Ventricular Tachycardia or Fibrillation Storm in Coronavirus Disease

Abstract

Ventricular tachycardia (VT) or ventricular fibrillation (VF) storm associated with severe acute respiratory syndrome coronavirus 2 infection is a potentially fatal complication; the correlation of these 2 disorders, however, has not been well studied. This retrospective case series examined outcomes of 2 patients who were admitted for repeated implantable cardioverter-defibrillator shocks with or without syncope and observed to have VT/VF storms with COVID-19. Mechanisms of VT/VF storms in COVID-19 are multifactorial including myocarditis, systemic inflammation, hyperadrenergic state, hemodynamic instability, hypoxia, acidosis, and proarrhythmic drugs. A higher incidence of VT/VF storm is observed in patients with comorbidities and those requiring critical care, with some studies reporting increased mortality. In our cohort, 1 of the 2 patients succumbed to the complications from COVID-19, and the other patient was discharged to home in stable condition. Monitoring of life-threatening arrhythmias in the setting of COVID-19 may need to be adopted to prevent morbidity and mortality.

Figure 1

Case 1. Apical four-chamber view of left ventricle with Simpson disk summation method showing increased left ventricular end diastolic volume and diameter. Telemetry strip showing polymorphic ventricular fibrillation rhythm.

Figure 2

Case 2. Left atrium and moderately dilated left ventricle shown. Pacemaker leads present in the right ventricle. Telemetry strip showing ventricular tachycardia storm.

Figure 3

Potential mechanisms of VT/VF storm in COVID-19. Complications resulting from SARS-CoV-2 infection can lead to myocarditis, systemic inflammation, hypotension, hypoxia and acidosis, and a hyperadrenergic response. These along with the use of proarrhythmic drugs can lead to VT/VF storm which are more commonly observed in patients with multiple comorbidities who are critically ill. Abbreviations: COVID-19: coronavirus disease; ICD: implantable cardioverter-defibrillator; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; VF: ventricular fibrillation; VT: ventricular tachycardia.

Figure 4

Electrophysiological mechanisms underlying ventricular arrhythmias from hypoxia and hypercapnia [23]. Decreased partial pressure of oxygen, increased partial pressure of carbon dioxide, and decreased pH lead to reduced ATP, reduced upstroke velocity, and increased ROS. These electrophysiological changes with interplay of additional variables promote arrhythmia via non-reentrant and reentrant mechanisms. Source: Lee et al. [25]. Reproduced with permission. Abbreviations: ATP: adenosine triphosphate; PaCO₂: partial pressure of carbon dioxide; PaO₂: partial pressure of oxygen; ROS: reactive oxygen species; RyR: ryanodine receptors; SR: sarcoplasmic reticulum.

Figure 5

Acute treatment of new episodes of ventricular tachyarrhythmias (VT/VF) [40]. Recommendations for treatment of monomorphic and polymorphic ventricular arrhythmias based on clinical assessment and hemodynamic stability. The benefit of IV amiodarone treatment should be balanced against the polymorphic risk in patients taking QR-prolonging antiviral therapy. Reproduced from https://www.escardio.org/Education/COVID-19-and-Cardiology/ESC-COVID-19-Guidance with permission from The European Society of Cardiology 2021. Abbreviations: DC: direct current; ECMO: extracorporeal membrane oxygenation; IV: intravenous; LV: left ventricle; Pts: patients; TdP: torsade de pointes; VF: ventricular fibrillation; VT: ventricular tachycardia.