Serum enzyme determinations in the diagnosis and assessment of myocardial infarction.

DIAGNOSTIC ENZYMOLOGY has grown exponentially since elevated serum amylase was first associated with pancreatitis in 19081 and Karmen, Wroblewski, LaDue, and their associates demonstrated in 1954 that SGOT* and LDH activity in serum increased following myocardial infarction.2 Following Markert's elucidation of the nature of LDH isoenzymes3 their importance in differential diagnosis was emphasized.4 Serum CPK elevations following myocardial infarction were first reported by Dreyfus and his coworkers5 in 1960, and soon confirmed by Hess and MacDonald.6 Determination of SGOT, LDH, and CPK activity rapidly became cornerstones in the laboratory diagnosis of acute myocardial infarction in man. Activity of many enzymes including aldolase, malic dehydrogenase, isomerase, and ICD may increase following myocardial infarction.7 Serum GGT, a lysosomal enzyme, exhibits increased activity late, reaching a peak within 8 days and returning to normal approximately 1 month following the initial insult.8 SPK contrary to CPK is not elevated following intramuscular injections,9 while serum GAPDH elevation may precede increases in conventional enzymes and aid detection of extension of myocardial necrosis.10 However, since SGOT, LDH, and CPK determinations have become established criteria in the laboratory diagnosis of acute myocardial