Mair J, Artner-Dworzak E, Lechleitner P, Smidt J, Wagner I, Dienstl F, Puschendorf B
Department of Medical Chemistry and Biochemistry, University of Innsbruck, Austria.
Clin Chem. 1991 Jun;37(6):845-52.
Troponin T is a structurally bound protein found in striated muscle cells. We tested concentrations of its cardiac-specific isotype in peripheral venous blood samples serially drawn from 72 patients with confirmed myocardial infarction. Fifty-nine patients received thrombolytic treatment with intravenous streptokinase, urokinase, or recombinant tissue-type plasminogen activator; because of contraindications, the remaining 13 patients did not. Concentrations of troponin T in plasma, measured by an enzyme-linked immunosorbent assay, started increasing within a few hours after the onset of symptoms (median, 4 h; range, 1-10 h). The sensitivity of troponin T for detecting myocardial infarction was 100% from 10 to 120 h after the onset of symptoms; sensitivity on the seventh day after admission was 84%. Concentrations were increased for up to three weeks in some patients with late or high peak values. Successful reperfusion in Q-wave infarction obviously influences the release of troponin T into plasma, with all such cases showing peak values less than or equal to 26 h (median, 14 h) after the onset of symptoms. Troponin T concentrations in these patients returned to within the reference interval more rapidly than in nonreperfused subjects. In the 13 patients without fibrinolytic therapy, troponin T tended to peak approximately 48 h (median) after the onset of chest pain. Troponin T concentrations in patients for whom thrombolysis was unsuccessful resembled those in patients without fibrinolytic therapy. The specificity of the assay was 96% as tested in samples of 96 emergency-room patients. The reference interval (less than 0.5 micrograms/L) was established from samples of 100 healthy blood donors. Troponin T measurements are a specific and sensitive method for the early and late diagnosis of acute myocardial infarction and could, therefore, provide a new criterion in laboratory diagnosis of its occurrence.
肌钙蛋白T是一种存在于横纹肌细胞中的结构结合蛋白。我们对72例确诊心肌梗死患者连续采集的外周静脉血样本中其心脏特异性同种型的浓度进行了检测。59例患者接受了静脉注射链激酶、尿激酶或重组组织型纤溶酶原激活剂的溶栓治疗；由于存在禁忌症，其余13例患者未接受治疗。通过酶联免疫吸附测定法测得的血浆中肌钙蛋白T浓度在症状发作后数小时内开始升高（中位数为4小时；范围为1 - 10小时）。症状发作后10至120小时，肌钙蛋白T检测心肌梗死的敏感性为100%；入院第七天的敏感性为84%。一些晚期或峰值较高的患者其浓度升高可持续长达三周。Q波梗死患者成功再灌注明显影响肌钙蛋白T释放到血浆中，所有这些病例症状发作后峰值均小于或等于26小时（中位数为14小时）。这些患者的肌钙蛋白T浓度比未再灌注的患者更快恢复到参考区间内。在13例未接受纤维蛋白溶解治疗的患者中，肌钙蛋白T往往在胸痛发作后约48小时（中位数）达到峰值。溶栓治疗未成功的患者的肌钙蛋白T浓度与未接受纤维蛋白溶解治疗的患者相似。在96例急诊患者的样本中进行检测，该检测方法的特异性为96%。参考区间（小于0.5微克/升）是根据100名健康献血者的样本确定的。肌钙蛋白T测量是急性心肌梗死早期和晚期诊断的一种特异性和敏感性方法，因此可为其发生的实验室诊断提供新的标准。
