EFFECT OF REPERFUSION ON IN-111 ANTIMYOSIN MONOCLONAL-ANTIBODY UPTAKEBY SALVAGED AND NECROTIC MYOCARDIUM IN THE DOG

Objective: The aim was to investigate the ability of In-111-antimyosin monoclonal antibody (In-111-AMA) to differentiate between salvaged an d necrotic myocardium following reperfusion. Methods: Dogs submitted t o 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 In- 111-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 infa rct by dye perfusion and triphenyltetrazolium chloride, the heart slic es were imaged by scintigraphy and dissected into necrotic, viable isc haemic, and normal myocardium. Myocardial blood flow was estimated by microspheres and In-111-AMA uptake was expressed as the ratio of the c orresponding non-ischaemic tissue samples taken from opposite ventricu lar wall. Results: In-111-AMA ratios in necrotic and salvaged myocardi um 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 ra tios of 6. 1(1.1) and 3.0(0.3) times normal values. In contrast, ratio s of 43.6(5.6) and 5.6(0.9) (p<0.05) in necrotic and salvaged myocardi um, respectively, were found in reperfused group 2, giving a 7.8 to 1 factor between the two tissue areas of the risk territory. Clear delin eation between salvaged and necrotic tissue territories could be made on scintigrams only in group 2, which otherwise presented smaller infa rcts: 35.1(7.9)% of the risk area v 58.0(8.7)% in non-reperfused anima ls (p<0.05). In-111-AMA uptake by necrotic myocardium did not correlat e with collateral (group 1) or reperfusion blood flows (group 3), indi cating that the greater uptake in reperfused myocardium is flow indepe ndent. Conclusions: In-111-AMA does not clearly identify necrotic from viable ischaemic myocardium within 24 h of injection in a coronary ar tery occlusion model. Thus it may not be a sensitive enough method to evaluate infarct size progression. However, reperfusion greatly increa sed In-111-AMA uptake by the infarct in a flow independent manner, thi s may prove to be useful for clinical assessment of infarct size and r eperfusion injury.