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What literature is available describing the occurrence of bradycardia with remdesivir?

Remdesivir is a broad-spectrum antiviral with activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that has caused the worldwide pandemic of COVID-19.1 An Emergency Use Authorization (EUA) for remdesivir use to treat severe COVID-19 in hospitalized adult and pediatric patients was granted by the Food and Drug Administration (FDA) in May 2020.2 Subsequently, the drug received FDA approval for use in hospitalized adults and pediatric patients 12 years of age and older in October 2020. Remdesivir use in hospitalized patients weighing 3.5 kg to < 40 kg and for patients under 12 years of age weighing at least 3.5 kg is admissible under the EUA.

Common (≥ 5%) adverse drug reactions (ADRs) of remdesivir observed in phase 3 clinical trials include nausea and elevation in transaminases.1 Serious reactions or those that led to discontinuation included transaminase elevations, kidney injury, infusion site reactions, rash, and decreased heart rate (<1%). As the use of remdesivir has increased, data on its safety has also accumulated. An increasing number of case reports, retrospective, and prospective studies have been published reporting the occurrence of bradycardia with remdesivir use.3-21 The purpose of this review is to summarize the current published literature available describing the effect of remdesivir on heart rate (HR).

Literature Review
As summarized in Table 1, a number of case reports have described the onset of bradycardia, its sequelae, and management in patients who received remdesivir as a component of treatment for COVID-19.3-13 With respect to patient characteristics, there is no consistency in the age or past medical history of the patients affected. The onset of bradycardia was also inconsistent with signs occurring as early as within 6 hours of the first dose and as late as after the fourth dose. Severity of bradycardia varied but most patients remained asymptomatic. Bradycardia resolved either spontaneously or with remdesivir discontinuation and additional treatment was not required in most cases. Patients who required treatment received atropine as needed and/or a dopamine infusion of 3 or 5 mcg/kg/min.

Summaries of ADRs of COVID-19 treatments submitted to the adverse reporting databases of the World Health Organization (WHO), Vigibase, and the FDA’s adverse event reporting system (FAERS) have been published.14,15 According to global adverse reaction reporting between January 1, 2020 to December 31, 2020 on COVID-19 treatments to VigiBase, approximately 35% (5299/14,574) of the reports were related to remdesivir treatment.14 Of these, frequency of effects on HR were: 4.6% bradycardia, 1.1% HR decreased, 0.7% sinus bradycardia, 0.3% QT prolongation, and 0.4% dizziness. The authors concluded that these cardiac effects are not outlined in the labeling of remdesivir, were unexpected, and deserve attention. In FAERS reporting from January 1, 2020 to May 28, 2021, remdesivir was considered a possible cause of approximately 51% of ADRs reported for COVID-19 treatments.15 Bradycardia associated with remdesivir (5.37%) was significantly higher compared with other treatments. Occurrence of bradycardia was not found to be more common based on age or sex.

Prospective and retrospective studies (see Table 2) in larger populations have attempted to determine incidence and/or association of remdesivir with bradycardia.16-21 Incidence of bradycardia ranged from 21% to 46.8%.17-20 One prospective study demonstrated a reduction in HR from baseline but no cases of bradycardia.16 No significant sequelae or major intervention was required in any of these larger studies.

