Bhayana V, Henderson A R
Department of Laboratory Medicine, University Hospital (University of Western Ontario), London, Canada.
Clin Biochem. 1995 Feb;28(1):1-29. doi: 10.1016/0009-9120(94)00065-4.
To assess various biochemical markers of myocardial damage.
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.
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?
评估心肌损伤的各种生化标志物。
在将任何检测方法常规用作心肌损伤的生化标志物之前，必须严格评估其已发表的诊断效用证据。此类评估包括受试者操作特征曲线（ROC）分析、对所宣称的敏感性和特异性值的置信区间估计，以及串联和并联检测模式的效果。还必须确定检测的纳入规则（高特异性）和排除规则（高敏感性）决策阈值，这些阈值可能随症状出现后的时间而变化。缺血性心脏病的范围包括急性（猝死、非Q波和Q波梗死）和慢性（稳定型、不稳定型和变异型心绞痛）情况。心肌损伤的生化标志物在急性缺血性心脏病的诊断中最有价值，尽管越来越多地发现其中一些标志物在慢性缺血性心脏病中具有预后价值。酶活性标志物包括天冬氨酸转氨酶、肌酸激酶（及其同工酶和亚型）、乳酸脱氢酶及其同工酶。肌酸激酶同工酶-2也可以通过免疫法检测，由于其速度快且血液水平比相应活性升高得更早，这种检测方法的使用越来越多。市售的非酶标志物是肌红蛋白和肌钙蛋白T；肌钙蛋白I预计在1995年末上市。虽然肌红蛋白是心肌损伤的非特异性指标，但其诊断价值在于其在血液中的早期出现。肌钙蛋白T对心脏的特异性更高，但已发表的数据似乎表明肌钙蛋白I对心脏的特异性更强。症状出现后，肌钙蛋白水平与肌酸激酶同工酶-2的质量检测在大致相同的时间变得异常；因此，它们作为心肌损伤的早期标志物并无用处。
这些心肌损伤的非酶标志物的出现必须促使人们重新评估酶标志物的持续使用情况。它们是否必要，如果是，应该保留哪些？
