Histologic,ultrastructural, and enzymatic measurements of infarct size following coronary artery stenosis and occlusion

Coronary artery narrowing (CAN), which reduced resting coronary blood flow (BF) by 50%, was induced in 10 conscious dogs and was maintained for 4 hours. Five additional dogs (group 1) with complete coronary artery occlusion were compared to the dogs with CAN. serum isoenzymes of creatine phosphokinase (CK) and latate dehydrogenase (LD) were monitored hourly in all groups. After 36 hours, samples were obtained for regional myocardial BF, quantitative histology, and quantitative ultrastructural (EM) morphology. Six dogs with CAN had small infarcts (MI) of less than 1 gm and persistent myocardial cell injury (group 2). The other four dogs with CAN had only persistent myocardial cell injury by ultrastructural criteria (group 3). Peak serum CK activities in groups 2 and 3 were similar, as were MI sizes calculated from serum CK and myocardial depletion. MB CK was of diagnostic value in group 1 but not in groups 2 and 3. The ratio of $\text{LD}\text{1}\text{LD 2}$ had diagnostic value in all three groups. MI size by enzyme estimates was consistently higher than planimetered MI size at autopsy in both groups 1 and 2. All three groups had significant amounts of ultrastructural damage outside of histologically demonstrated MI. These findings suggest that (1) gross and histologic MI size determination of 36 hours after ischemia underestimate extent of damage, and (2) ultrastructural cell changes cause significant release of CK and LD in coronary disease (CAD).