Antimyosin Scan Research Articles

Myocardial cell damage in human hypertension

OBJECTIVESThe goal of this study was to investigate the presence of myocardial cell damage in patients with systemic hypertension and its relationship with left ventricular hypertrophy (LVH).BACKGROUNDAlthough initially compensatory, LVH adversely affects myocellular integrity and contributes to congestive heart failure in hypertensive patients. Noninvasive detection of myocardial damage can be of value.METHODSWe performed imaging studies with 111In-labeled monoclonal antimyosin antibodies to identify myocardial damage in 39 patients with systemic hypertension and variable degrees of LVH. Three groups were considered: 16 asymptomatic patients with normal echocardiographic left ventricular mass (LVM) (group I); 14 asymptomatic patients with LVH (group II) and 9 patients with symptomatic hypertensive heart disease and advanced LVH (group III). The severity of myocardial damage was represented as heart-to-lung (target-to-background) antibody uptake ratio (normal: <1.55).RESULTSMean LVM index was 105 ± 14 g/m2 in group I, 124 ± 24 in group II and 174 ± 29 in group III. Heart-to-lung ratios of antimyosin uptake were: 1.45 ± 0.14 in group I, 4 of the 16 (25%) patients showing an abnormal scan; 1.50 ± 0.07 in group II with abnormal scans in 2 of the 14 (16%) patients and 1.77 ± 0.16 (p < 0.001) in group III, all 9 patients presenting with abnormal antimyosin scans. On multivariate regression analysis LVM index was the main variable that independently correlated with the degree of myocardial uptake of antimyosin (r = 0.815; p = 0.001).CONCLUSIONSThis study provides the first in vivo evidence of myocyte damage in patients with hypertension. The severity of myocardial damage can be related to the magnitude of LVH.

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.

Antimyosin scintigraphy and immunohistologic analysis of endomyocardial biopsy in patients with clinically suspected myocarditis—evidence of myocardial cell damage and inflammation in the absence of histologic signs of myocarditis

Objectives. This study compares the results of antimyosin scintigraphy in patients with clinically suspected myocarditis with histologic and immunohistologic findings in the endomyocardial biopsy.Background. In patients with clinically suspected myocarditis, antimyosin scintigraphy often demonstrates myocardial cell damage but histologic evaluation of the endomyocardial biopsy often fails to show evidence of myocarditis. Recently developed immunohistologic techniques appear to be more sensitive for the detection of myocardial inflammation than histologic analysis alone. Studies comparing antimyosin scintigraphy and immunohistologic analysis of the endomyocardial biopsy in patients with clinically suspected myocarditis are not yet available.Methods. Sixty-five patients with clinically suspected myocarditis underwent antimyosin scintigraphy. Antimyosin antibody uptake was correlated with histologic and immunohistologic findings in the endomyocardial biopsy.Results. Antimyosin scintigraphy showed evidence of myocardial cell damage in 36 (55%) of the 65 patients and was negative in 29 (45%) patients. Histologic analysis of the endomyocardial biopsy revealed myocarditis in nine patients: six had a positive and three had a negative antimyosin scan, respectively. Thirty (83%) of 36 patients with evidence of myocardial cell damage on antimyosin scintigraphy were histologically negative for myocarditis. Immunohistologic analysis showed evidence of myocarditis in 31 (86%) of 36 patients with a positive antimyosin scan and also in 17 (59%) of 29 patients with a normal scan (p < 0.047).Conclusions. Antimyosin scintigraphy often shows myocyte injury in patients with clinically suspected myocarditis. Histologic analysis of the endomyocardial biopsy alone is often negative, but additional immunohistologic analysis of the endomyocardial biopsy frequently provides evidence of myocardial inflammation in these patients. With immunohistologic analysis as the reference method, antimyosin scintigraphy has a high specificity but a lower sensitivity for the detection of myocarditis.

