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Published on: January 16, 2019
Prolonged QT predicts prognosis in COVID-19
Zaki Akhtar1,2, Mark M Gallagher1,2, Yee Guan Yap3
1Department of Cardiology, Ashford and St Peter's NHS trust, Chertsey, Surrey, UK.
Insights
Coronavirus disease-2019 (COVID-19) illness can cause corrected QT interval (QTc) prolongation. This QTc prolongation is linked to increased mortality risk in COVID-19 patients.
Area of Science:
- Cardiology
- Infectious Diseases
- Critical Care Medicine
Background:
- Coronavirus disease-2019 (COVID-19) is a severe illness causing multi-organ dysfunction.
- Abnormal electrocardiograms, including QT prolongation, are associated with poor outcomes in COVID-19 patients.
- QT prolongation in COVID-19 has been previously linked to pharmacological effects.
Purpose of the Study:
- To investigate the effects of COVID-19 illness on the corrected QT interval (QTc).
- To determine if QTc prolongation is associated with mortality in COVID-19 patients.
Main Methods:
- A retrospective study of 293 consecutive COVID-19 patients admitted to the hospital.
- Comparison of demographic data, laboratory findings, and electrocardiograms between survivors and non-survivors.
- Multivariate Cox-regression analysis to identify predictors of mortality.
Main Results:
- Deceased patients were older and had higher levels of C-reactive protein and troponin.
- A significantly longer QTc interval was observed in non-survivors compared to survivors (461.1 ms vs 449.3 ms).
- QTc prolongation (>455 ms for males, >465 ms for females) was a significant predictor of mortality (HR 1.49).
Conclusions:
- QTc prolongation occurs during COVID-19 illness.
- QTc prolongation is associated with increased mortality risk in COVID-19 patients.
- Monitoring QTc interval may aid in risk stratification for severe COVID-19 outcomes.
Background:
Coronavirus disease-2019 (COVID-19) causes severe illness and multi-organ dysfunction. An abnormal electrocardiogram is associated with poor outcome, and QT prolongation during the illness has been linked to pharmacological effects. This study sought to investigate the effects of the COVID-19 illness on the corrected QT interval (QTc).
Method:
For 293 consecutive patients admitted to our hospital via the emergency department for COVID-19 between 01/03/20 -18/05/20, demographic data, laboratory findings, admission electrocardiograph and clinical observations were compared in those who survived and those who died within 6 weeks. Hospital records were reviewed for prior electrocardiograms for comparison with those recorded on presentation with COVID-19.
Results:
Patients who died were older than survivors (82 vs 69.8 years, p < 0.001), more likely to have cancer (22.3% vs 13.1%, p = 0.034), dementia (25.6% vs 10.7%, p = 0.034) and ischemic heart disease (27.8% vs 10.7%, p < 0.001). Deceased patients exhibited higher levels of C-reactive protein (244.6 mg/L vs 146.5 mg/L, p < 0.01), troponin (1982.4 ng/L vs 413.4 ng/L, p = 0.017), with a significantly longer QTc interval (461.1 ms vs 449.3 ms, p = 0.007). Pre-COVID electrocardiograms were located for 172 patients; the QTc recorded on presentation with COVID-19 was longer than the prior measurement in both groups, but was more prolonged in the deceased group (448.4 ms vs 472.9 ms, pre-COVID vs COVID, p < 0.01). Multivariate Cox-regression analysis revealed age, C-reactive protein and prolonged QTc of >455 ms (males) and >465 ms (females) (p = 0.028, HR 1.49 [1.04-2.13]), as predictors of mortality. QTc prolongation beyond these dichotomy limits was associated with increased mortality risk (p = 0.0027, HR 1.78 [1.2-2.6]).
Conclusion:
QTc prolongation occurs in COVID-19 illness and is associated with poor outcome.
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