Certain enzymes are present in cardiac muscle that are released when tissue necrosis occurs. Serum aspartate aminotransferase (AST, formerly oxaloacetic transaminase, or SGOT) is elevated at some time in 90%-95% of acute MI patients (literature range, 87%-97%). These statistics for sensitivity of the AST in acute MI are based on multiple sequential AST determinations and are therefore not valid for any single determination. Aspartate transaminase levels become elevated 8-12 hours after infarction, reach a peak 24-48 hours after infarction, and fall to normal within 3-8 days. The AST blood levels correlate very roughly with the extent of infarct and may be only transiently and minimally abnormal.

Besides myocardial injury, the AST level may become elevated because of acute damage to parenchymal cells of the liver, skeletal muscle, kidney, and pancreas. Abnormality due to liver cell injury is especially common (e.g., liver congestion, active cirrhosis, and acute or chronic hepatitis), but an increased AST level will occur with sufficient degrees of skeletal muscle injury (including trauma or extensive surgical damage) and is also found fairly frequently in acute pancreatitis. In some of these situations, myocardial infarct may have to be considered in the differential diagnosis of the patient’s symptoms. Chronic hypokalemia may elevate both AST and also creatine kinase (CK) levels; morphine and meperidine (Demerol) may temporarily raise AST levels, and AST elevations have been reported in occasional patients receiving warfarin sodium (Coumadin) anticoagulant therapy and in some patients taking large doses of salicylates.

The major drawbacks of the AST in diagnosis of acute MI are the many conditions (especially liver congestion) that can produce AST elevation.