Biochemical markers of myocardial damage

Abstract

Objective: To assess various biochemical markers of myocardial damage.

Methods and results: Before routinely using any test as a biochemical marker of myocardial damage, the published evidence for its diagnostic utility must be critically assessed. Such assessment includes receiver operator curve (ROC) curve analyses, confidence interval estimates of claimed sensitivity and specificity values, and the effects of testing in serial and parallel modes. It is also necessary to establish the test's rule-in (high specificity) and rule-out (high sensitivity) decision thresholds that may vary with time after the onset of symptoms. The spectrum of ischemic heart disease includes acute (sudden death, non-Q- and Q-wave infarctions) and chronic (stable, unstable, and variant angina) conditions. Biochemical markers of myocardial damage are of most value in the diagnosis of acute ischemic heart disease, although increasingly some of these markers are being found to possess a prognostic value in chronic ischemic heart disease. The markers of enzymatic activity include aspartate aminotransferase, creatine kinase (together with isoenzymes and isoforms), and lactate dehydrogenase and isoenzymes. Creatine kinase isoenzyme-2 may also be measured immunologically, and this type of assay is in increasing use both because of its speed and because its blood levels rise earlier than the corresponding activities. The commercially available nonenzymatic markers are myoglobin and troponin T; troponin I is expected to become available in late 1995. While myoglobin is a nonspecific indicator of myocardial damage, its diagnostic value is due to its early appearance in blood. Troponin T is more cardiac specific, but the published data appears to suggest that the cardiac specificity of troponin I is superior. Troponin levels become abnormal at about the same time after the onset of symptoms as mass assays of creatine kinase isoenzyme-2; therefore, they are not useful as early markers of myocardial damage.

Conclusion: The availability of these nonenzymatic markers of myocardial damage must force a reassessment of the continued use of the enzymatic markers. Are they necessary, and if so, which ones should be retained?