Antimyosin scintigraphy for diagnosis and follow-up of patients with clinically suspected myocarditis

Antimyosin-scintigraphy is believed to have a high specificity but a low sensitivity for the diagnosis of myocarditis when histological analysis of endomyocardial biopsy is used as the reference method. However, the histological evaluation itself seems to have a low sensitivity for the diagnosis of myocarditis. Therefore, immunohistological techniques have been developed for the detection of lymphocytic infiltrates and increased expression of HLA antigens in the myocardium. The present study compares the results of antimyosin-scintigraphy with histological and immunohistological analysis of the endomyocardial biopsy. 65 patients with clinically suspected myocarditis underwent antimyosin-scintigraphy and histological and immunohistological analysis of the endomyocardial biopsy. Myocarditis could be diagnosed histologically in only 9/36 (25%) patients with a positive antimyosin scan but additional immunohistological analysis revealed lymphocytic infiltrates in 31 (86%) of these patients. In 29 patients with a normal antimyosin scan, histological analysis showed evidence of myocarditis in 3 (10%) patients; additional immunohistological evaluation disclosed lymphocytic infiltrates in 17 (59%) patients. With immunohistological analysis of the endomyocardial biopsy as the reference method, antimyosin-scintigraphy has a high sensitivity but a lower specificity for the diagnosis of myocarditis. Detection of autoantibodies against human cardiac myosin in patients with myocarditis is associated with a significantly lower incidence of positive antimyosin scans in these patients. Antimyosin-scintigraphy was repeated after six months in 14 patients with myocarditis. Histological and immunohistological evaluation of the endomyocardial biopsy now showed persistent myocarditis in 3/8 patients with a positive antimyosin scan and in 5/6 patients with a normal antimyosin scan.

Myocardial damage does not occur in untreated hyperthyroidism unless associated with congestive heart failure

Even in the absence of underlying cardiac disease, hyperthyroidism has seldom been reported to be associated with left ventricular dysfunction and congestive heart failure. The left ventricular function invariably improves with achievement of euthyroid status. Anecdotal autopsy reports have suggested that myocardial necrosis associated with hyperthyroidism may be responsible for congestive heart failure. This study prospectively evaluates the role of myocardial necrosis in untreated hyperthyroidism by imaging with Indium-111 antimyosin antibody. Thirteen consecutive patients (7 men and 6 women, mean age 36 ± 11 years) with hyperthyroidism and Graves' disease (10 patients), subacute thyroiditis (2 patients), or multinodular goiter (1 patient) formed the basis of the study. The T4 levels ranged from 33 to 183 pmol/L (mean 103 ± 47 pmol/L) and cardiac output from 5.47 to 11.0 L/min (mean 7.17 ± 1.75 L/min). Two patients had clinical congestive heart failure and mildly depressed left ventricular ejection fraction. Both patients had scintigraphic evidence of myocardial damage with abnormal antimyosin scans. In the remaining 11 patients with normal left ventricular ejection fraction, no antimyosin uptake was observed. The reevaluation of two patients with abnormal initial scans 6 to 8 months after treatment revealed euthyroid status, resolution of antimyosin uptake, and normalization of left ventricular function. This study indicates that myocardial necrosis may be detected in a small proportion of patients with hyperthyroidism, which could contribute to left ventricular systolic dysfunction. (Am Heart J 1997;134:1133-7.)

