Localization of cardiac myosin-specific antibody in myocardial infarction.

Khaw, Ban An; Haber, Edgar; Smith, Thomas W.

doi:10.1172/jci108488

Cited by 132 publications

(49 citation statements)

References 21 publications

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“…Some possible explanations for this difference in image size are that (1) the methods of pixel counting and threshold setting were not comparable, (2) the timing of the scans favored pyrophosphate uptake, (3) unrecognized previous myocardial necrosis may have contributed to the overall pyrophosphate image, and (4) one of the two scanning techniques either does not label infarcted tissue or, conversely, labels noninfarcted tissue. The methods of pixel counting were similar for both antimyosin and pyrophosphate SPECT.…”

Section: Methodsmentioning

confidence: 99%

Scintigraphic quantification of myocardial necrosis in patients after intravenous injection of myosin-specific antibody.

et al. 1986

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The Fab fragments of antimyosin antibodies, labeled with 9mTc, were used in the scintigraphic examination of 30 patients with myocardial infarction. The ability to detect necrosis and determine its extent from the antimyosin scan were compared with the results of quantitative regional wall motion analysis by contrast ventriculography at 10 to 14 days and 99mTc-pyrophosphate imaging. Antimyosin images recorded by planar and single photon-emission computed tomography (SPECT) delineated areas of myocardial necrosis in 27 of 30 patients (90%) compared with a 91% sensitivity of pyrophosphate in 21 of 23 patients. Infarct size was determined by both antimyosin and pyrophosphate SPECT images. Results by both techniques showed a significant correlation with computer-derived hypokinetic segment length (r = .79 for both, p = .002) and peak creatine kinase (r = .9 for both, p < .01). Although sensitivity for and correlations with markers of necrosis were similar with both techniques, infarct size by pyrophosphate SPECT was 1.7 times larger than infarct size by antimyosin SPECT (p < .01). Certain zones in the infarct area were differentially labeled; the nature and irreversibility of injury within these zones remains to be clarified. Circulation 74, No. 3, 501-508, 1986. WE PREVIOUSLY described a method for localizing and quantifying regions of myocardial necrosis based on the binding of radiolabeled myosin-specific antibodies to cells that have lost the integrity of their plasma membranes.",2 Unlike other methods that are dependent on blood flow, concentration of antibody in the center of an infarct is greater than that at the periphery, with antibody concentration inversely proportional to blood flow.

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Section: Methodsmentioning

confidence: 99%

Scintigraphic quantification of myocardial necrosis in patients after intravenous injection of myosin-specific antibody.

et al. 1986

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“…8 In order to determine whether specific localization also occurred after intracoronary injection,`31I-Ab(Fab9) and '25I-N-IgG(Fab')2 were simultaneously injected into the hearts of four dogs Maximal uptake ratios of '31I-Ab(Fab')2 at the center ab')2 FIGURE 7. Ratios ofradioactivity (cpm/g) (Fab')2 in test region to normal myocardium for 1311-A b(Fab')2 and 125J-N-IgG(Fab')2 injected simultaneously into animals with nontransmural infarcts.…”

Section: Pathological Evaluationmentioning

confidence: 99%

Early imaging of experimental myocardial infarction by intracoronary administraion of 131I-labelled anticardiac myosin (Fab')2 fragments.

