DOI: https://doi.org/10.36347/sasjm.2025.v11i11.004

Pages: 1087-1091

Brugada syndrome (BrS) is a cardiac channelopathy caused by loss-of-function mutations in the SCN5A gene, leading to decreased sodium current and risk of malignant ventricular arrhythmias. Several psychotropic drugs, particularly antipsychotics with sodium channel–blocking properties, have been implicated in unmasking or inducing Brugada-type electrocardiographic (ECG) patterns. We report the case of a young man with treatment-resistant schizophrenia who developed a type-1 Brugada ECG pattern while receiving chlorpromazine, which normalized after drug withdrawal. These effects may be potentiated by high plasma concentrations, drug interactions, or predisposing SCN5A variants. Epidemiological studies suggest that patients with schizophrenia may present a higher prevalence of Brugada-like ECG patterns, possibly related to shared ion channel and autonomic dysfunction. Management of schizophrenia in patients with BrS requires careful antipsychotic selection and collaboration between psychiatry and cardiology to minimize arrhythmic risk. Drugs with minimal sodium channel–blocking activity are preferred alternatives. Regular ECG monitoring is recommended during treatment with sodium channel–blocking psychotropics, especially in resistant or poly-treated cases. Early recognition of drug-induced Brugada phenocopy allows safe continuation of psychiatric care while preventing fatal cardiac events.