Mechanisms contributing to myocardial accumulation of /sup 99m/Tc stannous pyrophosphate after coronary arterial occlusion

The relation between the accumulation of pyrophosphate and technetium-99m in myocardium with reversible and irreversible ischemic injury was studied in dogs subjected to transitory or persistent coronary arterial occlusion. Among four dogs with coronary occlusion maintained for less than 20 minutes, none had either increased MB creatine kinase (CK) (the ''myocardial'' CK isoenzyme) activity serum or a positive /sup 99m/Tc stannous pyrophosphate image. Seven dogs with coronary occlusion maintained for 30 or more minutes had elevated serum MB CK activity, and five of the seven had positive (abnormal) images. Thus, although false negative images may occur occasionally despite myocardial damage, both increased serum MB CK and abnormal images generally accompanied prolonged coronary occlusion. In contrast, ischemia without infarction was not associated with abnormal images. Both /sup 99m/Tc and 32P labeled pyrophosphate were accumulated extensively and proportionally in myocardium from zones of infarction, and uptake of both tracers was comparable although modest in isolated mitochondria. Similar results were obtained after myocardial infarction in animals with induced profound leukopenia. Thus, phagocytosis of the radiopharmaceutical agent by leukocytes migrating into the infarct is not an essential mechanism accounting for uptake. These results indicate that abnormal images reflect uptake of pyrophosphate, associated with /sup 99m/Tc, by irreversibly injured myocardium rather than leukocytic infiltration involved in the inflammatory response in the heart