Khaw¹,

Gold²,

Leinbach³

et al. 1978

Circulation

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SUMMARY We examined the feasibility of early imaging of myocardial infarcts by intracoronary injection of I3'l-labelled cardiac myosin-specific antibody (Fab')2. The left anterior descending coronary artery was occluded for 5 hours by a balloon catheter introduced through the carotid artery in 12 dogs. The catheter was withdrawn and 1 mCi 201TI was injected intravenously and 500 ,uCi of '"'I antibody were injected into the main left coronary artery. Six of these animals demonstrated evidence of myocardial infarction by ECG and subsequent triphenyl-tetrazolium chloride staining, while the others did not. In each of the infarcted animals, in vivo scintograms one-half hour after injection of isotope showed uptake of 131I in the anteroapical region of the heart corresponding to the region of absent 201TI uptake. This relationship was confirmed in the excised hearts and in heart slices. In slices, l311 uptake corresponded to regions that did not stain with triphenyltetrazolium chloride. In the six animals that did not show evidence for infarction after coronary occlusion, uptake of 131Iwas not demonstrated, either in vivo or in excised specimens. In four additional dogs subjected to the same procedure, I2'l-labelled (Fab')2 from nonimmune IgG was injected simultaneously into the left main coronary artery with "3'1-labelled canine myosin-specific antibody (Fab')2. The ratio of uptake between infarct center and normal tissue was 34.3 ± 1.5 (mean ± SEM) for the specific antibody fragment as contrasted to 6.6 + 0.4 for the nonimmune IgG fragment, indicating that intracoronary injection does not favor nonspecific sequestration of protein in regions of infarction. Thus, the intracoronary administration of myosin-specific antibody fragments leads to early and specific one-half hour imaging of myocardial infarcts.THE IDEAL AGENT for the scintigraphic identification of infarcted myocardium in vivo should be sensitive, specific and readily detectable. Attempts to develop such an agent that can be administered noninvasively have only been partially successful. Hot spot imaging agents such as 9smTc-pyrophosphate,l-4 'mTctetracycline,5 99mTc-glucoheptonate,6 and gallium-67 citrate7 accumulate in infarcted myocardium, but without ideal sensitivity and specificity, with an average delay after either injection of the radiopharmaceutical or onset of myocardial infarction of 24-48 hours. Radioiodine-labelled anticardiac myosin antibodies have been shown experimentally to be highly specific for necrotic myocardium.8"-1 However, this method also requires at least 48 hours after intravenous administration for the antibody uptake to attain an ideal concentration for visualization of the necrotic myocardium with an Anger camera.1'To increase the rate of antimyosin antibody uptake by the infarct, we have experimented with the intracoronary route of administration of the antimyosin antibody. This approach shows promise for the

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“…Still another method has depended on assay of 3 H-labeled amino acids fed to laboratory animals;"- 13 such procedures are not applicable to the study of human biopsy material. Determination of myosin by antibody techniques 14 is hindered by the unique solubility properties of the protein; the fact that complete extraction of the protein from the cellular matrix by nondenaturing solvents is not readily achieved can further complicate immunochemical assays.…”

mentioning

confidence: 99%

The structural proteins of normal and diseased human myocardium.

Frederiksen¹,

Hoffnung²,

Frederiksen³

et al. 1978

Circulation Research

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SUMMARY Microanalytical techniques have been developed for the quantitative determination of actomyosinand collagen from 20 to 30-mg (wet mass) samples of myocardium. Actomyosin is the major contractile protein complex and is, therefore, an index of functional muscle; collagen is the major protein of connective and scar tissue and is, therefore, an index of fibrosis. These proteins were determined in six myocardial samples from each of four normal, four ischemic, and three hypertrophied human hearts. As determined by electrophoresis in a denaturing medium, the concentration of actomyosin in normal myocardium is 69 /tg/mg wet tissue; the concentration in ischemic myocardium is not significantly different from normal, but is approximately 45% higher than normal in hearts with left ventricular hypertrophy. These observations indicate that hypertrophy is not simply an increase in total heart mass but, rather, involves an increase in actomyosin concentration in myocardial tissue as well. Collagen is determined from amino acid analysis of whole tissue for 4-hydroxyproline, an amino acid characteristic of this protein; the concentration of collagen in normal (6.1 /ig/mg wet tissue) myocardium are not significantly different from those in hypertrophied myocardium. In focal regions of ischemic hearts, however, collagen is increased 2-to 4-fold. The concentration of collagen in myocardial tissue correlates well (r = 0.947) with the degree of fibrosis determined by conventional histological techniques. This work represents (1) a more direct biochemical determination of contractile protein concentration in whole myocardium and (2) a more direct correlation of the biochemical assay for collagen with histological data than have been reported previously.

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Localization of cardiac myosin-specific antibody in myocardial infarction.

Cited by 132 publications

References 21 publications

Scintigraphic quantification of myocardial necrosis in patients after intravenous injection of myosin-specific antibody.

Scintigraphic quantification of myocardial necrosis in patients after intravenous injection of myosin-specific antibody.

Early imaging of experimental myocardial infarction by intracoronary administraion of 131I-labelled anticardiac myosin (Fab')2 fragments.

The structural proteins of normal and diseased human myocardium.

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