Attul Sharma*, Rachel Quint*, Fares Salem*, Zohal Rahimi*, Premsai Bondalapati*, Akashpreet Riar*
* American University of the Caribbean School of Medicine
Sodium and potassium channels are the most critical players in the maintenance of homeostasis and function in the human body. Specifically, sodium imbalance can affect normal cardiac function; however, laboratory results may not always reflect electrolyte disturbances associated with other unrecognized comorbidities, such as Brugada’s syndrome (BrS). BrS is a rare inherited autosomal dominant cardiac arrhythmia that can be mistaken for various anomalies, such as ventricular fibrillation. About one-third of BrS cases can be diagnosed through genetic analysis of several genes responsible for sodium, potassium, and calcium channel integrity, primarily SCN5A. First line therapy for patients with BrS is an Implantable Cardioverter Defibrillator (ICD). Alternatively, patients can be prescribed quinidine, a class 1A antiarrhythmic drug, which carries with it the risk of ventricular fibrillation. Extra precaution and recurrent monitoring should be undertaken as complications may arise with pharmacologic treatment. The purpose of this case report is to highlight the presentation and clinical importance of Brugada syndrome, a diagnosis that may be overlooked as a cause of sudden cardiac death.
We present a case of a 24-year-old healthy male presenting to the ER with a syncopal episode. The patient had no prior medical and his past medical history was negative for medications, infections, and abnormalities. He has a family history of heart disease with a grandfather who has had a defibrillator placed for heart failure. Upon ER arrival, the patient underwent a physical examination, laboratory testing, and a 12- lead ECG. The patient was subsequently diagnosed with ventricular fibrillation, which was then later identified as Brugada Syndrome.