Brugada syndrome is an inherited arrhythmogenic disease, characterised by a coved-type ST segment elevation in right precordial leads and an increased risk of sudden cardiac death due to ventricular arrhythmia. Electrocardiographic patterns of the disease is divided into three as: a) type I, characterized by a coved-type ST-segment elevation ≥ 2 mm in more than one right precordial lead (V1-V3), followed by negative T wave; b) type II, characterized by ST-segment elevation ≥ 2 mm in right precordial leads followed by positive or biphasic T waves, resulting in a saddleback configuration; and c) type III, defined as any of the 2 previous types if ST-segment elevation is ≤ 1 mm. Although genetic basis of the disease is described (mutations in SCN5A, a cardiac sodium channel gene, transmitted in an autosomal dominant pattern), there is a lack of information about its relationship with triggering factors, particularly toxins. Even though the literature knowledge mainly depends on case reports, in this review, our aim was to investigate the relationship between BrS and toxins, and create awareness on clinicians about this fatal entity.