Myocardial uptake of antimyosin antibody compared with serum myosin light chain I levels in patients with myocardial infarction.
ABSTRACT Myocardial accumulation of In-111-antimyosin (InAM) was evaluated in comparison with circulating serum myosin light chain I (LCI) level at the time of InAM injection. Seventeen consecutive patients were studied at various stages ranging from 6 days to 34 days after myocardial infarction (MI). The infarct area was positive for InAM uptake in all patients (100%), and significant myocardial uptake was observed in 14 patients (82.4%). The intensity of InAM uptake correlated with the infarct location shown by ECG and CAG. In contrast, 12 patients (70.6%) had normal or undetectable serum myosin LCI levels, with 5 being normal (0.42-2.5 ng/ml) and 7 undetectable (0.42 ng/ml or less). Only 5 patients (29.4%) had elevated serum myosin LCI levels at the time of InAM injection, and this elevation was slight, ranging from 3.4 to 4.5 ng/ml (mean: 3.75 ng/ml). Among patients with undetectable, normal, and elevated serum myosin LCI levels, there was no significant correlation between InAM uptake and the serum myosin LCI level. Thus, even after the serum myosin LCI level has decreased to normal, InAM can still bind to cardiac myosin in patients with MI, presumably until there is complete recovery from the hibernating myocardium due to ischemic damage.
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ABSTRACT: The diagnostic value of 111In-antimyosin (AM) imaging for identifying myocardial infarction was evaluated in comparison with 99mTc-pyrophosphate (PPi) imaging. Twenty-four patients with various stages of myocardial infarction, ranging from three days to nine months after the onset of infarction, underwent both AM and PPi scans. Of 26 infarct lesions AM scan identified 22 (85%), while PPi scans detected 10 (38%) (p less than 0.01). When less than a week had passed since the onset both scans demonstrated all infarct lesions. For seven subacute lesions studied within one to two weeks of onset, AM scans detected (100%), while PPi scans identified only 2 (29%). Furthermore, AM scans showed discrete myocardial uptake in 7 (64%) of those studied more than two weeks after onset. The intensity of AM uptake in the infarcts studied more than seven days after onset was less than that in acute infarcts studied within seven days of onset (p less than 0.05). These preliminary data indicate that the abnormal myocardial uptake of AM persists beyond the first two weeks when PPi no longer accumulates. Thus, AM scans can be considered to provide a sensitive diagnosis of subacute as well as acute myocardial necrosis.Journal of Nuclear Medicine 03/1990; 31(2):136-42. · 5.56 Impact Factor
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ABSTRACT: A radioimmunoassay for human cardiac myosin light chains (CM-LC) was developed and evaluated as a selective diagnostic test for acute myocardial infarction (AMI). The assay had a sensitivity of 1.0 ng/ml (+/- 2 standard deviations) in serum. Eighty-three patients with confirmed AMI all showed an elevated plasma concentration of CM-LC at some time during the course of their illness. Of 9 patients from whom early blood samples were obtained, 7 had diagnostic concentrations within 6 hours from the onset of chest pain. Only 2 had an elevated total creatine kinase level at this time. CM-LC concentrations peaked on days 2 to 4, but remained elevated in patients with large AMIs for more than 1 week. In preinfarction syndrome, 8 of 15 patients had elevated CM-LC levels at least once. Of 15 patients with stable angina pectoris, only 1 patient, who had congestive heart failure, showed elevated light chain levels. CM-LC levels were not detectable by this method in the sera of healthy persons (n = 72), patients with recent intramuscular injection (n = 3), or those with a variety of systemic illnesses (n = 14). In initial studies using an antiserum having 25% cross-reactivity between cardiac and skeletal muscle myosin light chains, 3 patients who had extensive skeletal muscle damage appeared to have elevated concentrations. Patients with this finding have not yet been examined with a more specific antiserum (8% cross-reactivity).(ABSTRACT TRUNCATED AT 250 WORDS)The American Journal of Cardiology 12/1984; 54(8):964-70. · 3.43 Impact Factor
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ABSTRACT: Myocardial infarct size was measured by single photon emission computed tomography (SPECT) following injection of indium-111 antimyosin in 27 patients (18 male and 9 female; mean age 57.4 +/- 10.5 years, range 37 to 75) who had acute transmural myocardial infarction (MI). These 27 patients represent 27 of 35 (77%) consecutive patients with acute Q-wave infarctions who were injected with indium-111 antimyosin. In the remaining 8 patients either tracer uptake was too faint or the scans were technically inadequate to permit infarct sizing from SPECT reconstructions. In the 27 patients studied, infarct location by electrocardiogram was anterior in 15 and inferoposterior in 12. Nine patients had a history of prior infarction. Each patient received 2 mCi of indium-111 antimyosin followed by SPECT imaging 48 hours later. Infarct mass was determined from coronal slices using a threshold value obtained from a human torso/cardiac phantom. Infarct size ranged from 11 to 87 g mean 48.5 +/- 24). Anterior infarcts were significantly (p less than 0.01) larger (60 +/- 20 g) than inferoposterior infarcts (34 +/- 21 g). For patients without prior MI, there were significant inverse correlations between infarct size and ejection fraction (r = 0.71, p less than 0.01) and wall motion score (r = 0.58, p less than 0.01) obtained from predischarge gated blood pool scans. Peak creatine kinase-MB correlated significantly with infarct size for patients without either reperfusion or right ventricular infarction (r = 0.66). Seven patients without prior infarcts had additional simultaneous indium-111/thallium-201 SPECT studies using dual energy windows.(ABSTRACT TRUNCATED AT 250 WORDS)The American Journal of Cardiology 05/1989; 63(12):777-83. · 3.43 Impact Factor