Myocardial technetium-99m-teboroxime activity in acute coronary artery occlusion and reperfusion: Relation to myocardial blood flow and viability

The purpose of this study was to test the hypothesis that ^99mTc- teboroxime retention within the heart depends at least in part on the presence of viable myocytes. Methods: We used a porcine model of acute myocardial infarction with reperfusion and compared the myocardial uptake of labeled microspheres at 1 hr of reperfusion with that of ^99mTc-teboroxime. Eleven domestic swine had measurements of hemodynamics and regional myocardial blood flow (microspheres) at baseline, at 10 and 50 min of left anterior descending (LAD) coronary artery occlusion and at 10 and 60 min of LAD reperfusion. Technetium-99m-teperoxime was injected intravenously at 60 min of reperfusion and the animal was killed 5-7 min later. The heart was then perfused with triphenyl tetrazolium chloride to identify infarcted and jeopardized myocardium in the occlusion zone and with Evans blue dye to mark normally perfused myocardium. After imaging, tissue sections were digested and colored microspheres were extracted and counted to determine myocardial blood flow. Results: After coronary occlusion, infarct zone (MIZ) to normal zone (NZ) blood flow ratios declined from 0.95 ± 0.27 (preocclusion) to 0.18 ± 0.15 at 10 min and 0.25 ± 0.35 at 50 min of occlusion (both p < 0.05). The MIZ:NZ count ratio at 60 min of reperfusion was less than the MIZ:NZ blood flow ratio in every animal and over the entire range of flow ratios (0.55-3.64). Conclusion: Technetium-99m-teboroxime requires viable myocytes for retention within the heart and is not exclusively a tracer of myocardial blood flow when imaged 5-7 min after injection. Additional in vivo imaging studies are required to determine the extent to which reduced retention of the tracer by reperfused but nonviable myocardium influences the appearance of clinical scans.