Cardiac Troponin for Assessment of Myocardial Injury in COVID-19: JACC Review Topic of the Week

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.

Keywords: cardiac troponin; coronavirus disease 2019; myocardial injury; type 2 myocardial infarction.

Graphical abstract

Figure 1

Incidence of Myocardial Injury in COVID-19 Frequency of myocardial injury increases with greater severity of illness. COVID-19 = coronavirus disease-2019.

Figure 2

Classification of Myocardial Injury in COVID-19 Increases in cTn should be categorized as chronic myocardial injury, acute nonischemic myocardial injury, or acute myocardial infarction. For several conditions, there is a spectrum and the most common category is indicated, but can present in other ways. CKD = chronic kidney disease; COVID-19 = coronavirus disease-2019; CRP = C-reactive protein; cTn = cardiac troponin; ESRD = end-stage renal disease; NT-proBNP = N-terminal pro–B-type natriuretic peptide; URL = upper reference limit.

Figure 3

Outcomes Patients with myocardial injury (blue bars) have a higher risk of death, arrhythmias, ARDS, and mechanical ventilation as compared with those without injury (red bars). ARDS = acute respiratory distress syndrome; VF = ventricular fibrillation; VT = ventricular tachycardia.

Figure 4

Relationship Between cTn and Mortality in COVID-19 Data from Shi et al. (6) showing that the higher the cardiac troponin (cTn), the worse the outcome, and vice versa. Abbreviations as in Figure 2.

Figure 5

Serial Cardiac Troponin Measurements to Distinguish Survivors From Nonsurvivors Data from Zhou et al. (2) showing stable (red line, survivors) versus dynamic (blue line, nonsurvivors) high-sensitivity (hs) cardiac troponin patterns.

Central Illustration

Conceptual Proposal to Use Cardiac Troponin in COVID-19 Baseline measurements can facilitate stage classification (52) and initial triage (steps 1 and 2), and serial measurements help with short- and long-term risk stratification (step 3). This information is likely to be most beneficial in those in whom disease stage and risk status is uncertain, where cTn can help with decisions about triage and level of care. ARDS = acute respiratory distress syndrome; CRP = C-reactive protein; CXR = chest x-ray; NT-proBNP = N-terminal pro–B-type natriuretic peptide.