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Figure 3 Patient Examples

Representative surface ECGs and unipolar electrograms in a control subject (A) and in 2 patients with Brugada syndrome (B and C) under baseline conditions (left panels) and after pilsicainide administration (right panels). (A) Brugada-type ECG was not observed in surface ECGs. Under baseline conditions, the epicardial ARI (221 ms) was shorter than the endocardial ARI (244 ms). After the administration of pilsicainide, the epicardial ARI (208 ms) was still shorter than the endocardial ARI (230 ms). (B) Under baseline conditions, type 1 ECG was observed in lead V₂(3ics) (*), and the epicardial ARI (239 ms) was longer than the endocardial ARI (187 ms). After the administration of pilsicainide, type 1 ECG was still observed in lead V₂(3ics) (*), and epicardial ARI (222 ms) was longer than endocardial ARI (190 ms). (C) Under baseline conditions, type 1 ECG was not observed in any of the surface ECG leads, and the epicardial ARI (210 ms) was shorter than endocardial ARI (248 ms). However, after administration of pilsicainide, the epicardial ARI, but not the endocardial ARI, was markedly prolonged (260 ms), and type 1 ECG appeared in lead V₂(3ics) (*). The epicardial ARI was 18 ms longer than the endocardial ARI (242 ms). Numbers indicate ARI. ARI = activation-recovery interval; ECG = electrocardiogram; RVOT-epi = uniploar electrogram of the epicardium at the right ventricular outflow tract; RVOT-endo = uniploar electrogram of the endocardium at the right ventricular outflow tract; * = type 1 ECG.