Drug-induced Brugada Syndrome

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

Disclosures

Europace. 2009;11(8):989-994. 

In This Article

Drug-induced Brugada Syndrome

Patients with proved Brugada syndrome can have normal ECG recordings at other times. Brugada syndrome can also be incompletely expressed in a family. Known or suspected mutation carriers may display a normal ECG or a partial non-diagnostic Brugada pattern of a saddle-shaped ST segment with or without elevation: the type 2 and 3 ECG patterns, respectively. In these cases, a diagnostic challenge with a sodium channel blocker such as ajmaline, flecainide, or pilsicainide may induce the full-blown type 1 ECG pattern and support the diagnosis in a family member.[1]

On the other hand, the Brugada sign has been described in asymptomatic patients after exposure to various drugs.[12] These patients normally do not have any symptoms or history of ventricular arrhythmias. In these asymptomatic patients, the abnormal ECG often can be reproduced by class 1A and 1C antiarrhythmic drugs, such as flecainide, procainamide, or ajmaline, which block the sodium channel.[13,14] Autonomic influence is also important: α-adrenergic blockade reduces the ST-segment elevation, whereas α-adrenergic stimulation has the opposite effect.[14] It has become apparent subsequently that sporadic cases of the Brugada ECG pattern without a family history of the condition may be 'unconcealed' by exposure to drugs with sodium channel blocking effects.[15,16] Theoretically, therefore, an acquired intervention that causes a sufficient imbalance of inward and outward currents in the right ventricular outflow tract may induce the surface ECG pattern in an individual, although the likelihood of arrhythmias is unclear. Whether this requires an underlying genetic predisposition or represents latent Brugada syndrome has not been established.

The characteristic ECG pattern of ST-segment elevation in V1 and V2 in the Brugada syndrome is dynamic; it is often intermittently present in affected individuals and can be unmasked by sodium channel blockers as mentioned above.[15,17–26] However, recently, many other pharmacological agents not related to class I antiarrhythmic agents have been reported to induce Brugada ECG pattern including tricyclic antidepressants (TCAs), fluoxetine, lithium, trifluoperazine, antihistamines, and cocaine. In a survey of 1000 normal subjects in whom two ECGs were systematically recorded, the prevalence of drug-induced Brugada syndrome (confirmed on a sodium channel blockade challenge) was reported to be 5 out of 1000.[16]

As published reports of the drug-induced Brugada sign have become increasingly prevalent, there is growing interest in the mechanisms responsible for this acquired ECG pattern and its clinical significance. It is possible that drug-induced Brugada syndrome may be due to an individual susceptibility that favours drug-induced ECG abnormalities, possibly as a result of an increase in a latent ion channel dysfunction similar to that in drug-induced long QT syndrome. However, further evidence is needed to confirm this postulation. In this paper, we will review the cases and evidence of drug-induced Brugada syndrome reported in the literatures.

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