Limitations in cardiac assessment at the bedside

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. Introduction In 2000, the Joint European Society of Cardiology/American College of Cardiology Committee proposed a new definition of myocardial infarction based predominantly on the detection of the cardiospecific biomarkers troponin T and troponin I in the appropriate clinical setting [1]. Given that cardiac troponin is highly sensitive for detecting even minimal myocardial-cell necrosis, these markers may become ‘positive’ even in the absence of thrombotic acute coronary syndromes [2]. This may occasionally be related to a spurious troponin elevation but may also be due to several nonthrombotic cardiac and systemic diseases [2-4]. Sepsis and other systemic inflammatory processes may lead to myocardial depression and cellular injury, greatly increased oxygen consumption, reduced microvascular circulation, and decreased oxygen delivery to the heart, ultimately resulting in the release of troponin into the systemic circulation [5]. The aim of this review is to go from bench to bedside to determine what evidence and interests are able to incite intensivists to evaluate the cardiac troponin plasma marker in the context of sepsis. Limitations in cardiac assessment at the bedside Abnormalities of cardiac function are frequent in patients with sepsis. Approximately 50% of patients with severe sepsis and septic shock may develop impairment of ventricular performance. Whereas evaluation of myocardial performance during septic shock is of critical importance to select the best therapeutic options, several factors complicate the diagnosis of sepsis-induced myocardial dysfunction in humans. Making accurate measurements of cardiac function is difficult and this is confounded by the inherent difficulty of excluding patients with true coronary insufficiency with sepsis. The available evaluation methods have their strengths and limitations, leading to an absence of consensus regarding the gold standard technique to assess cardiac function. In addition, most of the contractility indexes are affected by peripheral vasodilatation and changes in loading conditions observed in septic shock. In addition, catecholamine stress observed in sepsis stimulates the myocardium and may, therefore, mask myocardial depression. Since alteration of myocardial performance in sepsis may be related to structural abnormalities of the heart, biochemical markers could thus be useful in the diagnosis of sepsis-induced myocardial dysfunction. Recently, plasma cardiac troponin has been proposed as a biomarker that accurately detects myocardial dysfunction and provides prognosis information in septic patients. Review Bench-to-bedside review: Significance and interpretation of elevated troponin in septic patients Raphael Favory1,2 and Remi Neviere1 1Physiology Department, School of Medicine, EA2689 University of Lille, France 2Medical Intensive Care Unit, Universitary Hospital of Lille, France Corresponding author: Remi Neviere, [email protected] Published: 4 August 2006 Critical Care 2006, 10:224 (doi:10.1186/cc4991) This article is online at http://ccforum.com/content/10/4/224 © 2006 BioMed Central Ltd IL = interleukin; TNF = tumor necrosis factor.