DOI: 10.23937/2378-2951/1410277
Fever-Induced Brugada Syndrome (BrS): Clinical Case Presentation and Short Review on Brugada Syndrome
Almontasser Bella Kassier, MD*, Adnan Kassier, MD, Yashwant Agrawal, MD, and Jagadeesh K. Kalavakunta, MD
Ascension Borgess Hospital, Kalamazoo, MI, USA
Keywords
Brugada syndrome, Syncope, Arrhythmia, ICD
Introduction
In 1992, Brugada syndrome (BrS) was described for the first time as a pattern of ST-segment elevation in right precordial electrocardiography (EKG) leads with a high incidence of unexplained cardiac arrest (UCA) and sudden cardiac death (SCD) in patients with structurally normal hearts [
1]. It is associated with an autosomal dominant genetic predisposition. Therefore, in the case of diagnosed UCA or SCD, first-degree relatives are advised to be screened for cardiac abnormalities [
2]. The characteristic EKG changes of the Brugada pattern could sometimes be transient or variable over time. There are some known provoking factors such as fever, medications, and toxins [
3]. In this case, we present a 23-year-old Caucasian male patient with a long-standing history of substance abuse who presented with syncope. Electrocardiography performed by emergency medical services (EMS) showed a Brugada pattern.
Case Description
A 23-year-old Caucasian male patient with a long-standing history of substance abuse, presented with syncope. When emergency medical services arrived, the patient had supraventricular tachycardia of around 180 beats per minute and subsequently cardioverted at 50 J on site. They attempted to reverse the patient's somnolence with Narcan, first intranasal then intravenous, without improvement. Upon arrival at the emergency department, the patient had a witnessed episode of what appeared to be seizure activity with foaming through the mouth. EKG at the time showed a Brugada EKG pattern (Figure 1). He was febrile with a temperature of 103 F. The patient's toxicity profile was positive for both Amphetamine and cannabinoid. Creatine Kinase was > 4000 I Unit\L and Troponin I was 2.38 ng\ml which suggested rhabdomyolysis. While hospitalized, the patient had another seizure-like episode while on telemetry, which showed sinus rhythm at the time of syncope. Cardiac MRI was negative for structural abnormalities. His family history was significant for SCD in his 40-years-old aunt. We contemplated the idea of placing an implantable cardioverter defibrillator (ICD). However, since he had another seizure while on telemetry without EKG abnormalities, we opted to place an Implantable Loop Recorder (ILR) instead, before discharge.