Drug-induced Brugada Syndrome

Yee Guan Yap; Elijah R. Behr; A. John Camm


Europace. 2009;11(8):989-994. 

In This Article


In summary, it appears that potent sodium channel blockers and selected non-cardiac drugs may induce the type 1 Brugada ECG even in patients without any other features of the syndrome such as history of syncope or ventricular tachyarrhythmias. In some cases, the abnormal ECG appeared in some individuals only during the administration of a sodium channel blocker used to identify carriers of the disease within a family with a history of sudden death or Brugada syndrome. In other individuals, the diagnostic ECG was seen when the patients were exposed to the offending drugs for other medical reasons. In such patients, it is not clear whether or to what extent a genetic predisposition may be involved. The prognosis appears to be good provided the full-blown Brugada syndrome is not uncovered. Thus, in asymptomatic patients without a family history of sudden death, drug-induced Brugada sign is likely to be benign once the offending agent is discontinued.[12] Existing data in Brugada syndrome support this approach. For example, a registry study of patients with type 1 Brugada ECG pattern found that asymptomatic patients who developed the Brugada sign only after pharmacological challenge had no arrhythmic events at 27 ± 29 months.[70] These findings have been replicated by other groups. Once the offending agent has been removed, it is therefore reasonable to then treat the patient utilizing existing algorithms from the Second Consensus Conference of the Heart Rhythm Society and the European Heart Rhythm Association.[1] Canine ventricular wedge studies suggested that a flecainide-induced Brugada phenotype does not necessarily indicate the presence of an arrhythmic substrate; it does denote the ability of sodium channel block to create the conditions under which the arrhythmic substrate may readily develop.[71]


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