Table 1. Case reports of bradycardia after initiation of remdesivir.3-13
Patient characteristics
Intervention and outcome
Ching et al 20213
37-year-old male
Baseline HR = 102 bpm
Remdesivir dose not specified
HR: 40 to 44 bpm after second dose
Remdesivir discontinued on day 2
Day 6: HR increased to 56 to 58 bpm
Day 8 (2 days post-discharge): 60 to 70 bpm
No sequelae at 2-month follow-up
Eleftheriou et al 20214
Patient 1:
13.5-year-old female
Baseline HR = 80 bpm
Patient 2:
10-year-old female
Baseline HR = 80 bpm
Patient 3:
Baseline HR = 130 bpm
Remdesivir doses not specified
Patient 1: 
HR: 50 bpm after fourth dose
Patient 2: 
HR: 60 bpm after third dose
Patient 3: 
HR: 80 bpm after third dose
HR normalized within 24 h in all patients with either discontinuation or completion of remdesivir treatment
Jacinto et al 20215
78-year-old female
former tobacco user
Baseline HR range: 65 to 75 bpm
Baseline systolic BP range: 120 to 180 mm Hg
Baseline ECG: Left bundle branch block
Received remdesivir 200 mg on day 1 and 100 mg daily for 4 days
HR: 38 bpm 20 h after first dose
Symptomatic bradycardia with BP 73/50 mm Hg
ECG: sinus bradycardia with left bundle branch block
Refractory to atropine so dopamine 5 mcg/min was maintained for course of remdesivir therapy and HR maintained between 65 to 75 bpm
Dopamine titrated down and discontinued 18 h after last remdesivir dose; HR and ECG remained normal
Naranjo score=7 probable side effect
Selvaraj et al 2021672-year-old male
Lung cancer
Atrial fibrillation (no specific treatment)
Baseline HR range: 68 to 86 bpm
Baseline ECG: atrial fibrillation; right bundle branch block
Received remdesivir 200 mg on day 1 and 100 mg daily for 4 days
HR range: 30 to 40 bpm within 24 h of first dose and continued for duration of remdesivir treatment
Complete AV block on day 5 of treatment
AV block spontaneously resolved within 48 h of completion of remdesivir treatment
HR range on day 10: 52 to 58 bpm
Chow et al 2021716-year-old male
Obesity (BMI 43.9 kg/m2)
Baseline HR range: > 90 bpm
Received remdesivir 200 mg on day 1
HR range: 46 and 65 bpm over 12 h after first dose; reduction in HR started within 6 h after the first dose
Patient reported no symptoms specific to low HR
Remdesivir discontinued
HR range: 40 to 60 bpm for 2 days after discontinuation
HR at 14 days after discharge: 107 bpm
Sanchez-Cortez et al 2021813-year-old male
Baseline HR range: 80 to 90 bpm
Received remdesivir 200 mg on day 1, then 100 mg daily
HR: 40 bpm after 3rd dose
Asymptomatic, ECG-confirmed sinus bradycardia
Remdesivir discontinued upon bradycardia
HR normalized to 80 to 100 bpm within 24 h
Naranjo score 6=probable side effect
Day et al 2021959-year-old male
No significant PMH
Baseline HR range: 79 to 89 bpm
Baseline ECG: Normal sinus rhythm
Received remdesivir 200 mg on day 1, then 100 mg daily
HR: 50 bpm after third dose
ECG-confirmed sinus bradycardia
Fatigue, generalized weakness, and headache but no lightheadedness
Remdesivir discontinued upon bradycardia
HR normalized to 62 bpm 3 days after remdesivir was discontinued
Barkas et al 202110
36-year-old male
No significant PMH
Baseline HR: 92 bpm
Baseline ECG: Normal sinus rhythm
Received remdesivir 200 mg on day 1, then 100 mg daily
HR: 39 bpm after third dose
Asymptomatic; ECG-confirmed sinus bradycardia; other cardiac abnormalities ruled out
Remdesivir discontinued
HR normalized to 58 bpm measured on day 9 after remdesivir discontinuation
Abdelmajid et al 202111Patient 1:
55-year-old male
Active smoker
Baseline HR: 61 bpm
Baseline ECG: Normal sinus rhythm
Patient 2:
54-year-old female
No significant PMH
Baseline HR: 70 bpm
Baseline ECG: Normal sinus rhythm
Both patients received remdesivir 200 mg on day 1, then 100 mg daily
Patient 1:
HR: 31 bpm after fourth dose
ECG-confirmed sinus bradycardia
Thyroid and cardiac markers were normal
Patient 2:
HR range: 37 to 42 bpm after second dose
ECG: QT prolongation, then atrial fibrillation
Cardiac enzymes were normal
Symptomatic bradycardia with dizziness and fatigue
Patient 1:
Remdesivir discontinued on day 5 of treatment
HR increased to 54 bpm 2 days after remdesivir discontinuation and to 74 bpm before discharge
Patient 2:
Remdesivir discontinued before third dose with HR
Patient required ICU admission and received atropine as needed (if HR < 35 bpm) and dopamine 3 mcg/kg/min
HR normalized to above 60 bpm and ECG was normal within unspecified time frame after remdesivir discontinuation
Gubitosa et al 20201254-year-old female
Left bundle branch block
B-cell lymphoma
Baseline HR range: 60 to 70 bpm
Received remdesivir 200 mg on day 1, then 100 mg daily
HR: 38 bpm within 24 h of first dose and to 34 bpm on day 4 of treatment
Cardiac enzymes normal; other potential causes ruled out
ECG: sinus bradycardia and widened QRS complex
Symptomatic with dizziness, chest pressure and shortness of breath
Remdesivir discontinued after continued bradycardia
Atropine administered
HR normalized to 60 to 70 bpm with resolution of chest pain and dizziness within unspecified time frame after remdesivir discontinuation