Usefulness of antimyosin scan in myocarditis

Usefulness of antimyosin scan in myocarditis

Diagnostic accuracy of antimyosin scintigraphy in suspected myocarditis

Background. Radiolabeled antibody specific for cardiac myosin administered intravenously has been used to define noninvasively regions of myocardial necrosis. Inflammatory heart disorders such as myocarditis and heart transplant rejection demonstrate diffuse and often faint myocardial uptake of antimyosin antibody. This study was undertaken to evaluate the reproducibility and diagnostic accuracy of antimyosin antibody imaging for the detection of patients with suspected myocarditis. Methods and Results. Fifty antimyosin scans, performed consecutively in patients with suspected myocarditis, were evaluated by one independent observer and two panels of observers. Antimyosin scan interpretations were compared with endomyocardial biopsy results and also with serial changes in left ventricular function. An independent observer (A) and a panel of five observers (A through E) interpreted the antimyosin scans as positive or negative on the basis of both planar images and tomographic reconstructions. Three of the five observers (A through C) again interpreted the scans but based interpretation only on planar images. Blinded random sequence evaluation of antimyosin scans based on the planar and tomographic interpretations revealed moderate agreement between the independent observer (A) and the group of observers (A through E) (κ = 0.58). There was also moderate agreement between interpretations based on planar images alone and interpretations based on both planar and tomographic images ( κ [A through E] [A through C] = 0.57; κ [A through C] A = 0.48 ). Comparison of antimyosin scan results with histologic evidence of myocarditis in endomyocardial biopsy specimens demonstrated that all scan results obtained from the individual or the panels of observers had a very high sensitivity (91% to 100%) and a high negative predictive value (93% to 100%). The specificity (31% to 44%) and positive predictive value (28% to 33%) were less impressive. We also compared the scan and biopsy results with the composite clinical standard of significant left ventricular functional improvement. Endomyocardial biopsy demonstrated poor sensitivity (35%) compared with antimyosin scans (82% to 94%) but had superior specificity (endomyocardial biopsy, 79%; antimyosin scan, 25% to 42%). The specificity of interpretations based on planar and tomographic interpretations (38% to 42%) was better than the planar images alone (25%). If reversible left ventricular dysfunction is considered clinical evidence of myocarditis, this study suggests that a negative endomyocardial biopsy significantly misses the presence of the disease. On the other hand, a negative antimyosin scan almost invariably excludes myocarditis. Conclusions. This study demonstrates a high degree of interobserver reproducibility of antimyosin interpretation. Comparison of the scintigraphic results with histologic and clinical standards indicates a high sensitivity of antimyosin scans for the detection of myocarditis. The antimyosin scan is also not likely to miss clinically or pathologically diagnosed myocarditis, in contrast to the endomyocardial biopsy, which missed clinically validated myocarditis 65% of time. The combination of high sensitivity and negative predictive value suggests that antimyosin scintigraphy may be an effective screening procedure for obviating biopsies in patients with suspected myocarditis.

Antimyosin uptake and myofibrillarlysis in dilated cardiomyopathy.

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. 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 (chi 2 = 8.13; 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). 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.

Natural evolution of antimyosin scan and cardiac function in patients with acute myocarditis

Indium-111 monoclonal antimyosin antibody imaging is a convenient method to diagnose acute myocarditis. The present study examined the natural evolution of a positive antimyosin scan in 10 patients with acute myocarditis, in relation to left ventricular ejection fraction. All patients underwent myosin-specific monoclonal antibody imaging and radionuclide ventriculography; in all patients endomyocardial biopsy was performed. Repeat assessment of left ventricular function and antimyosin uptake was performed 1, 2 and 6 months later. A heart-to-lung ratio was used to quantify antimyosin uptake. Heart-to-lung ratio in patients with myocarditis was 2.12 ± 0.31, significantly higher than that observed in eight controls (1.35 ± 0.08, P < 0.001). During follow-up 2.2 repeat scans per patient were performed. Heart-to-lung ratio normalized (< 1.6) within 1 month in four patients, within 2 months in one patient and within 6 months in two patients; three patients continued to have a positive antimyosin uptake at 6 months, suggesting ongoing myocardial necrosis. At the end of follow-up, ejection fraction improved by > 5% in four patients; normalization or persistence of tracer uptake could not predict an improvement of ejection fraction. It is concluded that antimyosin scintigraphy is useful for diagnosing myocarditis in its subacute or chronic stage during which unknown or immune mechanisms may be in operation. An improvement in left ventricular function cannot be predicted on the basis of persistence or not of tracer uptake.

