Elevated Cardiac Troponin I in Sepsis and Septic Shock: No Evidence for Thrombus Associated Myocardial Necrosis

David R Altmann,Regulo Rodriguez,Micha T Maeder,Thomas Fehr,Wolfgang Korte,Peter Ammann,Hans Rickli,Philipp Haager,Gian-Reto Kleger,Adrian V Hernandez

doi:10.1371/journal.pone.0009017

Abstract

BackgroundElevated cardiac troponin I (cTnI) is frequently observed in patients with severe sepsis and septic shock. However, the mechanisms underlying cTnI release in these patients are still unknown. To date no data regarding coagulation disturbances as a possible mechanism for cTnI release during sepsis are available.Methodology/Principal FindingsConsecutive patients with systemic inflammatory response syndrome (SIRS), sepsis or septic shock without evidence of an acute coronary syndrome were analyzed. Coagulation parameters (clotting time (CT), clot formation time (CFT), maximum clot firmness (MCF), α-angle) were assessed in native whole blood samples, and using specific activators to evaluate the extrinsic and intrinsic as well as the fibrin component of the coagulation pathway with the use of rotational thrombelastometry (ROTEM).Thirty-eight patients were included and 22 (58%) were cTnI-positive. Baseline characteristics between TnI-positive and -negative patients were similar. The CT, CFT, MCF and the α-angle were similar between the groups with trends towards shorter CT in the extrinsic and fibrin activation.Conclusions/SignificanceWe found no differences in coagulation parameters analyzed with rotational thrombelastometry between cTnI-positive and -negative patients with SIRS, severe sepsis, and septic shock. These findings suggest that pathophysiological mechanisms other than thrombus-associated myocardial damage might play a major role, including reversible myocardial membrane leakage and/or cytokine mediated apoptosis in these patients.

Highlights

Elevated concentrations of cardiac troponin I are frequently observed in patients with severe sepsis and septic shock even in the absence of an acute coronary syndrome (ACS) [1]
Conclusions/Significance: We found no differences in coagulation parameters analyzed with rotational thrombelastometry between cardiac troponin I (cTnI)-positive and -negative patients with systemic inflammatory response syndrome (SIRS), severe sepsis, and septic shock
One might speculate that septic patients with increased troponin concentrations might show evidence of increased platelet reactivity; it has been shown that septic patients show increased plateletleukocyte interaction [9], which is found early in myocardial infarction [10] and which is associated with an increased troponin release in patients undergoing percutaneous coronary intervention; interestingly, this increase can be inhibited with the use of a GP IIb/IIIa inhibitor [11]

Summary

Introduction

Elevated concentrations of cardiac troponin I (cTnI) are frequently observed in patients with severe sepsis and septic shock even in the absence of an acute coronary syndrome (ACS) [1]. Elevated cardiac cTnI in this setting are associated with left ventricular dysfunction [2] and adverse outcome [3]. The mechanisms underlying cTnI release in patients with sepsis are still unknown, and a number of hypotheses have been formulated [4]. There is ample evidence from the literature that platelet properties such as reactivity and receptor density are associated with an increased risk of troponin release with reduced coronary perfusion [6,7,8]. Elevated cardiac troponin I (cTnI) is frequently observed in patients with severe sepsis and septic shock. The mechanisms underlying cTnI release in these patients are still unknown. To date no data regarding coagulation disturbances as a possible mechanism for cTnI release during sepsis are available

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