Myocardial infarctions and serum enzymes.

CLINICAL CHEMISTRY, Vol. 30, No. 8, 1984 1285 Measurement of certain enzymes in serum has been essential to the evaluation of acute myocardial infarction since the first reports (1) of elevated serum glutamic oxalacetic transaminase (as it was then called) in 1959. Over the past two decades, testing for increased serum creatine kinase (CK) and lactate dehydrogenase (LD) has become routine to assess myocardial damage. Lactate dehydrogenase can be separated into five isoenzymes by electrophoresis on agarose gel, and the LD-1 isoenzyme can be quantified immunochemically. The three creatine kinase isoenzymes (MM, MB, BB) can be assayed by immunoinhibition, an immunochemical method, radioinununoassay, or electrophoretic separation on agarose gel. After electrophoresis, the plates are examined under long-wave ultraviolet light for the presence or absence of the CK-MB band. The method most commonly applied for CK and LD assay is electrophoresis on agarose gel. Diagnosis of acute myocardial infarction is based on the triad of chest pain, electrocardiographic abnormalities (including ST segment elevation with evolution of Q waves), and increased LD and CK enzymes with specific isoenzyme patterns. Lactate dehydrogenase from myocardial tissue has a predominance of the LD-1 isoenzyme. In normal serum, LD-2 is the most prominent isoenzyme. The most commonly accepted pattern for assessing myocardial damage is a serum LD-1/LD-2 ratio greater than one. Myocardial necrosis is also suspected when CK is increased with CK-MB exceeding 4% of total CK. With use of a combination of LD1/LD-2 greater than one and elevated CK-MB, acute myocardial necrosis can be diagnosed with a sensitivity of 90% and specificity of 95% (2). However, there are other clinical states in which either the LD-1/LD-2 ratio may “flip” or CK-MB be increased. In I addition to the heart, erythrocytes and the renal cortex have a preponderance of LD-1. In pernicious anemia, hemolysis, and renal cortical infarction the LD isoenzyme patterns mimic myocardial infarction. The increase and time to peak value are important in differentiating these disorders. In infarction, the LD increase occurs 12 to 24 h after the onset of symptoms, and the peak value is usually seen between 48 and 72 h. This sequence would be unusual in hemolytic states. Erythrocyte damage is unlikely to produce an LD1ILD-2 ffip (3). Evaluation of blood samples at least every 12 h for the first two days after suspected myocardial damage assists in the clinical correlation of the isoenzyme pattern. In this issue Shahangian et al. (4) describe the LI) isoenzyme pattern for patients with electrical burns, thermal burns, or trauma. The isoenzyme pattern for the three groups is strikingly similar. The percentage of LD-1 is 1516%, which is within the normal range. The LD-1ILD-2 ratio for the three groups varies from 0.63 to 0.69. Only six patients have an LD-1ILD-2 ifip. This represents just 1% of their population not suspected of acute myocardial infarction. Creatine kinase is found in skeletal muscle, heart, brain, and the gastrointestinal tract when assayed by fluorescence scanning of electrophoretic media (5). CK-MB activity in the myocardium represents 15 to 46% of the total CK activity. There are traces of CK-MB present in other tissues, but most is confined to the heart. Increased serum CK-MB may occur in skeletal muscle trauma, Duchenne’s muscular dystrophy, cardiac valve replacement, electrical cardioversion, myocarditis, hypothermia, hyperthermia, Reye’s syndrome, and long-distance running (3, 6). Fortunately, the proportion of patients with elevated CK-MB in these disorders is low, and the absolute values are generally less than in acute myocardial infarction. Burn and trauma patients have uniformly increased total CK (4). Fifty-seven percent had CK-MB greater than 4%, including 16 patients with fractions greater than 10%. Clinical data, electrographic abnormalities, and technetium pyrophosphate scans did not support a diagnosis of myocardial necrosis. The increased CK-MB in these patients may be explained by the inconsistent reports on the normal amount of CK-MB in skeletal muscle or the possibility of individual varistion of CK-MB among patients. In those individuals with increased CKMB activity, the LD-1ILD-2 ratio is less than one in all cases. This supports the high predictive accuracy of the combination of LD-1ILD-2 flip and increased CK-MB in the diagnosis of acute myocardial necrosis (7). Myocardial damage is best assessed by combining the clinical history, electrocardiogram, and CK and LD isoenzymes. Samples of serum for enzyme analysis should be performed frequently enough to determine the increase and peak of increased activity in serum. Burn and trauma patients have increases in LD and CK that can be differentiated from myocardial infarction. The presence of an LD1/LD-2 flip and concomitant increase in serum CK-MB remain in the most sensitive and specific indicators of acute myocardial damage.