Perspective on the clinical application of troponin in heart failure and states of cardiac injury

Bass, Almasa; Patterson, J. Herbert

doi:10.1007/s10741-008-9124-8

Cited by 8 publications

(4 citation statements)

References 79 publications

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“…Cardiac tissue damage, like cell death or necrosis with myofilament injuries, will inevitably cause cTn elevation. Meanwhile, the severity of cardiac damage can be reflected by the level of increased cTn ( Bass et al, 2010 ). Mir and Heinzerling have reported that some cases with PD-1/PD-L1 inhibitor immunotherapy-related heart failure, cardiomyopathy, myocarditis, and myocardial fibrosis may manifest normal troponin levels ( Heinzerling et al, 2016 ; Mir et al, 2018 ).…”

Section: Diagnosismentioning

confidence: 99%

PD-1/PD-L1 Inhibitor-Associated Myocarditis: Epidemiology, Characteristics, Diagnosis, Treatment, and Potential Mechanism

Dong

Kong

et al. 2022

Front. Pharmacol.

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Immune checkpoint inhibitors (ICIs) induce T-cell activation against cancer cells, and due to their anti-tumor function in multiple cancers, ICIs have been considered an important option for oncotherapy. PD-1/PD-L1 inhibitors are now widely used as ICIs for many types of cancers in clinical practices. Myocarditis induced by anti-PD-1/PD-L1 agents is uncommon but shows potentially fatal toxicity. In this review, we attempted to conclude the incidence, characteristics, diagnosis, and treatments, as well as illustrate the potential pathogenesis from the perspectives of T-lymphocyte infiltration, disturbance of regulatory T cells, cytokines, macrophage-mediated inflammatory response, and synergistic effect of PD-1/PD-L1 and CTLA4.

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Section: Diagnosismentioning

confidence: 99%

PD-1/PD-L1 Inhibitor-Associated Myocarditis: Epidemiology, Characteristics, Diagnosis, Treatment, and Potential Mechanism

Dong

Kong

et al. 2022

Front. Pharmacol.

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“…2 The use of biomarkers as a tool in outcome prediction for these patients is a relatively novel concept for which there is an expanding evidence base. Cardiac smooth muscle troponin (cTn) is well established as a sensitive and early indicator of cardiac injury 3 but further to this cardiac role, studies in critically ill patients have demonstrated an association between elevated cTn levels and increased morbidity, mortality and length of stay in both unselected medical and non-cardiac surgical patients. 4–7 It remains unclear whether the different cTn subunits, troponin I (cTnI), troponin T (cTnT) and C (cTnC), are of equivalent diagnostic and prognostic significance in the non-acute coronary syndrome setting.…”

Section: Introductionmentioning

confidence: 99%

Cardiac troponin T is associated with mortality in patients admitted to critical care in a UK major trauma centre: a retrospective database analysis

Crewdson

Thompson

Thomas

2018

Journal of the Intensive Care Society

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Background: Elevated levels of cardiac troponin T are associated with poor outcome in critically ill patients and have been proposed as a prognostic marker in major trauma. This study investigated the relationship between cardiac troponin T levels on admission to intensive care unit (ICU) and all-cause mortality in major trauma patients. Methods: A retrospective database analysis of cardiac troponin T levels on admission to the ICU in major trauma patients between 1 August 2015 and 31 December 2016 at a UK Major Trauma Centre was performed. Results: Of the 243 patients, 69 (28.4%) died. Cardiac troponin T levels were significantly higher in patients who died compared to survivors: 42 vs. 13 ng/L, respectively (p < 0.0001); the odds of all-cause mortality increased significantly as troponin increased, independent of age or Acute Physiology and Chronic Health Evaluation score. Discussion: This confirms cardiac troponin T at ICU admission as a marker of mortality in major trauma. Elevated cardiac troponin T may be seen in patients without evidence of direct cardiac trauma.

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“…Although the clear pathophysiological process is not well characterised, it more likely represents a spectrum of changes ranging from cell death and frank necrosis with myofilament disruption to less severe and likely transient changes in the integrity and permeability of the sarcolemma membrane. This implies that irrespective of the causative factors, cardiac injury will inevitably lead to an elevated plasma level of cTn, and the level of increase reflects the severity of damage [22].…”

Section: Evidence Supporting the Hypothesesmentioning

confidence: 99%

An Hypothesis: Disproportion Between Cardiac Troponin and B-Type Natriuretic Peptide Levels—A High Risk and Poor Prognostic Biomarker in Patients With Fulminant Myocarditis?

Yu¹,

Zhang²,

Xiong

et al. 2021

Heart, Lung and Circulation

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In our clinical practice, we recently found some patients with severe fulminant myocarditis (FM) who showed persistently elevated cardiac troponin (cTn) levels and "seemingly normal" B-type natriuretic peptide (BNP) level, and who subsequently progressed to poor outcomes. Indeed, this sounds contrary to conventional wisdom, but it is not an accidental phenomenon. Fulminant myocarditis is a rapidly progressive disease associated with high mortality. Recent studies have shown that patients with FM are significantly more likely to require heart transplantation than those without FM. Prompt diagnosis of FM and the institution of advanced cardiac life support will save more lives. Cardiac troponin and BNP are widely used diagnostic markers. Cardiac troponin is a specific marker of cardiac injury and its level correlates with the severity of cardiac injury. However, plasma BNP has a dual identity; it is not only a marker of cardiac pressure/volume overload, but it is also a cardioprotective factor that provides effective neurohormonal compensation to maintain homeostasis. Similar to fulminant hepatitis (characterised by diffuse inflammation and massive parenchymal cell necrosis) sometimes showing disproportion between transaminase level and bilirubin level, the disproportion between cTn and BNP levels in FM seems to be consistent with its severe histopathological changes, including diffuse infiltration of the myocardium by inflammatory cells, as well as severe cardiomyocyte injury and necrosis. Moreover, in previous studies, a lower BNP level was found to be an adverse prognostic marker in end-stage heart failure. All these findings indicate that in patients with FM with a persistently high cTn level and ominous clinical presentation, a "seemingly normal" BNP level is not a friendly signal. We hypothesise that the combination of a persistently elevated cTn level and low BNP level in patients with FM indicates worse myocardial injury and poor prognosis.

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Perspective on the clinical application of troponin in heart failure and states of cardiac injury

Cited by 8 publications

References 79 publications

PD-1/PD-L1 Inhibitor-Associated Myocarditis: Epidemiology, Characteristics, Diagnosis, Treatment, and Potential Mechanism

PD-1/PD-L1 Inhibitor-Associated Myocarditis: Epidemiology, Characteristics, Diagnosis, Treatment, and Potential Mechanism

Cardiac troponin T is associated with mortality in patients admitted to critical care in a UK major trauma centre: a retrospective database analysis

An Hypothesis: Disproportion Between Cardiac Troponin and B-Type Natriuretic Peptide Levels—A High Risk and Poor Prognostic Biomarker in Patients With Fulminant Myocarditis?

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