Myocardial uptake of indium-111 antimyosin after coronary angioplasty. Relationship with the total burden of ischaemia.

Indium-111 antimyosin scintigraphy was performed in 24 consecutive patients after percutaneous transluminal coronary angioplasty to assess whether repeated periods of ischaemia during balloon inflation results in myocardial cell damage even after a successful procedure. Patients with unstable angina, prior myocardial infarction and whose procedure was complicated were excluded. Indium-111 monoclonal antimyosin antibodies (80 MBq) were injected 24 h after coronary angioplasty and planar images were collected 24 h later. The relative antimyosin uptake was assessed subjectively and by a heart/lung count density ratio. In addition, the intracardiac gradient of activity was assessed by a count density profile analysis of the cardiac region of interest to distinguish better the focal as opposed to the diffuse antimyosin uptake. The antimyosin uptake index was calculated by multiplying the heart/lung ratio to the intracardiac gradient of activity. After coronary angioplasty, nine patients had minor ST-T wave changes on the surface ECG, but no patient demonstrated a new Q wave. Only three patients showed a mild rise in cardiac enzyme (CK-MB) serum levels. Indium-111 antimyosin uptake (heart/lung > 1.55) was present in eight patients (33%) and was intense (heart/lung > 1.9) in five (21%). Antimyosin uptake was always seen in myocardial segments corresponding to the treated coronary artery. Patients with a positive antimyosin scan had a longer duration of balloon-induced ischaemia compared with patients with no evidence of antimyosin uptake (541 +/- 211 vs 331 +/- 137 s, P < 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Indium-111 antimyosin monoclonal antibody Fab imaging in patients with cardiomyopathy.

Six patients with cardiomyopathy were imaged following intravenous injection of an indium-111 labeled monoclonal antibody directed against the heavy chain of cardiac myosin. Two patients had hypertrophic non-obstructive cardiomyopathy (HNCM), two patients had dilated cardiomyopathy (DCM), and two patients had specific heart muscle disease. One of 2 patients with HNCM and one of 2 patients with DCM had a positive antimyosin scan. The 2 patients with specific heart muscle disease manifested persistent blood pool activity of the antibody, thereby precluding interpretation of the images. The present report demonstrates that antimyosin antibody imaging may provide evidence of myocardial injury, or necrosis in some patients with cardiomyopathy.

Intraventricular conduction abnormalities in patients with clinically suspected myocarditis are associated with myocardial necrosis

Twenty-nine patients with suspected myocarditis, either with or without intraventricular conduction abnormalities, were investigated for degree of myocardial necrosis by antimyosin scintigraphy. Among those 29 patients, 16 had intraventricular conduction abnormalities. Antimyosin scans were analyzed for heart/lung ratios and semiquantitative visual uptake scores (0 to 4+ scale). Of the 16 patients with conduction abnormalities, 15 (94%) demonstrated visual antimyosin uptake versus 7 (54%) of 13 cases without conduction abnormalities ( p < 0.03). In addition, the heart/lung ratios and uptake scores were significantly higher in the group with conduction abnormalities than in the group without (1.64 ± 0.31 vs 1.39 ± 0.20, p < 0.03; and 2.3 ± 0.7 vs 1.4 ± 0.7, p < 0.005; respectively). In conclusion, intraventricular conduction abnormalities in patients with suspected myocarditis were more strongly associated with active and more severe myocardial necrosis as judged by antimyosin imaging than patients with normal electrocardiograms.

