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急性冠状动脉综合征中心肌肌钙蛋白的释放:是缺血还是坏死?

Release of cardiac troponin in acute coronary syndromes: ischemia or necrosis?

作者信息

Wu A H, Ford L

机构信息

Department of Pathology and Laboratory Medicine, Hartford Hospital, CT, USA.

出版信息

Clin Chim Acta. 1999 Jun 30;284(2):161-74. doi: 10.1016/s0009-8981(99)00078-9.

DOI:10.1016/s0009-8981(99)00078-9
PMID:10451243
Abstract

Analysis of cardiac troponin T and I have been shown to be effective in detecting minor myocardial injury in cardiac patients who present with acute coronary syndromes (ACS). Determination of minor myocardial injury is significant, as these patients have a higher short-term morbidity and mortality than other unstable angina patients with normal concentrations for these markers. In this report, two theories are given as to why cardiac troponin is superior to other markers such as CK-MB for risk stratification. The 'low cut-off concentration model' is based on the fact that troponin is not increased in patients with skeletal muscle disease or injury, resulting in low baseline concentrations of the cardiac isoforms in the absence of active cardiac disease. This enables the use of low decision limits. Troponin also has a higher myocardial tissue content relative to CK-MB, thereby also increasing its clinical sensitivity to irreversible injury. In the 'reversible ischemia model', cytoplasmic free troponin T and I leak across the membrane of myocytes as the result of reduced coronary blood flow. Jeopardized myocardial tissue can recover with acute recanalization. Support for this model comes from clinical observations and animal studies.

摘要

对心肌肌钙蛋白T和I的分析已被证明在检测患有急性冠状动脉综合征(ACS)的心脏病患者的轻微心肌损伤方面是有效的。确定轻微心肌损伤具有重要意义,因为这些患者的短期发病率和死亡率高于这些标志物浓度正常的其他不稳定型心绞痛患者。在本报告中,给出了两种关于为什么心肌肌钙蛋白在风险分层方面优于其他标志物(如肌酸激酶同工酶MB)的理论。“低临界浓度模型”基于这样一个事实,即患有骨骼肌疾病或损伤的患者肌钙蛋白不会升高,导致在无活动性心脏病时心脏同工型的基线浓度较低。这使得能够使用低判定限。相对于肌酸激酶同工酶MB,肌钙蛋白的心肌组织含量也更高,从而也增加了其对不可逆损伤的临床敏感性。在“可逆性缺血模型”中,由于冠状动脉血流减少,细胞质游离肌钙蛋白T和I会穿过心肌细胞膜泄漏。濒临危险的心肌组织可通过急性再灌注恢复。对该模型的支持来自临床观察和动物研究。

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