Gupta et al 202013Patient 1:
26-year-old female
Baseline HR range: 80 to 100 bpm
Baseline ECG: normal sinus rhythm
Patient 2:
77-year-old female
Baseline HR: 67 bpm
Baseline ECG: Normal sinus rhythm
Both patients received remdesivir 200 mg on day 1, then 100 mg daily
Patient 1:
HR: 40 to 50 bpm after third dose
ECG: sinus bradycardia; prolonged QT interval and T wave abnormality
Patient 2:
HR: 48 bpm after third dose
ECG: sinus bradycardia
Patient 1:
Remdesivir discontinued upon bradycardia
HR returned to baseline and QT interval shortened 3 days after remdesivir discontinuation.
Patient 2:
Remdesivir discontinued upon bradycardia
HR returned to baseline 2 days after remdesivir discontinuation
Abbreviations: AV, atrioventricular, BMI, body mass index; BP, blood pressure; bpm, beats per minute; COPD, chronic obstructive pulmonary disease; ECG, electrocardiogram; HR, heart rate; HTN, hypertension; ICU, intensive care unit; PMH, past medical history.
Table 2. Studies evaluating incidence and risk of bradycardia with remdesivir treatment.16-21 
Study type
Definition of bradycardia
Brunetti et al16
Prospective cohort of
COVID-19 patients treated with remdesivir (N=52)
At baseline:
56% male
76% > 50 years
53% at least 1 CV comorbidity
57% HTN
Bradycardia (HR < 60 bpm)
Symptomatic bradycardia (bradycardia + clinical symptoms*)
HR reduction was significantly reduced from a baseline of 85 bpm to 70 bpm (p<0.05)
Reduction observed in the first days of treatment
The extent of HR reduction was proportional to the baseline HR (p<0.001)
No episodes of bradycardia, symptomatic bradycardia or QTc prolongation.
No patients discontinued remdesivir
HR reduction is observed with remdesivir; however, extent of reduction was not significant to cause bradycardia or symptoms
Perhaps, the improvement in symptoms of COVID-19 is causing HR reduction as patients may be presenting with higher baseline HR
Kumar et al+, 17, 18
Multicenter, retrospective analysis
COVID-19 positive patients admitted between March and August 2020 (N=1053)
Absolute bradycardia (HR < 60 bpm)
Profound bradycardia (HR < 50 bpm)
Episodes occurring on 2 separate measures at least 4 h apart during hospitalization
28.7% of those receiving remdesivir developed absolute bradycardia
Incidence of profound bradycardia in patients receiving remdesivir was not reported
Bradycardia resolved with remdesivir discontinuation in some cases (full analysis is pending)
Pallotto et al19
Single-center, retrospective analysis
COVID-19 positive patients admitted between September and December 2020
Cases (n=62): full course of remdesivir with no prior history of bradycardia
Controls (n=79): did not receive remdesivir
Transient bradycardia: HR < 60 bpm for 2 consecutive measures or < 50 bpm on 1 measure
Transient bradycardia:
46.8% cases vs 27.8% controls; p=0.023 (OR, 2.15, 95% CI 1.05 to 4.4, p=0.036)
No symptomatic bradycardia or ECG changes were observed
All patients had received full course of remdesivir treatment
No adverse sequelae reported from transient bradycardia
Attena et al20
Single-center, prospective, observational study
COVID-19 positive patients hospitalized between September and December 2020
Remdesivir treatment (n=100)
No remdesivir treatmennt-control group (n=66)
ECG-detected sinus bradycardia
Extreme sinus bradycardia: HR < 50 bpm
ECG-detected sinus bradycardia on day 5: 21/100 (21%) remdesivir group vs 2/66 (3%) control group (p=0.001)
Extreme sinus bradycardia: 4/21 (19%) of patients with bradycardia who received remdesivir
Female sex, low resting HR, and high baseline D-dimer were associated with incident sinus bradycardia
Sinus bradycardia was reversed upon remdesivir discontinuation in all cases
No interventions were required for bradycardia, specifically
Touafchia et al21
Retrospective comparative study using Vigibase reports of patients with COVID-19 up to September 23, 2020
Remdesivir ADR reports (n=2603)
Hydroxychloroquine, lopinavir/ritonavir, tocilizumab, or glucocorticoids ADR reports (n=3971)
Cases: reports containing terms ‘bradycardia’ or ‘sinus bradycardia’ found in MedDRA dictionary
Non-cases: any other adverse events
94/2509 (3.7%) remdesivir vs. 88/3883 (2.3%) other treatments; ROR 1.65 (1.23 to 2.22) **
Of the 94 cases, 75 (80%) were serious and 16 (17%) were fatal
Median onset of bradycardia: 2.4 days (range 1 to 6)
Specific interventions for bradycardia not described
*clinical symptoms= syncope or presyncope, transient dizziness or light-headedness, heart failure, or confusion; **ROR=exposure odds among reported cases of bradycardia over the exposure odds among reported non-cases; + original analysis18 evaluated occurrence of bradycardia in all COVID-19 patients and results presented here were in response to a comment to the authors on remdesivir.17
Abbreviations: ADR, adverse drug reaction; bpm, beats per minute; CI, confidence interval; CV, cardiovascular; ECG, electrocardiogram; HR, heart rate; HTN, hypertension; OR, odds ratio; ROR, reporting odds ratio.

