uptake (antimyosin index) also was determined. Antimyosin uptake was positive in seven (100%), nine (90%) and no (0%) patients in Groups A, B, and C, respectively. The antimyosin index in Groups A and B was 2.46 +/- 0.49 and 2.04 +/- 0.24, respectively, findings were significantly higher than that in Group C (1.51 +/- 0.13) (p less than 0.01). Positive biopsy findings were noted in only two patients in Group A. Thus, antimyosin uptake was increased in dilated phase hypertrophic cardiomyopathy and dilated cardiomyopathy, which suggests ongoing necrotic changes in these patients.     

Imaging of acute myocardial infarction in pigs with Indium-111 monoclonal antimyosin scintigraphy and MRI

Indium-111 antimyosin F(ab')2 was used in a series of scintigraphic studies on experimentally induced myocardial infarctions in pigs. Antimyosin distribution recorded by planar images of in vivo pigs and by single photon emission computed tomography (SPECT) of excised hearts delineated areas of myocardial necrosis if infarct volume exceeded 3.3 cm3. Scintigraphic images were compared with magnetic resonance images (MRI) obtained from excised hearts and with photographs of slices of the hearts. Infarct size and localization determined with antimyosin were compared. The MR images, with or without gadolinium-DTPA (Gd-DTPA), of the in vivo pigs were all false-negative; some myocardial wall thinning and high bloodpool signals were visible. Results show that both the antimyosin and the MR technique are specific methods for the visualization of induced myocardial necrosis in this animal model. However, the use of antimyosin is limited to a period ranging from 24 to 72 hours after infarction.     

Imaging of cardiac transplantation rejection in primates using two new antimyosin agents.

Indium-111-labeled monoclonal antimyosin Fab has been used to image myocardial infarction, myocarditis and cardiac transplant rejection with localization in myocytes that have suffered irreversible loss of cell membrane integrity. Technical factors potentially limiting clinical usefulness of 111In antimyosin include dosimetry (72 hr half-life of 111In), slow blood clearance of antibody proteins delaying optimal imaging to 24 to 48 hr postinjection and nontarget organ uptake. Therefore, two new antimyosin imaging agents experimentally shown to potentially improve dosimetry, shorten time from injection to imaging or decrease nonspecific cell binding were evaluated in a primate cardiac transplant model. The two agents evaluated were polylysine 111In-antimyosin (0.023 mg Fab modified with a 3.3 kd polymer of polylysine and labeled with 111In) and 99mTc-antimyosin (0.5 mg Fab' antimyosin labeled using the RP-1 ligand technique). A total of eight baboons were studied: three with heterotopic (cervical) xenographs, three with orthotopic allographs and two control animals. Each animal was injected first with 12-23 mCi of 99mTc-RP-1 antimyosin and 5-16 hr after completion of imaging, was injected with 0.72-1.88 mCi of 111In-polylysine antimyosin (PIs) and reimaged 12-48 hr later. The imaging results were compared to the histology of the animals. Biexponential curves were fit to the blood sample data and rate constants were determined and expressed as T1/2 values. There were no significant differences between the two agents in either the early fast components or the late slow components. On planar imaging, there was blood-pool activity at 10-12 hr postinjection of both agents, but by 16-24 hr postinjection, blood pool was negligible on the 111In-PIs scans. Both agents were concentrated in the rejected cardiac tissue. The slow blood-pool clearance combined with the 6 hr half-life of 99mTc-RP-1 AMA make this agent less promising for detection of diffuse myocardial uptake than 111In Fab modified with polylysine.     

111In-antimyosin Fab scintigraphy in cardiovascular diseases: (multicenter clinical trial)

In a multicenter study, a total of 380 patients with myocardial infarction, myocarditis and cardiomyopathy underwent 111In-Antimyosin Fab myocardial imaging. 111In-Antimyosin Fab was administered intravenously and myocardial images were obtained 48 hours later. Only 3 patients developed mild adverse effects. Human antimouse antibodies were detected in 7 patients. Positive scans in patients with myocardial infarction were seen in 92/119 (77%) within 2 weeks after the onset of myocardial infarction, in 58/71 (82%) at 3-4 weeks, in 20/22 (91%) at 4-8 weeks and 17/31 (55%) thereafter. The location of myocardial damage delineated by 111In-Antimyosin Fab imaging was concordant with the infarct location by ECG and coronary angiography. In patients with myocarditis, 111In-Antimyosin Fab uptake was positive in 7/12 (58%) within 8 weeks and 6/17 (35%) thereafter. Positive 111In-Antimyosin Fab scans were seen in 12/36 (33%) in dilated cardiomyopathy and in 17/19 (89%) in hypertrophic cardiomyopathy. Although the mechanism of persistently positive 111In-Antimyosin Fab images in the subacute to chronic stage of myocardial infarction and myocarditis remains to be clarified, 111In-Antimyosin Fab may be useful for the detection of the diseases and in evaluating the prognosis of patients with cardiomyopathy.