Severe Myocardium Suppression in Two Congenital Heart Disease Patients After Remdesivir Use

Background Remdesivir, the first antiviral agent against SARS-CoV-2 fully approved by the FDA, induces ECG abnormalities and impairs cardiac function. Remdesivir interferes with mitochondrial dynamics in vitro, herein, we report on two pediatric patients with a history of congenital heart disease (CHD) who developed profound cardiogenic shock after remdesivir administration. Patient 1 A 10-year-old boy with hypoplastic left heart syndrome was admitted for SARS-CoV-2 infection with a high viral load. After receiving remdesivir, the patient experienced refractory hypotension and a widening of the QRS duration, followed by cardiac arrest. Despite treatment with multiple inotropes and vasopressors, the patient required venoarterial extracorporeal membrane oxygenation (VA-ECMO) for cardiogenic shock and ultimately died of intracranial hemorrhage. Patient 2 A 15-year-old boy with pulmonary atresia and ventricular septal defect after corrective surgeries was admitted for SARS-CoV-2 infection. After receiving remdesivir, the patient developed hypotension, ultimately requiring VA-ECMO due to profound shock and multiorgan failure. Despite stabilization, the patient remained comatose and eventually succumbed to a severe intra-abdominal infection. Conclusion In our proposed model, remdesivir may impair cardiac function, especially at high viral loads, by interfering with mitochondrial quality control and augmenting the cytokine storm. Certain CHDs lead to ventricular overload, rendering cardiomyocytes susceptible to remdesivir-induced mitochondrial dysfunction. Moreover, the sudden onset of shock and the protracted nature of its progression observed in the two patients were in line with the pharmacokinetics of remdesivir. We recommend that remdesivir be used with caution in patients with CHD with right ventricle failure and single-ventricle circulation.