COVID-19 and Cardiac Effects
Cardiac effects, including viral myocarditis, heart failure, cardiomyopathy, myocardial infarction, thromboembolism, and arrhythmias (including bradycardia), as a complication of COVID-19 have been described.18, 22-26 Entry of SARS-CoV-2 into cardiomyocytes and inflammation causing a prothrombotic state are some proposed mechanisms leading to these cardiac effects.22,24 In a meta-analysis on cardiac manifestations in COVID-19 illness, the  incidence of acute cardiac injury was found to be 15%.22 In other observational studies, 8% to 17% of patients had arrhythmia-related events including atrial fibrillation (21%), sinus bradycardia (8%), and heart block (8%).18 In pediatric patients, cardiac manifestations have included cardiogenic shock, electrocardiogram (ECG) changes, and myocardial infarction.23

Kumar and colleagues studied the incidence of bradycardia in 1053 patients hospitalized for COVID-19 between March and August of 2020.18 Absolute bradycardia (HR < 60 bpm) and profound bradycardia (HR < 50 bpm) with episodes occurring on 2 separate measures at least 4 hours apart during hospitalization were the primary outcomes. Approximately 25% (n=262 patients) had absolute bradycardia and 13% (n=137) had profound bradycardia. Mortality rate was significantly higher in patients who had profound vs. absolute bradycardia (25.5% vs. 17.7%, p<0.01). Patients with HR 60 bpm.

A report by Bhasin and colleagues describes a case of complete heart block in a patient with myocarditis due to COVID-19.25 The patient received treatment for COVID-19 with remdesivir with no worsening of cardiac consequences.

Remdesivir’s active metabolite, a nucleoside triphosphate, is an inhibitor of the SARS-CoV-2 polymerase involved in viral replication.1,5 One suggested mechanism for its effect on HR is the metabolite’s resemblance to adenosine 5′ triphosphate (ATP) which suppresses the sinoatrial and atrioventricular node activity and increases vagal tone.5,16 Another postulation is the reduction in HR observed with treatment of COVID-19 may be an indicator of response to therapy.16

Current literature describing the occurrence of bradycardia with remdesivir treatment includes published case reports, ADR database reporting, small prospective, observational, and retrospective studies. Based on the data currently available, the association between bradycardia and remdesivir remains inconclusive as some cases have reported transient bradycardia and resolution with continuation of remdesivir treatment as well as successful use of remdesivir in a patient with heart block. Clinicians should obtain baseline HR and an ECG in patients with COVID-19.27 If remdesivir treatment is initiated, close attention should be given to daily HR measures during the course of treatment. Management of bradycardia, should it occur, depends on patient symptoms and comorbid conditions. Remdesivir should be considered a potential cause and, if suspected, management (based on available literature) can include continued monitoring, discontinuation of remdesivir, and treatment for persistent/symptomatic bradycardia with dopamine and atropine (as needed). Given the cardiac effects of COVID-19, cardiac monitoring with or without remdesivir treatment may be warranted.22,27


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  26. Bhasin V, Carrillo M, Ghosh B, Moin D, Maglione TJ, Kassotis J. Reversible complete heart block in a patient with coronavirus disease 2019. Pacing Clin Electrophysiol. 2021 Jul 21:10.1111/pace.14321. doi: 10.1111/pace.14321
  27. Prutkin JM, Knight BP, Parikh N. COVID-19: arrhythmias and conduction system disease. In: Post TW, ed. UpToDate. UpToDate; 2021. Accessed September 30, 2021.

Prepared by:
Rita Soni, PharmD, BCPS
Clinical Assistant Professor, Drug Information Specialist
University of Illinois at Chicago College of Pharmacy

October 2021

The information presented is current as of September 22, 2021. This information is intended as an educational piece and should not be used as the sole source for clinical decision-making.