Key result
Hydroxychloroquine in COVID-19 is linked to a ~12 ms QTc increase with no ventricular arrhythmias.
Why the study?
The extent of hydroxychloroquine-induced QTc prolongation and its relation to COVID-19 severity and arrhythmic events were unclear.
Does hydroxychloroquine alone or in combination with azithromycin cause severe QTc prolongation or ventricular arrhythmias in patients with COVID-19?
Cohort (n=2,014)
Yes
Does hydroxychloroquine alone or in combination with azithromycin cause severe QTc prolongation or ventricular arrhythmias in patients with COVID-19?
Absolute Event Rate: 439.2% vs 427.6%
p-value: p=<0.001
Hydroxychloroquine therapy in COVID-19 patients is associated with a low incidence of severe QTc prolongation and no observed ventricular arrhythmias, suggesting safety concerns regarding its arrhythmogenic potential may have been overestimated.
Modest QTc rise without arrhythmias in retrospective data warrants no prescribing change for HCQ in COVID-19; leaves open need for randomized safety confirmation.
Objective To evaluate the extent of hydroxychloroquine-induced corrected QT (QTc) prolongation and its relation to COVID-19 infection severity and incidence of polymorphic ventricular arrhythmias and sudden arrhythmic deaths. Design A large-scale cohort study with retrospective analysis of baseline and on-therapy QT interval corrected using Bazett and Fridericia formulas. Setting A multicentre study involving eight secondary and tertiary care hospitals of the Abu Dhabi Health Services Company (SEHA), United Arab Emirates. Participants 2014 patients consecutively admitted with PCR-confirmed SARS-CoV-2 infection between 1 March 2020 and 1 June 2020. Interventions Treatment with hydroxychloroquine alone or in combination with azithromycin for at least 24 hours and with a baseline ECG and at least one ECG after 24 hours of therapy. Main outcome measures Maximal QTc interval prolongation and its relationship to clinical severity, polymorphic ventricular tachycardia and sudden arrhythmic death while on treatment. Results The baseline QTc(Bazett) was 427.6±25.4 ms and the maximum QTc(Bazett) during treatment was 439.2±30.4 ms (p<0.001). Severe QTc prolongation (QTc ≥500 ms) was observed in 1.7%–3.3% of patients (Fridericia and Bazett, respectively). There were no cases of polymorphic ventricular arrhythmia or hydroxychloroquine-related arrhythmic death. QTc prolongation was more pronounced in combination therapy compared with hydroxychloroquine alone (22.2 ms vs 11.0 ms, p<0.001) and in patients with higher COVID-19 clinical severity (asymptomatic: 428.4±25.4 ms, severe COVID-19 infection: 452.7±35.7 ms, p<0.001). The overall in-hospital mortality was 3.97% and deceased patients had longer on-therapy QTc(Bazett) than survivors (459.8±21.4 ms vs 438.4±29.9 ms, p<0.001). Conclusions The incidence of severe QTc prolongation with hydroxychloroquine was low and not associated with ventricular arrhythmia. The safety concerns surrounding the use of hydroxychloroquine may have been overestimated; however, caution should be exercised when using hydroxychloroquine in patients with risk factors for QT prolongation.
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Kadri et al. (2022) conducted a cohort in COVID-19 infection (n=2,014). Hydroxychloroquine alone or in combination with azithromycin vs. Baseline was evaluated on Maximal QTc interval prolongation (p=<0.001). Hydroxychloroquine therapy in COVID-19 patients was associated with a modest increase in maximum QTc interval (439.2 ms vs 427.6 ms at baseline, p<0.001), with no cases of ventricular arrhythmia.
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