Prellwitz W, Hafner G, Rupprecht H J, Meyer J
Institut für Klinische Chemie und Laboratoriumsmedizin, Johannes-Gutenberg-Universität Mainz.
Med Klin (Munich). 1996 Jun 15;91(6):336-42.
In consideration of own investigations and analysis of the most important publications of other authors, a critical interpretation of the concentrations of Troponin T (cut off: < 1 microgram/l) and Troponin I (cut off: < 0.4 microgram/l) was done in patients with acute and chronic muscle diseases, with chronic renal failure, with acute myocardial infarction, and stable and unstable angina pectoris, after coronary angioplasty, following cardiac surgery and critical care patients.
In all cases with acute damage of the skeletal muscles (post operationem) the concentrations of TnT and TnI were in normal ranges. - In patients with chronic muscle diseases (M. Duchenne, Dermatomyositis) in 75% the TnT concentrations increased, while TnI concentrations were < 0.4 microgram/l. - In end stage renal disease patients undergoing chronic maintenance hemodialysis we found in 39% constantly elevated concentrations of TnT. TnI in all cases were in normal range. - In acute myocardial infarction in 97% of all patients both Troponins were increased, beginning 2 to 4 hours after onset. A normalization was observed between the 5th and 9th day. Very important is the differentiation between stable, and instable angina pectoris. In stable angina the concentration of both Troponins were in normal range, in contrast in 33 to 41% of all patients with unstable angina TnT and TnI were increased, in 9 to 16% even if the ECG showed no alteration. Elevated TnT or TnI concentrations predicted a significantly increased mortality. After coronary angioplasty and heparin treatment all patients had once more an elevation of TnT and TnI 8 and 27 hours after the invasive therapy. One of these substantial reasons for these minor myocardial cell necrosis is beside the endothelial injury the activation of the platelets and the coagulation system. - During the therapy with hirudin increases of TnT and TnI was not observed. Following cardiac surgery (ACVB) 6 to 48 hours after aortic unclamping 76 patients with TnI < 1 microgram/l had no perioperative myocardial infarction, while 14 patients with TnI concentrations > 1 microgram/l in 71.4% (n = 10) developed an acute infarction. - In patients in critical care units we observed only increased TnI concentrations in shock, especially in septic shock with multiple organ failures.
考虑到自身研究以及对其他作者最重要出版物的分析,对急性和慢性肌肉疾病、慢性肾衰竭、急性心肌梗死、稳定型和不稳定型心绞痛、冠状动脉成形术后、心脏手术后以及重症监护患者的肌钙蛋白T(临界值:<1微克/升)和肌钙蛋白I(临界值:<0.4微克/升)浓度进行了批判性解读。
在所有骨骼肌急性损伤(术后)的病例中,肌钙蛋白T和肌钙蛋白I的浓度均在正常范围内。——在慢性肌肉疾病(杜兴氏肌营养不良症、皮肌炎)患者中,75%的患者肌钙蛋白T浓度升高,而肌钙蛋白I浓度<0.4微克/升。——在接受慢性维持性血液透析的终末期肾病患者中,我们发现39%的患者肌钙蛋白T浓度持续升高。所有病例中的肌钙蛋白I均在正常范围内。——在急性心肌梗死患者中,97%的患者两种肌钙蛋白均升高,发病后2至4小时开始升高。在第5天至第9天观察到恢复正常。稳定型和不稳定型心绞痛的鉴别非常重要。在稳定型心绞痛中,两种肌钙蛋白的浓度均在正常范围内,相比之下,在所有不稳定型心绞痛患者中,33%至41%的患者肌钙蛋白T和肌钙蛋白I升高,9%至16%的患者即使心电图无改变也是如此。肌钙蛋白T或肌钙蛋白I浓度升高预示死亡率显著增加。冠状动脉成形术和肝素治疗后,所有患者在侵入性治疗后8小时和27小时肌钙蛋白T和肌钙蛋白I再次升高。除内皮损伤外,这些轻微心肌细胞坏死的重要原因之一是血小板和凝血系统的激活。——在使用水蛭素治疗期间,未观察到肌钙蛋白T和肌钙蛋白I升高。心脏手术后(冠状动脉搭桥术),在主动脉阻断解除后6至48小时,76例肌钙蛋白I<1微克/升的患者未发生围手术期心肌梗死,而14例肌钙蛋白I浓度>1微克/升的患者中,71.4%(n = 10)发生了急性梗死。——在重症监护病房的患者中,我们仅在休克患者中观察到肌钙蛋白I浓度升高,尤其是在伴有多器官功能衰竭的脓毒性休克患者中。