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?