Abstract 1824: Pilsicainide, a Pure Sodium Channel Blocker, Enhances the Arrhythmogenic Endocardial Substrate in Brugada Syndrome.
Background: Epicardial electrical abnormalities, especially those in right ventricular (RV) outflow tract, are likely to be involved in the arrhythmogenic substrates in Brugada syndrome (BS). However, the involvement of endocardial substrate remains to be examined. The aim of this study was to examine whether pilsicainide, a pure sodium channel blocker, influences the endocardial substrates in BS.
Methods: Pilsicainide (1 mg/kg, IV in 10 min) was administered to 14 consecutive patients with suspected BS who underwent programmed ventricular stimulation. VF was induced in 8 patients (all males, 46±SEM yrs) but not in the remaining 6 patients (all males, 43±SEM yrs). The ECG pattern and the intracardiac conduction properties were measured to evaluate the endocardial substrates.
Results: Pilsicainide significantly elevated ST level in the right precordial leads in VF-induced patients more than in non VF-induced patients (V2, 0.22±0.06 vs. 0.02±0.11 mV, P±0.001). Endocardial potential measurement demonstrated that the onset of the potentials in the RV inflow or outflow tract from the earliest QRS, when measured in the vicinity of the administration of pilsicainide, was significantly delayed in VF-induced patients compared with non VF-induced patients (Δ duration, 23±6 vs. 5±8 msec, P<0.001). The delay was significantly correlated with the enhancement of the ST elevation in V2 (Fgure 1⇓) and the severity of late potentials (RMS40) of single averaged ECG (Figure 2⇓).
Conclusions: These results suggest that the endocardial substrate is also involved in the pathogenesis of BS, which could be distinguished by the response to sodium channel blockers, such as pilsicainide.