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Myocardial injury is seen in many patients with severe COVID-19. These researchers compared myocardial injury related to severe COVID-19 in 243 hospitalized, intubated patients with that in a prior cohort of 506 patients from the myocardial injury acute respiratory distress syndrome (MI-ARDS) study who had lung injury due to primary pneumonia. Plasma troponin, a marker for myocardial injury, was measured within 24 hours of intubation.
Troponin levels were elevated in similar proportions of non-COVID ARDS patients (49.6%) and COVID-19 patients (51%); 16% of COVID-19 patients had levels >10 times the upper limit of normal (UNL). After adjusting for age, sex, and creatinine, independent predictors of elevated troponin levels were chronic kidney disease, higher lactate levels, leukocytosis, higher ferritin, and lower fibrinogen levels. Mortality was incrementally greater with higher troponin levels (e.g., 22.7% with normal troponin levels, 61.5% with troponin >10×UNL) but not after adjustments for age, sex, creatinine, bilirubin, PaO2/FiO2 ratio, vasopressor use, and lactate levels. After adjusting for all these factors except lactate levels, COVID-19 was associated with significantly lower odds of myocardial injury than non-COVID ARDS (odds ratio, 0.55). COVID-19 patients had significantly higher mortality than non-COVID ARDS patients (36.2% vs. 26.4%). In an unadjusted analysis, mortality was similar among ARDS patients with and without myocardial injury and COVID-19 patients without myocardial injury, while COVID-19 patients with positive troponin had the highest mortality. This difference lost significance after adjustments (for all factors except lactate).
Metkus TS et al. Myocardial injury in severe COVID-19 compared to non-COVID acute respiratory distress syndrome. Circulation 2020 Nov 13; [e-pub]. (https://doi.org/10.1161/CIRCULATIONAHA.120.050543)
Comment
Unlike COVID-19–mediated myocarditis and myocardial injury seen in multisystem inflammatory syndrome (MIS) in children and young adults, myocardial injury is actually less common in COVID-19 ARDS than in non-COVID ARDS after adjustment for age, renal failure, and degree of critical illness. Thus, while considerable attention has been drawn to MIS-associated myocardial injury, the vast majority of COVID-19–mediated cardiac injury is caused by global multiorgan dysfunction of critical illness in older patients and those with comorbidities. Further research is needed to distinguish these and to determine if they warrant distinct therapeutic approaches.