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[不稳定型和稳定型心绞痛患者经皮冠状动脉腔内血管成形术后肌钙蛋白T的释放情况]

[Release of troponin T following PTCA in patients with unstable and stable angina pectoris].

作者信息

Ries M W, Rupprecht H J, Dudsjak H, Hafner G, Meyer J

机构信息

II. Medizinische Klinik, Johannes-Gutenberg-Universität Mainz.

出版信息

Z Kardiol. 1999 Nov;88(11):914-21. doi: 10.1007/s003920050369.

Abstract

It is still uncertain to what extent PTCA contributes to a rise of the myocardial ischemic marker troponin T. The purpose of this study was to determine the release of troponin T in patients with unstable and stable angina pectoris pre- and post-PTCA. Serial troponin T measurements were performed in 66 patients with unstable angina (group A) and 55 patients with stable angina pectoris (group B) pre-PTCA and 4, 8 and 24 hours post-PTCA. In group A, 39 (59%) patients with unstable angina pectoris showed pathologic troponin T concentrations (troponin T > or = 0.1 ng/ml); in 27 (41%) patients already pre-PTCA the troponin T was elevated beyond the normal values. Medians of troponin T rose from initially 0.045 ng/ml pre-PTCA to a maximum of 0.21 ng/ml 8 hours post PTCA. In group B medians of troponin T were at all times within normal limits; there was no rise in the observation interval. Using the Chi-square test there were statistically significant differences between group A and B regarding the troponin T values pre- and post-PTCA. In group A medians of total creatine kinase ranging between 24 U/L and 30 U/L were to all times within normal limits. Also in group B medians of total creatine kinase were always within normal limits. Statistically significant differences between the two groups could not be shown. Our study could show a difference in the periinterventional course of the ischemic marker troponin T in patients with unstable and stable angina pectoris. The data indicate a PTCA induced reversible ischemia of the cardiac muscle cell with additional release of the cytoplasmatic bound part of troponin T in patients with unstable angina pectoris. Troponin T also appears to be a more sensitive marker of very short myocardial ischemia than creatine kinase.

摘要

经皮冠状动脉腔内血管成形术(PTCA)在多大程度上导致心肌缺血标志物肌钙蛋白T升高仍不确定。本研究的目的是确定不稳定型和稳定型心绞痛患者在PTCA术前和术后肌钙蛋白T的释放情况。对66例不稳定型心绞痛患者(A组)和55例稳定型心绞痛患者(B组)在PTCA术前以及术后4、8和24小时进行了系列肌钙蛋白T测量。在A组中,39例(59%)不稳定型心绞痛患者肌钙蛋白T浓度呈病理性升高(肌钙蛋白T≥0.1 ng/ml);在27例(41%)患者中,术前肌钙蛋白T就已升高超过正常值。肌钙蛋白T的中位数从PTCA术前最初的0.045 ng/ml升至PTCA术后8小时最高的0.21 ng/ml。在B组中,肌钙蛋白T的中位数在所有时间均在正常范围内;观察期间没有升高。使用卡方检验,A组和B组在PTCA术前和术后的肌钙蛋白T值存在统计学显著差异。在A组中,总肌酸激酶的中位数在24 U/L至30 U/L之间,所有时间均在正常范围内。B组中总肌酸激酶的中位数也始终在正常范围内。两组之间未显示出统计学显著差异。我们的研究表明,不稳定型和稳定型心绞痛患者在介入治疗期间缺血标志物肌钙蛋白T的病程存在差异。数据表明,在不稳定型心绞痛患者中,PTCA诱导心肌细胞可逆性缺血,并额外释放细胞质结合部分的肌钙蛋白T。肌钙蛋白T似乎也是比肌酸激酶更敏感的极短时间心肌缺血标志物。

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