Abstract
Brugada syndrome is a rare cardiac condition characterized by distinctive electrocardiogram patterns, predisposing individuals to fatal arrhythmias. While primarily linked to a loss-of-function mutation in the SCN5A gene, acquired forms of the syndrome have been associated with various factors, including drug use. We present a case of a 31-year-old female who presented to the emergency department unresponsive following cocaine use and developed type 1 Brugada ECG patterns alongside an incomplete right bundle branch block in V1-V3, ST elevations with biphasic waves, and diffuse repolarization abnormalities with J point deviations while in the intensive care unit. This study aimed to discuss the complexity of managing drug-induced Brugada-like findings and highlights the need for further research into the mechanisms underlying cocaine-induced cardiac effects. We aimed to discuss potential mechanisms for the impact of cocaine as its role as a sodium channel blocker and its potential effects on connexin 43 in the context of Brugada syndrome. This study also reinforced the importance of differentiating between true Brugada syndrome and other similar ECG changes for appropriate care management.