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The authors review the use of increases in cardiac troponin (cTn) for the diagnosis of cardiac disease due to COVID-19 for risk stratification. Increased cTN is indicative of acute or chronic myocardial injury in patients with COVID-19 and is associated with adverse outcomes. COVID-19 is associated with direct cardiac injury and can cause acute myocardial infarction, myocarditis, stress cardiomyopathy, and acute heart failure. In addition, primary non-cardiac conditions such as pulmonary embolism, critical illness, and sepsis cause myocardial injury.
The use of serial cTn may aid in risk stratification, decision making especially for imaging, and disease phenotyping in patients hospitalized with COVID-19.
This abstract is available on the publisher's site.
Increases in cardiac troponin (cTn) indicative of myocardial injury are common in patients with COVID-19 and 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 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 non-cardiac conditions such as pulmonary embolism, critical illness, and sepsis probably cause more of the myocardial injury. The structured use of serial cTn 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.