Prolonged QT Interval in a Patient With Coronavirus Disease-2019: Beyond Hydroxychloroquine and Azithromycin

Abstract

Recent reports have suggested an increased risk of QT prolongation and subsequent life-threatening ventricular arrhythmias, particularly torsade de pointes, in patients with coronavirus disease-2019 (COVID-19) treated with hydroxychloroquine and azithromycin. In this article, we report the case of a 75-year-old female with a baseline prolonged QT interval in whom the COVID-19 illness resulted in further remarkable QT prolongation (>700 ms), precipitating recurrent self-terminating episodes of torsade de pointes that necessitated temporary cardiac pacing. Despite the correction of hypoxemia and the absence of reversible factors, such as adverse medication effects, electrolyte derangements, and usage of hydroxychloroquine/azithromycin, the QT interval remained persistently prolonged compared with the baseline with subsequent degeneration into ventricular tachycardia and death. Thus, we highlight that COVID-19 illness itself can potentially lead to further prolongation of QT interval and unmask fatal ventricular arrhythmias in patients who have a prolonged QT and low repolarization reserve at baseline.

Keywords: COVID-19; cardiac arrhythmia; prolonged QTc; torsade de pointes.

Figure 1.

Electrocardiogram on admission demonstrates atrial fibrillation with premature ventricular complexes, a ventricular rate of 95 beats per minute, and corrected QT of 473 ms. Bazett formula is used to correct the QT interval (QTc) for heart rate. There is no consensus regarding the measurement of QT interval in patients with atrial fibrillation. Some suggest averaging the measured QT interval over 10 beats or averaging the QT intervals with the shortest and longest preceding RR intervals. In the above electrocardiogram, it is difficult to discern the QT interval for 10 successive beats. Hence the QT interval is calculated by averaging the shortest and longest QT interval.

Figure 2.

Electrocardiogram obtained during the previous hospitalization 6 months ago while on sinus rhythm demonstrates sinus bradycardia with a heart rate of 55 beats per minute and corrected QT (QTc) of 498 ms as per Bazett formula.

Figure 3.

Chest X-ray on admission shows patchy bilateral opacities.

Figure 4.

Computed tomography of the thorax shows diffuse bilateral ground-glass opacities.

Figure 5.

Electrocardiogram on hospital day 2 demonstrates sinus bradycardia with a ventricular rate of 54 beats per minute, inferolateral deep T-wave inversions, and corrected QT of 718 ms per Bazett formula. Notably, the heart rate decreased significantly compared with day 1, and rhythm reverted to sinus likely related to intubation, mechanical ventilation, and usage of sedative agents such as propofol.

Figure 6.

The telemetry strip on day 5 demonstrates a self-terminating episode of polymorphic ventricular tachycardia. Note the varying amplitude, axis, and duration of QRS complexes suggestive of torsade de pointes (TdP). At the beginning of the strip, there are 2 runs of bigeminy (narrow complex QRS followed by a premature ventricular complex [PVC] at the end of the T-wave). The PVC rising in the third beat initiates TdP.

Figure 7.

Electrocardiogram on day 20 demonstrates atrial fibrillation with prolonged QTc of 622 ms. The QT intervals are corrected for preceding RR intervals using Bazett formula and averaged over 9 successive beats in lead V4.

Figure 8.

The telemetry strip on day 20 demonstrates ventricular tachycardia associated with hemodynamic collapse.