Myocardial Injury in Severe COVID-19 Patients

Quick Takes

  • Among patients hospitalized in Wuhan, China with severe COVID-19 during the early stages of the pandemic, increased age, comorbidities, and elevated CRP were associated with elevated cTn-I.
  • Based on the available data, short-term in-hospital death was more common among hospitalized patients with an elevated cTn-I.
  • Additional studies may help better assess whether myocardial involvement by the SARS-CoV-2 virus is a cause of death, or simply a marker of underlying comorbidities and the extent of the viral disease.

Study Questions:

What are the characteristics and clinical significance of myocardial injury among patients with severe coronavirus disease 2019 (COVID-19)?

Methods:

Consecutive patients with severe COVID-19 admitted to a university hospital and its satellite facilities in Wuhan, China in early 2020 were included in this retrospective study. Severe and critically ill disease was defined by the presence of any of the following: respiratory rate >30 breaths/minute, oxygen saturation ≤93%, PaO2/FiO2 ratio ≤300 mm Hg, respiratory failure requiring mechanical ventilation, shock, or respiratory failure combined with other organ failure requiring intensive care unit treatment. Patients <18 years of age and patients without assessment of cardiac biomarkers including cardiac troponin I (cTn-I) were excluded. Clinical outcomes including discharge, mortality, and length of stay were monitored until February 23, 2020. Clinical, laboratory, and treatment data were collected and compared between patients who died and those who survived. Risk factors for death and myocardial injury were analyzed using multivariable regression models.

Results:

Of 2,253 cases with confirmed COVID-19 hospitalized between January 1 and February 23, 2020, there were 1,002 unique cases of severe disease, and 671 with severe disease and available medical data. The median age was 63 years (interquartile range, 50-72 years), and 48% were male; the median time from symptom onset to the end of follow-up was 23 days, and from hospital admission to the end of follow-up was 17 days. A total of 62 patients (9.2%) died, with significant differences between survivors and nonsurvivors involving multiple clinical variables. There was a higher prevalence of myocardial injury among patients who died compared to survivors (75.8% vs. 9.7%, p < 0.001). The area under the receiver operating characteristic (ROC) curve of initial cTn-I for predicting in-hospital mortality was 0.92 (95% confidence interval [CI], 0.87-0.96; sensitivity 0.86, specificity 0.86; p < 0.001). In multivariable models, cTn-I was associated with an increased risk of death both using the ROC curve-derived cTn-I threshold of 0.026 ng/ml (hazard ratio [HR], 4.56; 95% CI, 1.28-16.28; p = 0.02) and treating cTn-I as a continuous variable (HR, 1.25; 95% CI, 1.07-1.46; p = 0.04). In multivariable logistic regression, “senior age,” comorbidities (including hypertension, coronary heart disease, chronic renal failure, and chronic obstructive pulmonary disease), and elevated level of C-reactive protein (CRP) were associated with enzyme evidence of myocardial injury.

Conclusions:

The authors concluded that the risk of in-hospital death among patients with severe COVID-19 can be predicted by markers of myocardial injury; and that “senior age,” evidence of an inflammatory response, and cardiovascular comorbidities were significantly associated with elevated cardiac enzymes.

Perspective:

In the throes of a pandemic, any knowledge might be taken as helpful. This early report from a single academic hospital and its satellites in Wuhan, China, suggests that elevated cTn-I as a marker of myocardial injury is common among patients with severe COVID-19; is associated with increased age (described in the manuscript as an undefined “senior age”), other comorbidities, and elevated CRP; and is associated with increased short-term in-hospital mortality. The differences between association and either causation or prediction should be stressed. With a relatively small sample size compared to the current world burden of COVID-19, and with data limited to a single center at the very onset of the pandemic, it is difficult to know how broadly to extrapolate these data. However, evidence of myocardial injury among patients with severe COVID-19 appears to be associated with an increased risk of death; additional studies may help better assess whether myocardial involvement by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus is a cause of death, or simply a marker of underlying comorbidities and the extent of the viral disease.

Clinical Topics: Prevention, Hypertension

Keywords: Biological Markers, Coronary Disease, Coronavirus, COVID-19, C-Reactive Protein, Critical Illness, Hospital Mortality, Hypertension, Patient Discharge, Primary Prevention, Pulmonary Disease, Chronic Obstructive, Renal Insufficiency, Chronic, Respiratory Rate, Risk Factors, SARS Virus, Shock, Troponin I


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