Ostrow et al. (1956) quote one case of Fiedler's myo- carditis in which the S.G.O.T. was elevated as one would expect, and Chesler (1958) reports elevated levels in diphtheritic myocarditis.Nydick et al. (1955a, 1955b) give an interesting account of its elevation in acute rheumatic carditis.The latter at any rate cannot often be confused with myocardial infarction, and no such difficulty arose in the present series. SummarySerial daily estimations of serum glutamic oxalacetic transaminase (S.G.O.T.) for at least 10 days have been made in 34 acute episodes of myocardial infarction occurring in 28 patients.The results have been com- pared with changes in erythrocyte sedimentation rate (E.S.R.), temperature, and electrocardiogram.Estimations of S.G.O.T. are most useful (a) when the electrocardiogram is obscured by previous myocardial infarction, arrhythmias, bundle-branch block, left ven- tricular strain, and digitalis; (b) when extension of myocardial infarction is suspected; and (c) to distinguish between acute coronary insufficiency and myocardial infarction.There was no rise in S.G.O.T. in 8.8% of the cases of fresh myocardial infarction.The maximum elevation of S.G.O.T. roughly corre- sponds with the electrocardiographic estimation of the size of the infarct only if other causes of a raised trans- aminase can be excluded.The most important of these in myocardial infarction is centrilobular necrosis of the liver secondary to cardiac failure.In small infarctions serial estimations of S.G.O.T. may show a characteristic curve even though the peak does not exceed 40 units.
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Bruce et al. (1958) studied this question.
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