High sensitivity troponin measurement in critical care: Flattering to deceive or ‘never means nothing’?

Abstract

Introduction Troponin elevation is central to the diagnosis of acute type 1 myocardial infarction. It is, however, elevated in a range of other conditions, including type 2 myocardial infarction, and this setting is increasingly associated with adverse clinical outcomes. Patients within intensive care frequently have at least one organ failure together with a range of co-morbidities. Interpretation of troponin assay results in this population is challenging. This clinical uncertainty is compounded by the introduction of ever more sensitive troponin assays. Areas covered The aims of this review are to (a) describe the currently available literature about the use of troponin assays in intensive care, (b) analyse the challenges presented by the introduction of increasingly sensitive troponin assays and (c) assess whether the role of troponin assays in intensive care may change in the future, dependent upon recent and ongoing research suggesting that they are predictive of outcome regardless of the underlying cause: the ‘never means nothing’ hypothesis.

Thrombotic complications in 2928 patients with COVID-19 treated in intensive care: a systematic review

“…Thus, whilst many early reports in patients with COVID-19 equated a troponin rise with myocardial infarction, typically this is more like to be related to sepsis and associated systemic inflammatory response, pro-coagulant status, and myocarditis. Without regular screening with cardiac biomarkers, in the absence of major ECG changes, myocardial injury in patients with COVID-19 can be frequently missed and yet is associated with an increased mortality [62,63]. Likewise, stroke can be very challenging to recognise in patients who are intubated and ventilated, due to masking of clinical signs and symptoms with sedation and neuromuscular blockade.…”

Septic cardiomyopathy: Diagnosis and management

“… [68] However, troponin elevation is frequently observed in critically ill patients regardless of reasons for admission. Furthermore, assays for troponin have become increasingly sensitive, [70] and the association between troponin and hospital mortality is substantially attenuated after controlling for confounding factors. [71] The causes of troponin elevation are likely multifactorial, and increases are associated with myocardial membrane leakage and/or cytokine apoptosis, but not macrothrombi.…”

Distribution of contemporary sensitivity troponin in the emergency department and relationship to 30-day mortality: The CHARIOT-ED substudy

“…The CHARIOT-ED substudy increased illness severity has been demonstrated to be closely associated with cTn elevation, not only in ED, but also in the context of sepsis and patients admitted to intensive care. [23][24][25][26][27] The most important observation of this study is that increasing cs-cTnI concentrations (regardless of the manufacturer's 99th percentile value) are associated with increasing 30-day mortality. Furthermore, the AUCs of 0.863 and 0.859 suggest that cs-cTnI testing on admission, outside of the context of acute T1MI, could provide useful prognostic information for clinicians about the patients newly presented to them.…”