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To assess myocardial infarction quantitatively in 15 mm thick transverse sections of the canine heart in vivo we utilized a new technique, positron emission transaxial tomography (PETT) and cyclotron-produced 11C-palmitate (11C-P) injected intravenously. Results were compared to regional myocardial creatine phosphokinase (CPK) depletion, diminished 14C-palmitate accumulation in tissue extracts, and infarction estimated morphometrically 48 hours after coronary occlusion. CPK activity and 14C-P content declined in parallel in transmural biopsies (N=44) from normal and ischemic zones (r=.92) in six dogs; and infarct in 10 mm thick cross sections of the entire left ventricle estimated morphometrically (N=26) in six other animals correlated with CPK depletion in contiguous 2.5 mm thick slices (r=.92). When the percentage of infarction in 15 mm thick cross sections was assessed tomographically in six other dogs 48 hours after coronary occlusion with 11C-P injected intravenously, results correlated with infarction in corresponding cross sections from the same hearts estimated morphometrically (r=.97, N=9) and by analysis of CPK depletion (r=.93, N=9). Thus, PETT permits estimation of infarction in cross sections of the left ventricle in vivo after intravenous injection of 11C-palmitate.

Quantification of infarction in cross sections of canine myocardium in vivo with positron emission transaxial tomography and 11C-palmitate.