INTRODUCTION: Na+ channel blockers are used to treat atrial fibrillation (AF). However, the effects of Na+ channel blockers on the electrophysiologic properties of pulmonary veins (PVs) are not well characterized. The aim of the present study was to evaluate the effect of the pure Na+ channel blocker pilsicainide on the PVs. METHODS AND RESULTS: PV mapping using a basket catheter was performed in 28 patients with paroxysmal AF. Twenty-eight PVs, including 20 left superior and 8 right superior PVs, were studied. Programmed stimulation was performed in the distal PV and PV-left atrial (LA) junction before and after infusion of pilsicainide (1 mg/kg). Pilsicainide significantly prolonged the effective refractory period (ERP) of the distal PV from 163 +/- 44 msec to 192 +/- 53 msec (P < 0.001), PV-LA junction from 227 +/- 48 msec to 235 +/- 52 msec (P < 0.05), and LA appendage from 225 +/- 55 msec to 245 +/- 48 msec (P < 0.05). Pilsicainide significantly prolonged the conduction time from the distal PV to PV-LA junction from 45 +/- 14 msec to 70 +/- 26 msec (P < 0.0001). In 3 of 5 patients who experienced AF termination with pilsicainide, PV-LA conduction block was observed just before AF termination. CONCLUSIONS: Pilsicainide can modify ERP heterogeneity and conduction properties in the PV and at the PV-LA junction. Because the PV and PV-LA junction have important roles as substrates for AF maintenance, pilsicainide may terminate AF by pharmacologic PV isolation.
INTRODUCTION: Na+ channel blockers are used to treat atrial fibrillation (AF). However, the effects of Na+ channel blockers on the electrophysiologic properties of pulmonary veins (PVs) are not well characterized. The aim of the present study was to evaluate the effect of the pure Na+ channel blocker pilsicainide on the PVs. METHODS AND RESULTS: PV mapping using a basket catheter was performed in 28 patients with paroxysmal AF. Twenty-eight PVs, including 20 left superior and 8 right superior PVs, were studied. Programmed stimulation was performed in the distal PV and PV-left atrial (LA) junction before and after infusion of pilsicainide (1 mg/kg). Pilsicainide significantly prolonged the effective refractory period (ERP) of the distal PV from 163 +/- 44 msec to 192 +/- 53 msec (P < 0.001), PV-LA junction from 227 +/- 48 msec to 235 +/- 52 msec (P < 0.05), and LA appendage from 225 +/- 55 msec to 245 +/- 48 msec (P < 0.05). Pilsicainide significantly prolonged the conduction time from the distal PV to PV-LA junction from 45 +/- 14 msec to 70 +/- 26 msec (P < 0.0001). In 3 of 5 patients who experienced AF termination with pilsicainide, PV-LA conduction block was observed just before AF termination. CONCLUSIONS:Pilsicainide can modify ERP heterogeneity and conduction properties in the PV and at the PV-LA junction. Because the PV and PV-LA junction have important roles as substrates for AF maintenance, pilsicainide may terminate AF by pharmacologic PV isolation.