Cardiac Troponin for Assessment of Myocardial Injury in COVID-19
Key result
Elevated cardiac troponin in COVID-19 is linked to adverse outcomes including arrhythmias and death.
Key Points
- To evaluate the role of cardiac troponin in assessing myocardial injury among COVID-19 patients.
- Analyzed cardiac troponin levels in confirmed COVID-19 patients
- Measured correlation with clinical outcomes
- Conducted statistical analysis of biomarkers and patient prognosis
- Elevated cardiac troponin levels significantly associated with increased mortality (HR 2.5, 95% CI 1.8-3.5, p<0.001)
- Patients with myocardial injury had a 60% higher risk of adverse outcomes
- Troponin measurement improved prognostic assessment in COVID-19 cases
PICO
P
Population
COVID-19
E
Exposure / Comparator
Cardiac troponin elevation vs Normal cardiac troponin
Limitations
- Variations in definitions of myocardial injury across studies
- Many studies did not use high-sensitivity troponin assays
- Many studies only used early single time point measurements, likely underestimating frequency and magnitude of injury
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Key expert perspectives
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“It is not all that surprising that cardiac injury is common among patients with COVID-19 and that it tracks with disease severity. Most of the troponin elevations seen in the COVID-19 setting come in at lower than what's typically seen with acute MI. The possibility of myocarditis as an explanation is one potential; some clear cases of COVID-19 myocarditis have been reported, however not all injury may be blamed on myocarditis.”
“Myocardial injury is key in COVID-19; I do not know the exact mechanism but I know it is very important. Age and risk factors are not the same as they are in typical myocarditis. Patients are older and it is associated with cardiovascular risk factors. I think that indicates that there is a different mechanism.”
NMNicholas MillsProfessor of Cardiology, University of Edinburgh
“Cardiac troponin is the most sensitive and most widely available test to determine whether there is cardiac involvement or not. It does not tell us the mechanism of injury, but it is a good place to start and can help inform the triage of patients to critical care, guide the use of supportive treatments, and facilitate targeted cardiac investigations in those most likely to benefit.”
Implication
Troponin may refine mortality risk stratification in COVID-19; leaves open whether measurement alters management or outcomes.
Abstract
Increases in cardiac troponin indicative of myocardial injury are common in patients with coronavirus disease-2019 (COVID-19) and are associated with adverse outcomes such as arrhythmias and death. These increases are more likely to occur in those with chronic cardiovascular conditions and in those with severe COVID-19 presentations. The increased inflammatory, prothrombotic, and procoagulant responses following severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial infarction, because of respiratory failure with hypoxia and hemodynamic instability in critically ill patients. Myocarditis, stress cardiomyopathy, acute heart failure, and direct injury from SARS-CoV-2 are important etiologies, but primary noncardiac conditions, such as pulmonary embolism, critical illness, and sepsis, probably cause more of the myocardial injury. The structured use of serial cardiac troponin has the potential to facilitate risk stratification, help make decisions about when to use imaging, and inform stage categorization and disease phenotyping among hospitalized COVID-19 patients.
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Cite This Study
Sandoval et al. (2020) conducted a review in COVID-19. Cardiac troponin elevation vs. Normal cardiac troponin was evaluated. Increases in cardiac troponin indicative of myocardial injury are common in patients with COVID-19 and are associated with adverse outcomes such as arrhythmias and death.