IN THE PAST few years, determination of the serum or plasma activity of predomninantly intracellular enzyme systenms has become a valuable adjunct in the study of disease. Since the original report of LaDue et al.1 many groups have investigated the levels of serum glutamic oxalacetic transaminase activity in a wide variety of conditions. Both myocardiuni and liver contain high concentrations of this enzyme, and clinical experienee has demonstrated the value of repeated determinations of blood transamiliase activity in the diagnosis and evaluation of myocardial infaretion and liver disease.2 In animals an uncomplicated acute meyocardial infaretion is associated with inereases in serum glutamic oxalacetic transaminase activity that correlate roughly with the amount of infarcted muscle.3-6 In the majority of patients sufferilng from an acute myocardial infaretion, the changes in blood enzyme activity resemble those produced in the experimelntal animal; after the first day, the level increases, usually to less than 400 units. and then graduallv falls to normal within a 3or 4-day period.7 Infrequently, however, the blood enzyme activity soars to very high levels followiing an acute myocardial infaretion. In animal experiments, such high levels of enzyme activity have been recorded only in instanees of very large infarets.3 6 Occasional patients have been cited with very high seruiii levels of glutamic oxalacetic transaminase activity prior to death from a myocardial infaretion, and autopsy disclosed central necrosis of the liver.7' 8 It has been postulated that the liver nmay contribute to these unusual levels of blood enzymne activity.8' 9 There has lnot, however, been ani extensive clinical survey of this problemn.