Case Presentation: A 34-year-old woman with a medical history of chronic hypertension, paraplegia secondary to a motor vehicle accident, and chronic substance use disorder managed with buprenorphine presenting with persistent tachycardia. On admission, her electrocardiogram (EKG) revealed sinus tachycardia, and she tested positive for influenza. She was initiated on oseltamivir (Tamiflu) at 1 AM. Within two hours, telemetry monitoring detected new-onset bradycardia. A repeat EKG demonstrated junctional bradycardia with nonspecific ST-T wave changes. A subsequent EKG revealed sinus bradycardia. The differentials included thyroid dysfunction, autonomic dysregulation due to spinal cord injury, and structural cardiac abnormalities. Thyroid studies were normal. Although autonomic dysfunction was considered given to her paraplegia, the patient’s baseline was typically tachycardia. A transthoracic echocardiogram showed no structural cardiac abnormalities. Given the temporal relationship between oseltamivir administration and the onset of bradycardia, and recognizing similar reports in post-marketing surveillance data, oseltamivir was discontinued as a precaution. Following discontinuation, her heart rate normalized in 2 to 3 hours. She was also treated for chronic osteomyelitis and then discharged home.
Discussion: Neuraminidase inhibitors (Oseltamivir and Remdesivir) are commonly used to treat influenza, reducing flu-related morbidity and mortality [1]. Although generally well-tolerated, they can cause cardiovascular side effects like tachyarrhythmias and QT interval prolongation [2]. For Oseltamivir specifically, there are few documented cases of serious cardiovascular effects, such as bradycardia, tachycardia, arrhythmias, often due to insufficient monitoring for these reactions [3]. The mechanism behind these effects is unclear, but it is hypothesized that it may prolong atrial action potential duration, increase atrial refractoriness and lead to bradycardia, and even to atrial standstill. Interestingly, this electrophysiologic effect is being studied for potential anti-atrial fibrillatory use [4].For hospitalists, medication-related bradyarrhythmia represents a crucial patient safety issue. Hospitalized patients routinely receive oseltamivir early in their course, often before a full diagnostic picture is established. This case underscores the importance of continuous telemetry monitoring, timely recognition of medication-induced rhythm disturbances, and careful reassessment of treatment risks versus benefits. The rapid resolution of bradycardia following drug cessation further supports causality and emphasizes the need for vigilance in the acute-care setting.
Conclusions: Oseltamivir-induced bradycardia is a rare but clinically important adverse effect that may be overlooked in hospitalized patients. Despite the widespread use of Oseltamivir, the incidence of bradycardia may be underreported due to limited clinician awareness. Increased awareness among hospitalists is essential, given the widespread use of oseltamivir and the vulnerability of hospitalized patients to medication-related complications. Further research is warranted to better characterize the incidence and mechanism for oseltamivir-associated bradycardia.