Abstract

Objective: To investigate the relation between the wall motion abnormalities and sodium channel abnormalities in cases of the Brugada syndrome.

Design: Consecutive prospective case–control study in a single hospital.

Setting: Tertiary referral centre.

Patients: 13 consecutive patients with Brugada syndrome and 13 age and sex matched control subjects.

Interventions: Each subject underwent electron beam computed tomography (EBT) and a 12 lead ECG before and after disopyramide injection.

Main outcome measures: QRS width and the magnitude of ST segment elevation in the 12 lead ECG; wall motion by EBT.

Results: After disopyramide, EBT revealed deterioration of focal wall motion abnormalities in the right ventricular outflow tract region in eight of the 13 patients (62%). Prolongation of the QRS width after disopyramide injection in lead V2, which usually reflects the electrical activity in right ventricular outflow tract region, was greater in these eight patients (p < 0.01) than in the other five patients, in whom wall motion did not change after disopyramide. The degree of augmentation of ST segment elevation did not differ significantly between the two groups

Conclusions: The deterioration of wall motion abnormalities in the right ventricular outflow tract region after disopyramide suggests the presence of functional abnormalities of the sodium channel. Some patients with Brugada syndrome may have arrhythmogenic substrates with abnormal responses to sodium channel blockers.