The coronavirus disease 2019 (COVID-19) pandemic has affected >8 million patients and caused >400 thousand deaths to date.¹ Recent reports indicate that myocardial injury is frequent among patients with COVID-19. Here we summarize 10 key points about myocardial injury and COVID-19.

1. The term myocardial injury applies to any patient in whom at least one cardiac troponin (cTn) concentration is above the 99th percentile upper reference limit (URL).

Following recommendations from the Task Force for the Universal Definition of Myocardial Infarction, the term myocardial injury (acute or chronic) applies to any patient in whom at least one cTn concentration is above the 99th percentile URL.

2. Myocardial injury is common in patients with COVID-19.

The exact frequency of myocardial injury in patients with COVID-19 is difficult to ascertain due to variations in cTn assays and thresholds used, studied populations, as well as the number and timing of samples obtained. The incidence is likely higher when using high-sensitivity cTn assays and evaluating populations with higher illness severity compared to when using contemporary assays and evaluating populations with lower illness severity.

3. Following careful clinical evaluation, patients with cTn increases indicative of myocardial injury, including those with COVID-19, should be classified as (a) chronic myocardial injury, (b) acute nonischemic myocardial injury, or (c) acute myocardial infarction (MI).

Following careful clinical evaluation and understanding of the clinical context in which cTn measurements were obtained, clinicians tasked to evaluate patients with cTn increases (COVID-19 or non-COVID-19 related) should classify patients as having (a) chronic myocardial injury, (b) acute nonischemic myocardial injury, or (c) acute MI.

4. Chronic myocardial injury, a term that applies to those with chronic stable (<20% change) cTn increases, can be frequently encountered in patients with COVID-19 given the older age and high prevalence of chronic cardiovascular conditions observed in these patients.

Patients diagnosed with COVID-19 are often older and with comorbidities. These latter issues are important because cTn is a marker of not only acute but also chronic structural myocardial disease. Studies report that patients with COVID-19 often have chronic cardiovascular conditions such as hypertension, cardiomyopathy, coronary artery disease, or heart failure. When more severe, all these conditions can be explanations for chronic stable increases >99th percentile URL.

5. Acute nonischemic myocardial injury, a term that applies to patients with dynamic rising and/or falling cTn concentration without clinical evidence of myocardial ischemia, is probably the predominant mechanism for cTn increases in patients with COVID-19.

Emerging reports suggest that acute nonischemic myocardial injury is likely the predominant reason for cTn increases. It can be due to cardiac etiologies such as acute heart failure, myocarditis, stress cardiomyopathy, or direct severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) injury. It can also be due to several primary non-cardiac etiologies such as critical illness and pulmonary embolism. Despite emerging reports of myocarditis in patients with COVID-19, cTn increases should not always be considered to be due to myocarditis. Clinical context, pre-test probability, and careful evaluation of the signs and/or symptoms should inform the suspected probable nature of cTn increases.

6. There is a theoretical increased risk for acute MI in patients infected with SARS-CoV-2.

Patients with acute infection, viral or bacterial, are known to have increased inflammatory, prothrombotic, and procoagulant responses. Data from several COVID-19 studies confirm that this is also the case for COVID-19. Conceptually, the risk for type 2 MI is higher because of the respiratory failure with hypoxia and hemodynamic disturbances that occur in COVID-19 with severe illness. Type 2 MIs are common in the critically ill when ischemia is present. Further data are needed on MI subtypes, but several recent ST-segment elevation MI analyses suggest its frequency is reduced and focus on the concern that patients are not seeking attention or presenting late.

7. Not all cTn increases >99th percentile URL require additional noninvasive or invasive evaluations.

Clinicians are often tempted to pursue more evaluation in patients with cTn increases. This is not always necessary, especially if the increases are due to myocardial injury (no clear ischemia) or type 2 MI (ischemia present). This is conceptually important overall and even more so during the COVID-19 pandemic. Given the risk for health care personnel exposure, imaging studies or invasive procedures should be reserved for those scenarios in which interventions are expected to provide clinical benefit and impact patient management.

8. Except for rare circumstances, cTn increases >99th percentile URL are true positives for acute or chronic myocardial injury that are associated with adverse outcomes. The higher the concentration, the worse the outcome.

Increases in cTn are indicative of myocardial injury. Using high-sensitivity cTn assays, it is infrequent to encounter analytical issues that lead to false positives. Clinicians, however, often see elevations as laboratory nuisances and dismiss them, forgetting the important prognostic significance of those elevations. Although actionable measures are not always clear or possible, cTn increases identify patients at higher risk for adverse short- and long-term outcomes. COVID-19 studies have shown that myocardial injury, irrespective of the nature of the elevations, is associated with a higher risk for death and arrhythmias. Further, data from Guo et al.² and Shi et al.³ show that patients with myocardial injury have higher incidence of complications such as acute respiratory distress syndrome and kidney injury.

9. The structured use of serial cTn, along with other inflammatory and thrombotic markers, among patients presenting to the hospital with SARS-CoV-2 infection may facilitate COVID-19 stage classification, patient triage, and risk stratification.

For patients presenting to the hospital with COVID-19, in addition to routine clinical evaluation, the standardized measurement of cTn for the detection of myocardial injury along with other inflammatory (e.g., C-reactive protein, ferritin, IL6, and procalcitonin) and thrombotic (D-dimer) markers may facilitate understanding whether patients are in stage I (early infection), stage II (pulmonary phase), or stage III (hyperinflammatory phase). Further, as a continuous prognostic marker, the initial cTn measurement may help triage patients, and subsequent serial measurements may help identify lower-risk patients with stable concentrations or higher-risk patients with increasing patterns. The latter may need additional evaluations.

10. No specific therapies exist for myocardial injury due to COVID-19.

For patients with COVID-19 with cTn increases, usual clinical practice guidelines apply to those with type 1 MI, heart failure or cardiomyopathy, and arrhythmias. Individualized care for each condition is required in those with acute nonischemic myocardial injury. Most cases of type 2 MI and acute and chronic myocardial injury can be managed conservatively.

References

1. Sandoval Y, Januzzi JL Jr, Jaffe AS. Cardiac Troponin for the Diagnosis and Risk-Stratification of Myocardial Injury in COVID-19: JACC Review Topic of the Week. J Am Coll Cardiol 2020;Jul 3:[Epub ahead of print].
2. Guo T, Fan Y, Chen M, et al. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol 2020;Mar 27:[Epub ahead of print].
3. Shi S, Qin M, Shen B, et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol 2020;Mar 25:[Epub ahead of print].

Clinical Topics: Acute Coronary Syndromes, Cardiovascular Care Team, COVID-19 Hub, Dyslipidemia, Heart Failure and Cardiomyopathies, Atherosclerotic Disease (CAD/PAD), ACS and Cardiac Biomarkers, Lipid Metabolism, Heart Failure and Cardiac Biomarkers

Keywords: Acute Coronary Syndrome, COVID-19, Coronavirus, severe acute respiratory syndrome coronavirus 2, Coronary Artery Disease, C-Reactive Protein, Critical Illness, Interleukin-6, Takotsubo Cardiomyopathy, Myocarditis, Respiratory Distress Syndrome, Triage, Prognosis, Ferritins

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