Lethal Arrhythmia (Torsade de Pointes) in COVID-19: An Event Synergistically Induced by Viral Associated Cardiac Injury, Hyperinflammatory Response, and Treatment Drug?

Abstract

Arrhythmias in patients with coronavirus disease 2019 (COVID-19) are prevalent and deserve special attention because they are associated with an increased risk of fatal outcome. The mechanism of arrhythmia in COVID-19 remains unclear. Here, we report our first case of confirmed COVID-19 with documented Torsade de Pointes (TdP). A 64-year-old woman, previously healthy, presented to our emergency department with progressive shortness of breath, dry cough, and 1 week of fever. She was treated with chloroquine phosphate, meropenem, and ciprofloxacin. After 5 days of admission, her condition deteriorated and she was admitted to the intensive care unit. The patient had two episodes of malignant arrhythmias within 24 hours. The former was TdP, and the latter was a fatal pulseless ventricular tachycardia that occured even after chloroquine was discontinued. There was evidence of cardiac injury shown by increased serum level of troponin I. We propose a synergistic concept of lethal arrhythmia due to direct severe acute respiratory syndrome coronavirus (SARS-CoV)-2-associated cardiac injury, hyperinflammatory response, and drug-induced arrhythmia.

Epidemiology, risk factors and prognosis of cardiovascular disease in the Coronavirus Disease 2019 (COVID-19) pandemic era: a systematic review

“…Another interesting point is the effect of SARS-CoV-2 on the cardiovascular system, as it may cause or conduce to acute cardiovascular events, microvascular thrombosis, myocardial damage, and arrhythmias [12,[66][67][68].…”

In-depth review of cardiopulmonary support in COVID-19 patients with heart failure

“…Recent studies have shown that COVID-19 is associated with acute myocardial involvement which described as an acute cardiac injury[ 3 , 12 , 13 ]. A suspicion of cardiac involvement in COVID-19 is best described by an elevation in cardiac biomarker [high-sensitivity troponin (hs-TnI)] above 99 th percentile upper reference limit[ 13 , 22 ]. Early reports had been analyzed, with notable findings suggest an increased level of cardiac troponin was associated with admission to intensive care and higher in hospital mortality[ 12 , 23 - 26 ].…”

“…Careful observation of the heart rate and rhythm are vitals in the clinical settings. Atrioventricular block, atrial fibrillation, polymorphic ventricular tachycardia and pulseless electrical activity have been closely associated with COVID-19 despite of the unknown mechanism of how these rhythms abnormalities may develop[ 22 , 35 ]. QT prolongation is constantly a thread, considering that QT prolongation is an independent risk factor of adverse outcome in advanced heart failure[ 36 ].…”

In-depth review of cardiopulmonary support in COVID-19 patients with heart failure

“…A lower pulmonary function is commonly found in HF patients and is contributed mainly by chronic obstructive pulmonary disease (COPD) [20]. Combination of underlying parenchymal disease and elevated left ventricular filling pressure leads to the development of pulmonary hypertension [21]. In COVID-19 infection, respiratory failure and acute respiratory distress syndrome (ARDS) further exacerbates pulmonary vasoconstriction and interstitial edema.…”