BIOCHEMICAL MARKERS OF MYOCARDIAL DAMAGE

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 diagnosti c utility must be critically assessed. Such assessment includes receiv er operator curve (ROC) curve analyses, confidence interval estimates of claimed sensitivity and specificity values, and the effects of test ing in serial and parallel modes. It is also necessary to establish th e test's rule-in (high specificity) and rule-out (high sensitivity) de cision 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 vari ant angina) conditions. Biochemical markers of myocardial damage are o f most value in the diagnosis of acute ischemic heart disease, althoug h increasingly some of these markers are being found to possess a prog nostic value in chronic ischemic heart disease. The markers of enzymat ic activity include aspartate aminotransferase, creatine kinase (toget her with isoenzymes and isoforms), and lactate dehydrogenase and isoen zymes. Creatine kinase isoenzyme-2 may also be measured immunologicall y, and this type of assay is in increasing use both because of its spe ed and because its blood levels rise earlier than the corresponding ac tivities. The commercially available nonenzymatic markers are myoglobi n and troponin T; troponin I is expected to become available in late 1 995. 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 leve ls 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 availab ility of these nonenzymatic markers of myocardial damage must force a reassessment of the continued use of the enzymatic markers. Are they n ecessary, and if so, which ones should be retained?