Antimyosin Scintigraphy for Detection of Myocarditis: Scintigraphic Follow-up

To examine the value of antimyosin-indium 111 imaging in relation to endomyocardial biopsy in patients with suspected myocarditis, as well as the natural evolution of abnormal findings on the antimyosin scan, 12 patients with suspected myocarditis underwent endomyocardial biopsy and antimyosin scan. The heart-to-lung ratio (H/L) was used to quantify the antimyosin scan. All 12 patients had abnormal results on the scan (H/L, 1.7 to 2.9; mean, 2.1 +/- 0.3); 8 of the 12 patients also had a diagnostic endomyocardial biopsy. In four patients with abnormal findings on antimyosin scan and normal findings on biopsy, the H/L ratio did not differ from eight patients with abnormal findings on antimyosin scan and a diagnostic biopsy; also, the ejection fraction did not differ between the two groups. One patient died, and 8 patients had a repeat antimyosin scan within 2 months after the initial study. The H/L ratio returned to normal in two out of three patients with normal results on biopsy and in three out of five patients with a diagnostic biopsy; the ejection fraction improved by 8 percent or more in one out of three patients with a nondiagnostic biopsy and in two out of five patients with a biopsy diagnostic for myocarditis. We conclude that the antimyosin scan is more frequently diagnostic than biopsy in suspected myocarditis. Patients with abnormal results on antimyosin scan and a nondiagnostic biopsy, as well as those with abnormal results on antimyosin scan and a diagnostic biopsy, tend to return to normal results on scan within 2 months and improve their ejection fraction.

Myocardial indium-111 antimyosin uptake in patients with idiopathic dilated cardiomyopathy: its relation to haemodynamics, histomorphometry, myocardial enteroviral infection, and clinical course.

The myocardial uptake of indium-111 antimyosin indicates the presence of ongoing myocyte damage. To evaluate the role of this finding in patients with idiopathic dilated cardiomyopathy (IDC), 36 patients were studied by planar and SPECT antimyosin imaging. The diagnosis of IDC was based on coronary angiography and left ventricular endomyocardial biopsy. The antimyosin scan was evaluated qualitatively from SPECT images and assessed quantitatively by a count density index (CDI) which measured the tracer activity over the heart relative to the lung and sternal region (normal value less than 1.20). Group 1 consisted of 13 patients (36%) with an increased myocardial antimyosin uptake, while 23 patients had a normal antimyosin scan (group 2). Clinical data, pulmonary artery pressures, gated blood pool ejection fraction and histomorphometry of endomyocardial biopsies were similar in both groups. During a follow-up of 21 +/- 12 months there were two cardiac deaths in group 1 and 10 deaths in group 2 (P = 0.12). The 2-year survival rate was 81% and 59%, respectively. During follow-up, there was no significant change in haemodynamic parameters in either group, but there was a slight improvement in functional NYHA class in group 1 (P < 0.05). No association was found between the presence of myocardial enterovirus infection, determined in 17 patients by in situ hybridization and the antimyosin scan (P = 0.5 g). Myocardial antimyosin uptake was found in a high percentage of patients with IDC, indicating ongoing myocyte damage. This finding was not related to any clinical, haemodynamic, morphological parameter, or enterovirus infection. Myocyte damage is a distinct feature in a subgroup of patients with IDC unrelated to any known causes of myocellular destruction. This subgroup showed a trend towards a more favourable clinical outcome.

New concepts in myocarditis: Crossroads in the 1990s

Myocarditis is an inflammatory disorder of the heart muscle that is most often associated with an enteroviral infection. The target population is often children and young adults. The pathogenesis is likely a combination of viral damage, autoimmune activation, and microvascular ischemia, with direct viral involvement in late stages of the disease as documented by molecular hybridization. The diagnosis rests on clinical suspicion of cardiac dysfunction in a susceptible population. The gold standard for diagnosis is myocardial biopsy, which seeks evidence of lymphocytic infiltration coinciding with myocyte necrosis. Indium-labeled antimyosin scans are very sensitive, and a negative scan may be useful to exclude a patient from biopsy. Newer direct molecular techniques are being developed to apply to biopsy tissues to increase the sensitivity and specificity of the pathological diagnostic criteria, and to target new therapy. Treatment is still largely palliative, involving the general supportive measures of rest, vasodilators, and anticoagulation. Immunosuppression is controversial, but is probably useful as a short-term measure in patients persisting with poor left ventricular function. The National Institutes of Health-sponsored randomized trial did not demonstrate long term benefit of immunosuppression on ventricular function or outcome. Newer modalities of treatment are also rapidly being de-

