Cardiac troponin, along with inflammatory and thrombotic markers, may aid clinicians in determining stage classification and stratifying risk for myocardial injury among patients with coronavirus disease 2019 (COVID-19), according to a review article published in the Journal of the American College of Cardiology.

Increases in cardiac troponin that are suggestive of myocardial injury are common in patients with COVID-19 and are associated with arrhythmias and death. These increases more frequently occur in patients who have chronic cardiovascular conditions and in those who present with severe COVID-19.

Elevated troponin levels above the 99th percentile can be classified as chronic myocardial injury, acute nonischemic myocardial injury, or acute myocardial infarction. Chronic myocardial injury “is likely the etiology for many [patients with] COVID-19 because of the high prevalence of chronic cardiovascular conditions,” noted the researchers. “These elevations are true positives for myocardial injury and associated with an adverse prognosis even without intercurrent disease.”

Multiple mechanisms may lead to acute nonischemic myocardial injury, with common cardiac etiologies including myocarditis, stress cardiomyopathy, and acute heart failure. “Critical illness, acute pulmonary embolism, and sepsis can also cause cardiac troponin increases without overt myocardial ischemia that are categorized as acute nonischemic myocardial injury,” noted the review authors.


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There is an increased risk for acute atherothrombosis (type 1 myocardial infarction) due to the inflammatory responses evoked by infection that can directly affect atherosclerotic plaques and increase procoagulant and prothrombotic activity, the researchers noted. “A higher risk for myocardial oxygen supply-demand mismatch (type 2 myocardial infarction) exists due to the responses to acute infection, including the release of interleukins, [tumor necrosis factor]-α, and catecholamines, as well as the consequences of hypoxia, acidosis, and hypo- or hypertension,” they commented.

Although imaging is used to clarify the etiologies of these events, its use is problematic during the COVID-19 pandemic owing to the risk for infection among healthcare personnel. National and international recommendations have been developed for the COVID-19 pandemic regarding the selective use of noninvasive and invasive cardiac imaging modalities. “All emphasize that for patients with suspected or confirmed COVID-19, cardiac imaging requires strong clinical information that the results will impact patient management,” according to the authors. “Given these constraints, serial cardiac biomarker measurements may be valuable in helping to decide when to employ imaging in patients with COVID-19.”

The researchers pointed out that not all patients with cardiac troponin increases >99th percentile (or even with an increasing pattern) require imaging. If the increases are mild or modest, stable over time, and comporting to underlying comorbidities, imaging may not be needed.

To date, there are no established therapies for myocardial injury associated with COVID-19. “For patients with myocardial injury, in general, the same concepts apply for patients with and without COVID-19,” stated the investigators. “Management decisions should be based on serial measurements that facilitate decision-making.”

Patients who have cardiac troponin increases that are not marked and stable (without a significant rise and/or fall) “likely reflect chronic myocardial injury; particularly if there is a facile explanation such as chronic heart failure, cardiomyopathy or chronic kidney disease,” noted the researchers. “These patients do not require additional therapies except for treatment of their underlying conditions. Patients with acute nonischemic myocardial injury require individualized care for the specific conditions that caused the cardiac troponin increase…. For patients with overt myocardial ischemia in whom acute myocardial infarction is diagnosed, those whose clinical presentation is thought to be most consistent with type 1 myocardial infarction should be managed accordingly and receive evidence-based care. Those in whom acute atherothrombosis is thought to be less likely and type 2 myocardial infarction is suspected can be managed conservatively. ”The enhanced inflammatory and prothrombotic responses following infection with severe acute respiratory syndrome coronavirus 2 increase the risk for acute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial infarction, according to the researchers. “The structured use of serial cardiac troponin testing has the potential to facilitate risk stratification, help make decisions about when to use imaging, and inform stage categorization and disease phenotyping among hospitalized patients [with COVID-19],” they concluded.

Disclosures: Drs Sandoval, Januzzi, and Jaffe reported affiliations with the diagnostics and pharmaceutical industries. Please see the original reference for a full list of disclosures.

Reference

Sandoval Y, Januzzi JL Jr, Jaffe AS, et al. Cardiac troponin for the diagnosis and risk-stratification of myocardial injury in COVID-19 [published online July 3, 2020]. J Am Coll Cardiol. doi:2020.06.068