Prevalence and Impact of Myocardial Injury in Patients Hospitalized With COVID-19 Infection
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Key result
Elevated troponin I is linked to ~3-fold higher mortality in hospitalized COVID-19 patients.
- HR 3.03
- 95% CI 2.42 to 3.80
- P<0.001
- n=2,736
Why the study?
The degree of myocardial injury, reflected by troponin elevation, and associated outcomes among US hospitalized patients with COVID-19 were unknown.
Key Points
- To describe the prevalence and degree of myocardial injury as reflected by troponin elevation and evaluate its association with in-hospital mortality among patients hospitalized with COVID-19.
- Retrospective cohort study of 2,736 patients with laboratory-confirmed COVID-19 admitted to 1 of 5 Mount Sinai Health System hospitals in New York City between February 27, 2020, and April 12, 2020.
- Troponin-I concentrations (normal value <0.03 ng/ml) were measured within 24 h of hospital admission, and clinical data were captured from electronic health records.
- Across the cohort of 2,736 patients, 985 (36%) exhibited elevated troponin concentrations, and 506 (18.5%) died during hospitalization.
- Mild myocardial injury (troponin I >0.03 to 0.09 ng/ml; n = 455; 16.6%) was significantly associated with death after adjusting for clinical factors (adjusted hazard ratio: 1.75; 95% CI: 1.37 to 2.24; p < 0.001).
- Greater myocardial injury (troponin I >0.09 ng/dl; n = 530; 19.4%) was significantly associated with a higher risk of death (adjusted HR: 3.03; 95% CI: 2.42 to 3.80; p < 0.001).
Study Design
Type
Cohort (n=2,736)
Multicenter
Yes
PICO
P
Population
2,736 adults hospitalized with laboratory-confirmed COVID-19 and a troponin measurement within 24 hours of admission, followed for a median of 5.75 days.
E
Exposure / Comparator
Elevated troponin I (>0.09 ng/ml) vs Normal troponin I (0.00 to 0.03 ng/ml)
O
Primary Outcome
Mortality — HR 3.03 (2.42 to 3.80), p=<0.001
Main Result
Hazard Ratio: 3.03 (95% CI 2.42–3.8)
p-value: p=<0.001
Limitations
- Limitations inherent to the use of electronic health records for patient-level data without manual chart review verification
- Some patients had not completed their hospital course at the time of data freeze
- Use of anticoagulation and antiviral therapy was not included due to incomplete data
- Natriuretic peptide levels were not available for more than two-thirds of the study cohort
- Troponin concentrations were not available in 323 patients who had fewer comorbidities
- Not possible to ascertain mechanisms of death including cardiovascular and noncardiovascular causes
Discussion
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Key expert perspectives
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“It's kind of scary, actually, how much the risk goes up with elevated troponin.”
“It is not all that surprising that cardiac injury is common among patients with COVID-19 and that it tracks with disease severity. Most of the troponin elevations seen in the COVID-19 setting come in at lower than what's typically seen with acute MI. The possibility of myocarditis as an explanation is one potential; some clear cases of COVID-19 myocarditis have been reported, however not all injury may be blamed on myocarditis.”
“I think that the finding in terms of [cardiac injury's] relationship to mortality is striking.”
Implication
Randomized trial describes myocardial injury effects in hospitalized COVID-19 patients, indicating increased mortality risk.
Cite This Study
Lala et al. (2020) conducted a cohort in COVID-19 (n=2,736). Elevated troponin I (>0.09 ng/ml) vs. Normal troponin I (0.00 to 0.03 ng/ml) was evaluated on Mortality (HR 3.03, 95% CI 2.42 to 3.80, p=<0.001). Elevated troponin I (>0.09 ng/ml) was significantly associated with a higher risk of mortality (adjusted HR 3.03) compared to normal troponin levels in patients hospitalized with COVID-19.
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