Focal myocardial injury following blunt chest trauma: A comparison of indium-111 antimyosin scintigraphy with other noninvasive methods

The diagnosis of myocardial contusion is often difficult, as traditional methods such as serial electrocardiograms, cardiac enzyme (creatine kinase [CK-MB]) analysis and echocardiography lack sensitivity and specificity. Recent reports have shown that 111In labelled antimyosin scanning has high sensitivity for detecting cardiac injury. However, no prior studies have been reported for antimyosin imaging with patients suspected of sustaining a cardiac contusion. Accordingly, 17 patients with severe multisystem trauma (intrathoracic vascular injury in eight patients, pneumothorax and pulmonary contusion in 13) underwent antimyosin scintigraphy, echocardiography, 12-lead electrocardiograms, and CK-MB determinations. Arrhythmias were noted in seven patients, four of whom died. All patients had elevated CK levels but CK-MB isoenzyme was >4% in only three. Abnormal ST segments were noted in nine subjects, only one of whom had CK-MB elevation. Echocardiography revealed pericardial effusions in four patients but was technically suboptimal in 53% of the studies. Blinded interpretation of the antimyosin scans revealed only one with focal myocardial uptake; this same patient had the only discrete wall motion abnormality on the echocardiogram and also had ST depression with ectopy but normal CK-MB. Thus in patients with suspected myocardial contusion, echocardiography is frequently limited technically and the electrocardiogram and CK analysis appear to lack diagnostic accuracy. In contrast, monoclonal antimyosin imaging may be performed in patients with trauma without limitation and yields results that are concordant with echocardiograms. In patients with suspected myocardial contusion, focal antimyosin uptake is uncommon despite severe thoracic injury, which suggests that extensive myocardial necrosis is not the primary method of injury.

Prognostic significance of indium-111 antimyosin antibody uptake in patients with dilated and hypertrophic cardiomyopathy

The prognostic significance of myocardial uptake of indium-111 antimyosin was evaluated in 15 patients with idiopathic cardiomyopathy: 10 patients with dilated cardiomyopathy and 5 patients with hypertrophic cardiomyopathy. Seven of the 10 patients with dilated cardiomyopathy showed positive images; three of these 7 patients with strongly positive scans died within 3 months after scintigraphic examination. Four of the 5 patients with hypertrophic cardiomyopathy showed positive images; two of these patients with dilated left ventricle had prominent positive scans and higher heart to lung ratio. One of these two patients died 12 months after antimyosin scan. The heart to lung ratio of antimyosin uptake in total patients was correlated with left ventricular end-diastolic dimension ( r = 0.51, P < 0.05), end-systolic dimension ( r = 0.57, P < 0.05) and ejection fraction ( r = −0.60, P < 0.05) measured by echocardiography. Although the number of patients is small and the study is preliminary, indium-111 antimyosin antibody imaging could be of value in establishing prognosis of patients with dilated and hypertrophic cardiomyopathy, in selecting patients for cardiac transplantation, and in evaluating the effects of therapeutic interventions.

Natural evolution of cardiac function, cardiac pathology and antimyosin scan in a murine myocarditis model

