Bench-to-bedside review: Significance and interpretation of elevated troponin in septic patients

被引:61
作者
Favory, Raphael
Neviere, Remi [1 ]
机构
[1] Univ Lille, Dept Physiol, Sch Med, EA2689, Lille, France
[2] Univ Hosp Lille, Med Intens Care Unit, Lille, France
来源
CRITICAL CARE | 2006年 / 10卷 / 04期
关键词
D O I
10.1186/cc4991
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
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.
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页数:6
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共 43 条
[31]   Cytokine-induced modulation of cardiac function [J].
Prabhu, SD .
CIRCULATION RESEARCH, 2004, 95 (12) :1140-1153
[32]   Myocardial injury in critically ill patients - Relation to increased cardiac troponin I and hospital mortality [J].
Quenot, JP ;
Le Teuff, G ;
Quantin, C ;
Doise, JM ;
Abrahamowicz, M ;
Masson, D ;
Blettery, B .
CHEST, 2005, 128 (04) :2758-2764
[33]   NH2 terminal pro-brain natriuretic peptide plasma level as an early marker of prognosis and cardiac dysfunction in septic shock patients [J].
Roch, A ;
Allardet-Servent, J ;
Michelet, P ;
Oddoze, C ;
Forel, JM ;
Barrau, K ;
Loundou, A ;
Perrin, G ;
Auffray, JP ;
Portugal, H ;
Papazian, L .
CRITICAL CARE MEDICINE, 2005, 33 (05) :1001-1007
[34]   Common causes of troponin elevations in the absence of acute myocardial infarction - Incidence and clinical significance [J].
Roongsritong, C ;
Warraich, I ;
Bradley, C .
CHEST, 2004, 125 (05) :1877-1884
[35]   Serum cardiac troponin T as a prognostic marker in early sepsis [J].
Spies, C ;
Haude, V ;
Fitzner, R ;
Schröder, K ;
Overbeck, M ;
Runkel, N ;
Schaffartzik, W .
CHEST, 1998, 113 (04) :1055-1063
[36]   Polyethylene glycol-superoxide dismutase prevents endotoxin-induced cardiac dysfunction [J].
Supinski, Gerald S. ;
Callahan, Leigh A. .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2006, 173 (11) :1240-1247
[37]   A myocardial cytotoxic process is involved in the cardiac dysfunction of meningococcal septic shock [J].
Thiru, Y ;
Pathan, N ;
Bignall, S ;
Habibi, P ;
Levin, M .
CRITICAL CARE MEDICINE, 2000, 28 (08) :2979-2983
[38]   Myocardial cell injury in septic shock [J].
Turner, A ;
Tsamitros, M ;
Bellomo, R .
CRITICAL CARE MEDICINE, 1999, 27 (09) :1775-1780
[39]   Troponin in septic and critically ill patients [J].
van Bockel, EAP ;
Tullekan, JE ;
Ligtenberg, JLM ;
Zijlstra, JG .
CHEST, 2005, 127 (02) :687-688
[40]   Cardiac troponin I release and cytokine response during experimental human endotoxaemia [J].
van Bockel, EAP ;
Tulleken, JE ;
Kobold, ACM ;
Ligtenberg, JJM ;
van der Werf, TS ;
Spanjersberg, R ;
Zijlstra, JG .
INTENSIVE CARE MEDICINE, 2003, 29 (09) :1598-1600