An unexpected diagnosis: Brugada Syndrome in a healthy Kenyan male athlete

In this report, we describe an unexpected finding of Brugada Syndrome (BrS) in a young Kenyan athlete presenting with multiple episodes of syncope. This diagnosis could be the index case of BrS in the country, a diagnosis that is well described in Asia and the West, but rarely in Sub-Saharan Africa. A healthy 25-year-old male patient was referred by his teammate for episodes of syncope while playing field hockey. He noted that he has been healthy all his life with no significant medical history. His first episode of syncope was in late 2024, around October. He noted a prodromal episode of dizziness, fatigue and visual changes before passing out. He came to after about 30 seconds to 1 minute with no significant changes in his sensorium. He noted no fevers, no history of anaemia, no chest pain, no palpitations, no seizures or known cardiac history in the family. He subsequently had had two more episodes since then. His last episode was in the last week of March 2025. He had borderline bradycardic pulse in the mid 50s, with no murmurs, rubs or gallops, with a single, intact and non-displaced point of maximal impulse; normal JVP and no peripheral oedema. Radial, brachial and posterior tibial pulses were normal. Lungs had normal air movement without wheezing, rales or rhonchi. Abdominal exam had no organomegaly. His EKG revealed a normal sinus rhythm with a heart rate of 55 bpm, but with a prolonged PR interval of about 250 milliseconds; the right precordial leads V1 to V3 revealed elevated and coved ST segments diagnostic of type I Brugada Syndrome. A 12-hour Holter monitor revealed sinus bradycardia with persistent ventricular dysrhythmia, were consistent with the EKG, consistent with type I Brugada Syndrome. His echocardiogram revealed a normal left ventricle with mild concentric hypertrophy and normal function and an EF of 65 to 70%. Brugada syndrome (BrS) is a known leading cause of sudden cardiac death in young patients with structurally normal hearts. It is an autosomal dominant sodium channelopathy that causes a coved elevation in the ST segment in the right precordial leads that can degenerate in to a ventricular arrhythmia (polymorphic ventricular tachycardia or ventricular fibrillation) resulting in convulsive syncope and death.