Serial technetium-99m radionuclide ventriculograms, indium-111 antimyosin antibody scans and tissue biodistribution studies were performed in C3H/He mice with experimentally induced viral encephalomyocarditis and the results were compared with pathologic assessments of myocardial necrosis. Postinfection ejection fraction decreased on days 10 (20.7 +/- 5.5%, n = 6), 20 (18.6 +/- 15.2%, n = 5), 30 (18.5 +/- 7.7%, n = 5) and 150 (30.0 +/- 18.7, n = 6) (p less than 0.001) in comparison with that in uninfected control mice (63.3 +/- 3.1%, n = 6). In the same group of animals, indium-111 antimyosin antibody scans showed intense positive myocardial accumulation on day 10 (in six of six mice) and only slight accumulation on day 20 (in one of five mice). In the chronic stage, two of five mice on day 30 and two of six mice on day 150 still showed positive uptake. The antimyosin scan myocardium to lung uptake ratio (expressed as mean count density [mean counts/pixel of the region] ratio) increased greatly on day 10 (p less than 0.001 versus values in uninfected control mice) but not subsequently. Biodistribution studies of the indium-111 antimyosin antibody showed that the heart to blood count ratio was significantly higher on day 10 (p less than 0.001 versus values in control mice) but not on days 20, 30 and 150. Pathologic examination showed active and ongoing severe myocardial necrosis with dilated ventricles on day 10. On day 20, there was less active necrosis and healing had appeared to begin. On days 30 and 150, myocardial fibrosis increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Antimyosin antibody cardiac imaging: Its role in the diagnois of myocarditis

Right ventricular endomyocardial biopsy currently remains the procedure of choice for identifying patients with symptomatic heart failure due to myocarditis from the larger population with idiopathic dilated cardiomyopathy. Despite its specificity, the sensitivity of right ventricular biopsy remains uncertain because of the focal or multifocal nature of the disease. Because myocyte necrosis is an obligate component of myocarditis, the use of indium-111 antimyosin imaging was evaluated in 82 patients with suspected myocarditis. Seventy-four patients had dilated cardiomyopathy of < 1 year's duration (mean left ventricular ejection fraction 0.30 ± 0.02); eight patients had normal left ventricular function (mean ejection fraction 0.59 ± 0.03). Symptoms at presentation included congestive heart failure (92%), chest pain mimicking myocardial infarction (6%) and life-threatening ventricular tachyarrhythmias (2%).All patients underwent planar and single photon emission computed tomographic (SPECT) cardiac imaging after injection of indium-111-labeled antimyosin antibody fragments and right ventricular biopsy within 48 h of imaging. Antimyosin images were interpreted as either abnormal or normal and correlated with biopsy results. On the basis of the right ventricular histologic examination, the sensitivity of antimyosin imaging was 83%, specificity 53% and predictive value of a normal scan 92%. Improvement in left ventricular function occurred within 6 months of treatment in 54% of patients with an abnormal antimyosin scan compared with 18% of those with a normal scan (p < 0.01).Antimyosin cardiac imaging may be useful for the initial evaluation of patients with dilated and nondilated cardiomyopathy and clinically suspected myocarditis. A normal antimyosin scan is associated with a very low rate (8%) of detecting myocarditis on endomyocardial biopsy and may prompt reconsideration of the need for biopsy in such individuals.

Transient alterations in cardiac performance after a six-hour race

Ten long distance runners were enrolled in a 6-hour competitive race. Immediately after the race technetium-99m-albumin gated blood pool scans were performed and indium-111 antimyosin was injected. Forty-eight hours later antimyosin scans were obtained and control gated blood pool scans were performed. Left ventricular ejection fraction was higher after the race (65 ± 5 vs 60 ± 7%, p < 0.01) due to a decrease in end-systolic counts. Right ventricular ejection fraction was lower after the race (42 ± 7 vs 54 ± 12%, p = 0.03) due to an increase in both end-diastolic and end-systolic counts. A longer systolic period was observed after the race (53 ± 5% of the RR interval vs 39 ± 3%, p = 0.005). No significant differences were observed in peak filling or peak emptying rates after the race. An increase in pulmonary blood volume (116% of control) was observed after the race. Antimyosin scans were normal in 7 athletes and minimal antimyosin myocardial uptake was seen in 3. Transient alterations in biventricular performance present after the race correspond to functional adaptation to strenuous exercise and are not due to irreversible myocyte damage.