What are the cardiovascular adverse effects and underlying cellular mechanisms of antiviral therapies used for COVID-19?
This review highlights the importance of considering cardiovascular adverse effects and their cellular mechanisms when prescribing antiviral therapies for COVID-19.
Antiviral therapeutics have made a critical contribution in mitigating the symptoms and clinical outcomes of the coronavirus disease of 2019 (COVID-19), in which a single-stranded RNA viral pathogen, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), causes multi-organ injuries. Several antivirals were widely prescribed to treat COVID-19, either through the emergency use authorization (EUA) by the governmental regulatory agencies (i.e., remdesivir, paxlovid, molnupiravir, and the SARS-CoV-2-targeted monoclonal antibodies - tixagevimab and cilgavimab), as well as the repurposed use of the existing antiviral or antimalarial drugs (e.g., hydroxychloroquine, chloroquine, and ivermectin). Despite their efficacy in ameliorating COVID-19 symptoms, some adverse side-effects of the antivirals were also reported during the COVID-19 pandemic. Our current review has aimed to gather and extrapolate the recently published information concerning cardiovascular adverse effects caused by each of the antivirals. We also provide further discussion on the potential cellular mechanisms underlying the cardiovascular adverse effects of the selected antiviral drugs, which should be carefully considered when evaluating risk factors in managing patients with COVID-19 or similar infectious diseases. It is foreseeable that future antiviral drug development assisted with the newest artificial intelligence platform may improve the accuracy to predict the structures of biomolecules of antivirals and therefore to mitigate their associated cardiovascular adversities.
Chen et al. (Mon,) studied this question.