Effect of reperfusion on 111In-antimyosin monoclonal antibody uptake by salvaged and necrotic myocardium in the dog.

OBJECTIVE

The aim was to investigate the ability of 111In-antimyosin monoclonal antibody (111In-AMA) to differentiate between salvaged and necrotic myocardium following reperfusion.

METHODS

Dogs submitted to a 24 h left anterior descending coronary artery occlusion (group 1, n = 10) or to a 90 min occlusion followed by a 22.5 h reperfusion (group 2, n = 11, group 3, n = 5) were given radiolabelled microspheres and 111In-AMA after 75 min of ischaemia (groups 1 and 2), or after 19.5 h of reperfusion (group 3). After delimiting the area at risk and the infarct by dye perfusion and triphenyltetrazolium chloride, the heart slices were imaged by scintigraphy and dissected into necrotic, viable ischaemic, and normal myocardium. Myocardial blood flow was estimated by microspheres and 111In-AMA uptake was expressed as the ratio of the corresponding non-ischaemic tissue samples taken from opposite ventricular wall.

RESULTS

111In-AMA ratios in necrotic and salvaged myocardium were respectively 5.4(SEM 1.9) and 3.2(0.5) times the normal value, giving a 1.7 to 1 factor between the two areas in dogs with permanent occlusion (group 1). Similar results were obtained in group 3 with ratios of 6.1(1.1) and 3.0(0.3) times normal values. In contrast, ratios of 43.6(5.6) and 5.6(0.9) (p < 0.05) in necrotic and salvaged myocardium, respectively, were found in reperfused group 2, giving a 7.8 to 1 factor between the two tissue areas of the risk territory. Clear delineation between salvaged and necrotic tissue territories could be made on scintigrams only in group 2, which otherwise presented smaller infarcts: 35.1(7.9)% of the risk area v 58.0(8.7)% in non-reperfused animals (p < 0.05). 111In-AMA uptake by necrotic myocardium did not correlate with collateral (group 1) or reperfusion blood flows (group 3), indicating that the greater uptake in reperfused myocardium is flow independent.

CONCLUSIONS

111In-AMA does not clearly identify necrotic from viable ischaemic myocardium within 24 h of injection in a coronary artery occlusion model. Thus it may not be a sensitive enough method to evaluate infarct size progression. However, reperfusion greatly increased 111In-AMA uptake by the infarct in a flow independent manner, this may prove to be useful for clinical assessment of infarct size and reperfusion injury.