Favory Raphael, Neviere Remi
Physiology Department, School of Medicine, EA2689 University of Lille, France.
Crit Care. 2006;10(4):224. doi: 10.1186/cc4991.
Because no bedside method is currently available to evaluate myocardial contractility independent of loading conditions, a biological marker that could detect myocardial dysfunction in the early stage of severe sepsis would be a helpful tool in the management of septic patients. Clinical and experimental studies have reported that plasma cardiac troponin levels are increased in sepsis and could indicate myocardial dysfunction and poor outcome. The high prevalence of elevated levels of cardiac troponins in sepsis raises the question of what mechanism results in their release into the circulation. Apart from focal ischemia, several factors may contribute to the microinjury and minimal myocardial cell damage in the setting of septic shock. A possible direct cardiac myocytotoxic effect of endotoxins, cytokines or reactive oxygen radicals induced by the infectious process and produced by activated neutrophils, macrophages and endothelial cells has been postulated. The presence of microvascular failure and regional wall motion abnormalities, which are frequently observed in positive-troponin patients, also suggest ventricular wall strain and cardiac cell necrosis. Altogether, the available studies support the contention that cardiac troponin release is a valuable marker of myocardial injury in patients with septic shock.
由于目前尚无独立于负荷条件来评估心肌收缩力的床旁方法，因此，一种能够在严重脓毒症早期检测心肌功能障碍的生物标志物将成为脓毒症患者管理中的有用工具。临床和实验研究报告称脓毒症患者血浆心肌肌钙蛋白水平升高，这可能提示心肌功能障碍和不良预后。脓毒症患者中心肌肌钙蛋白水平升高的高发生率引发了其释放入循环的机制是什么的问题。除了局灶性缺血外，在脓毒性休克情况下，多种因素可能导致微损伤和心肌细胞轻微损伤。有人推测，感染过程诱导并由活化的中性粒细胞、巨噬细胞和内皮细胞产生的内毒素、细胞因子或活性氧自由基可能具有直接的心肌细胞毒性作用。在肌钙蛋白阳性的患者中经常观察到的微血管功能障碍和局部室壁运动异常的存在，也提示心室壁应变和心肌细胞坏死。总之，现有研究支持这样的观点，即心肌肌钙蛋白释放是脓毒性休克患者心肌损伤的一个有价值的标志物。
