![]() ![]() The overarching goal of this study was to investigate RAB and its associated clinical characteristics and outcomes.įollowing University Medical Center of Southern Nevada institutional review board approval, a retrospective audit was performed on 600 consecutive patients at a single institution who were evaluated at hospital admission for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection as defined by the COVID-19 treatment guidelines panel of the National Institute of Health, identified via polymerase chain reaction (PCR) between Maand March 31, 2021. Given the current widespread use of remdesivir and the comparatively modest attention placed on its potential cardiac pharmacodynamic properties, a better understanding of the clinical implications of RAB is warranted. It is not entirely clear whether drugs used in the treatment of COVID-19 that have QT interval-prolonging properties or certain drug–drug interactions also induce bradycardia. The potential etiology for COVID-19 arrhythmogenicity is manifold and includes myocardial insults (infarction, myocarditis), hypoxic injury, a systemic inflammatory response, autonomic disturbance, and electrolyte abnormalities. Furthermore, patients with severe disease may be more prone to incident bradycardia. Bradycardia in the context of COVID-19 may be associated with increased rates of mortality. ![]() Likewise, the association between COVID-19 and sinus bradycardia is well documented in the literature. RAB appears to occur at a disproportionate rate when compared to other pharmaceuticals administered to patients with COVID-19, but only a few studies have appreciated the clinically relevant outcomes that result from the bradycardia. However, despite its wide utilization, there remains a paucity of data regarding the cardiac-related clinical outcomes of remdesivir. Remdesivir antiviral therapy has offered a potential decrease in recovery time for COVID-19 patients, with an acceptable side effect profile. Adenosine is known to exert a negative chronotropic and dromotropic effect by slowing sinoatrial automaticity GS-441524 may lead to RAB via a similar mechanism to adenosine. One proposed mechanism of RAB refers to remdesivir’s active metabolite, GS-441524, a nucleotide triphosphate derivative similar in structure to adenosine. RAB is fairly common, with a reported incidence of 21–60%. found an increased risk of reporting bradycardia following the use of remdesivir compared to other drugs, a finding consistent with a number of case reports and observational studies. ![]() One such phenomenon is remdesivir-associated bradycardia (RAB). Although the drug has been studied extensively in clinical trials, the cardiac side effect profile of remdesivir is not well studied. Remdesivir is an antiviral prodrug of a nucleotide analog and currently a mainstay therapy in the treatment of coronavirus disease 2019 (COVID-19). ![]()
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