Usefulness of Elevated Troponin to Predict Death in Patients With COVID-19 and Myocardial Injury

Perfusfind S.L.
Artículos Jan 1, 1970 0

Highlights

  • Patients with COVID-19 with elevated troponin have markedly increased risk of death.
  • Patients with elevated troponin were frequently admitted to intensive care units.
  • Risk with elevated troponin is independent of acute phase and inflammatory markers.
  • Risk with elevated troponin is independent of baseline cardiovascular disease.
Elevations in troponin levels have been shown to predict mortality in patients with coronavirus disease 2019 (COVID-19). The role of inflammation in myocardial injury remains unclear. We sought to determine the association of elevated troponin with mortality in a large, ethnically diverse population of patients hospitalized with COVID-19, and to determine the association of elevated inflammatory markers with increased troponin levels. We reviewed all patients admitted at our health system with COVID-19 from March 1 to April 27, 2020, who had a troponin assessment within 48 hours of admission. We used logistic regression to calculate odds ratios (ORs) for mortality during hospitalization, controlling for demographics, co-morbidities, and markers of inflammation. Of 11,159 patients hospitalized with COVID-19, 6,247 had a troponin assessment within 48 hours. Of these, 4,426 (71%) patients had normal, 919 (15%) had mildly elevated, and 902 (14%) had severely elevated troponin. Acute phase and inflammatory markers were significantly elevated in patients with mildly and severely elevated troponin compared with normal troponin. Patients with elevated troponin had significantly increased odds of death for mildly elevated compared with normal troponin (adjusted OR, 2.06; 95% confidence interval, 1.68 to 2.53; p < 0.001) and for severely elevated compared with normal troponin (OR, 4.51; 95% confidence interval, 3.66 to 5.54; p < 0.001) independently of elevation in inflammatory markers. In conclusion, patients hospitalized with COVID-19 and elevated troponin had markedly increased mortality compared with patients with normal troponin levels. This risk was independent of cardiovascular co-morbidities and elevated markers of inflammation.
 

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the novel coronavirus responsible for coronavirus disease 2019 (COVID-19), has rapidly spread across the globe, infecting millions of people and overwhelming health care systems. While COVID-19 primarily presents with pulmonary symptoms, markers of myocardial injury (i.e., elevated serum cardiac troponin serum) have been associated with increased mortality, particularly in patients with underlying cardiovascular disease.

 However, these series were either small, single-centered, evaluated one troponin assay, or had a large proportion of patients still admitted without an endpoint at the time of analysis. Furthermore, it remains unclear if elevated troponin levels are due to ischemic myocardial injury via atherosclerotic plaque rupture or coronary thrombotic events (type 1 myocardial infarction), indirect injury associated with and sepsis resulting in supply-demand mismatch (type 2 myocardial infarction), or a direct result of the inflammatory surge frequently observed in patients hospitalized with COVID-19.

 

 In this study, we further explored the relationship of elevated troponin levels with mortality, acute phase and inflammatory markers, and electrocardiogram evidence of acute myocardial infarction (AMI) in patients admitted with COVID-19 to the largest academic health system in New York State.

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