Case Presentation: A 19-year-old male with no known medical history presented to the ED after being found down and profusely diaphoretic by his parents. He was unresponsive to multiple doses of Ativan and Narcan. He was tachycardic to the 150s and had respiratory insufficiency, so he was intubated in the ED. Initial EKG showed sinus tachycardia without ST changes. UDS was positive for THC, and labs revealed elevated procalcitonin, D-Dimer, Potassium, and LDH. CTA of the chest showed no evidence of PE but did identify multilobar pneumonia. Follow-up testing confirmed that he was COVID-positive. While in the ED, the patient’s heart rate then rapidly decreased and a stat EKG was performed. The patient then converted into pulseless VFib and ROSC was achieved after CPR. The stat EKG immediately before the code was notable for a type 1 Brugada pattern. Further EKG showed resolution of the pattern, however, the patient ultimately expired from anoxic brain injury.

Discussion: Brugada Syndrome is a male-predominant genetic disorder with a prevalence of 0.1 – 1% that results in an increased risk of ventricular tachyarrhythmias and sudden cardiac death in people with hearts that appear structurally normal. Although it is inherited in an autosomal dominant pattern, variable expressivity can make it difficult to diagnose with family history alone. Thus, diagnosis is typically made by identifying the characteristic pseudo-right bundle branch block in leads V1 and V2 on EKG, but diagnosis is often delayed due to the transient nature of these EKG changes. As a result, Brugada Syndrome can remain undetected until it is unmasked by a trigger, commonly fever or cocaine use, or in our patient’s case Brugada Syndrome was triggered by COVID-19 infection.Patients with Brugada Syndrome typically first present after a syncopal episode or sudden cardiac arrest due to the apparent lack of cardiac abnormalities on routine testing. Although genetic mutations have been identified as a likely cause of Brugada Syndrome, cardiac arrhythmias typically do not appear until triggered, most commonly by fever. As such, a high degree of clinical suspicion of Brugada Syndrome is necessary any time young male patients present with syncope, cardiac arrest, or an abnormal EKG in the setting of a febrile illness. In the context of the recent COVID-19 pandemic, where high fevers may be associated with COVID-19 infection, physicians should be aware of underlying causes that can put young patients at risk of sudden cardiac death as a result of COVID-19-induced fevers. Additionally, aggressive antipyretic therapy should be considered in young patients with COVID-19 to decrease the chances of triggering Brugada Syndrome that could progress to sudden cardiac death.

Conclusions: We present a case in which fever due to COVID-19 infection revealed Brugada Syndrome in a previously healthy 19-year-old male. As Brugada Syndrome usually triggered most commonly by fever, physicians should have high index of suspicion in young male patients that present with syncopal episode or sudden cardiac arrest. Furthermore, aggressive supportive therapy such as antipyretics should be considered to decrease the likelihood of triggering Brugada Syndrome, and give definitive treatment with ICD placement or catheter ablation.

IMAGE 1: Figure 1. (A) Patient’s initial EKG showing sinus tachycardia without ST changes (B) Pre-cardiac arrest EKG showing type 1 Brugada pattern with coved ST-elevation in V1-V3 followed by negative T waves (C) Resolution of Brugada pattern on subsequent EKG