Abstract
An increase of serum glutamic oxalacetic transaminase (SGO-T) activity following myocardial infarction was first described by LaDue et al. 1 and subsequently confirmed by numerous investigators. 2-6 Much emphasis has been placed on elevated SGO-T values in substantiating the clinical impression of myocardial infarction, especially when the electrocardiogram reveals equivocal changes, previous infarction, left bundle branch block, or arrhythmia. 7-9 With increased understanding of the ubiquitous nature of GO-T distribution in human tissues, it has become apparent that liver necrosis 10-14 and a host of other disease states 5,6,15-21 can provoke a rise in SGO-T activity. Thus, confusion may still exist when there is elevated SGO-T activity in the absence of electrocardiographic evidence of heart muscle damage. Obstructive biliary tract disease causes a rise in SGO-T activity, 22,23 and this rise may be unrelated to hepatic necrosis. 24 The demonstration of high GO-T activity in bile 25 further serves to
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