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

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.

Severe Pneumococcal Pneumonia Causes Acute Cardiac Toxicity and Subsequent Cardiac Remodeling

“…In addition, Corrales-Medina et al showed recently in a cohort study that 10-30% of adults (without clinical history of cardiac disease) admitted for 16 CAP, developed clinically relevant heart failure, arrhythmias, or acute coronary syndromes, up to 10 years after hospitalization (6-8). More commonly, up to 59% of patients admitted with sepsis develop a cardiac phenomenon called demand ischemia (i.e., mild troponin elevation and repolarization abnormalities in absence of myocardial infarction or coronary disease), rather than sepsis-induced cardiomyopathy or MACE (39)(40)(41). In our study, we found that all six previously healthy NHP with pneumococcal pneumonia, developed nonspecific cardiac changes that cannot be categorized as MACE but are consistent with what clinicians call demand ischemia.…”

Role of Admission Troponin‐T and Serial Troponin‐T Testing in Predicting Outcomes in Severe Sepsis and Septic Shock

“…Electrocardiography and echocardiography in these patients rarely demonstrate ischemic changes, and few patients have inducible ischemia on stress testing or occlusive coronary thrombus on autopsy 8, 26, 30. Postulated causes for troponin elevations in septic patients include ischemic mechanisms (eg, supply–demand imbalance or microvascular spasm or thrombosis) and nonischemic mechanisms (eg, reversible myocardial membrane leakage of cytosolic TnT pool or direct cellular toxicity from inflammatory mediators, microbial toxins, or excessive catecholamine levels) 7, 31, 32. While relative hypovolemia, inadequate resuscitation, and prolonged hypotension may contribute to myocardial injury in patients with septic shock, fluid resuscitation does not appear to influence the subsequent values of hs‐TnT on serial testing 12…”

Early Cardiac Arrest in Patients Hospitalized With Pneumonia

“…Sepsis can also cause abrupt cardiac arrest through effects independent of coronary ischemia, either through direct arrhythmogenic effects or through nonischemic myocardial injury and circulatory dysfunction. [25][26][27][28][29] While we were not able to investigate these mechanisms directly, we found myocardial ischemia/infarction as a possible cause in 6.3% of arrests in patients with pneumonia, and it was an active diagnosis in 13.4%. These are likely underestimates, as some cases of myocardial ischemia/infarction could have been undetected prior to an IHCA.…”