Potential Cardiotoxic Effects of Remdesivir on Cardiovascular System: A Literature Review

Maryam Nabati and Homa Parasee

Corona disease 2019 (COVID-19) pandemic continues to spread around the world with no efficacious treatment. Intravenous remdesivir is the only authorized drug for treatment of COVID-19 disease under an Emergency Use Authorization. Remdesivir is a 1′-cyano-substituted adenosine nucleotide prodrug which inhibits viral RNA synthesis. This metabolite is an adenosine analog but with a significantly longer half-life than adenosine. Adenosine is a powerful vasodilator that can cause profound hypotension which is followed by the compensatory release of catecholamines. It can also shorten atrial action potential and refractoriness and lead to atrial fibrillation (AF). These effects may also occur in ventricular cells and predispose patients to ventricular fibrillation. Remdesivir can also induce significant cytotoxic effects in cardiomyocytes that is considerably worse than chloroquine cardiotoxic effects. Remdesivir-induced cardiotoxicity is due to its binding to human mitochondrial RNA polymerase. On the other hand, remdesivir can increase field potential duration with decreased Na+ peak amplitudes and spontaneous beating rates in a dose-dependent manner that might induce prolonged QT interval and torsade de point. There are some reports of sinus bradycardia, hypotension, T-wave abnormalities, AF, and a prolonged QT interval and few cases of cardiac arrest and complete heat block following remdesivir infusion. It seems remdesivir have some cardiotoxic and proarrhythmic effects that are especially more pronounced in patients with previous cardiovascular diseases. The current safety profile of remdesivir is still not completely known and further prospective clinical trials are needed to assess its safety profile and potential adverse cardiovascular effects.

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