Localization of In-111 antimyosin Fab and 99mTc-pyrophosphate in reperfusion myocardial infarction model.

The myocardial uptake of In-111 antimyosin Fab and Tc-99m pyrophosphate was studied in dogs undergoing coronary artery occlusion for 90 minutes followed by reperfusion. The regional myocardial blood flow was determined by injecting Sc-46 labeled microsphere and was related to the relative concentrations of In-111 antimyosin and Tc-99m pyrophosphate. There was an inverse linear correlation between In-111 antimyosin Fab localization and the regional blood flow in both the subendocardial (r = 0.81) and subepicardial myocardium (r = -0.80). The greatest uptake of antimyosin was observed in areas of severe blood flow reduction (0-10% of normal). On the other hand, there was no correlation between the Tc-99m pyrophosphate uptake and the degree of blood flow reduction. Maximal subendocardial localization of Tc-99m degree of blood flow reduction. Maximal subendocardial localization of Tc-99m pyrophosphate was observed in areas where the blood flow was reduced to 31-50% of the normal. In the case of the subepicardium, the greatest uptake was localized to areas of 0 to 10% of the normal flow. In addition, there was significant myocardial uptake in regions where the blood flow was minimally reduced (greater than 81%). This study suggests that In-111 antimyosin Fab is a specific and quantitative tool in the evaluation of myocardial necrosis.