Electrophysiological effects of flecainide andsotalol in the human atrium during persistentatrial fibrillation

Aims Atrial fibrillation (AF) shortens the atrial action potentialand the atrial refractory period. These changes promote persistence of AF.Pharmacological prolongation of atrial action potential duration (APD) maytherefore help to prevent recurrent AF. In addition to prolonging APD,sodium channel blockers may prevent AF by inducing post–repolarizationrefractoriness (PRR). We studied whether two antiarrhythmic drugs (sotalol,flecainide) prolong APD or induce PRR in the fibrillating human atrium. Methods In 12 patients with persistent AF (11 male, 58 ± 5 yrs, 27 ± 7 monthsduration of AF), we recorded monophasic action potentials from the rightatrial appendage and inferior right atrium at baseline and 15 minutes afterintravenous administration of sotalol (1.5 mg/kg) or flecainide (2 mg/kg).APD and effective refractory periods (ERP) were determined. Results Bothdrugs prolonged APD90 during AF (flecainide from 109 ± 7 ms to 137 ± 10ms, sotalol from 108 ± 6 ms to 131 ± 8 ms, both p < 0.05 vs. baseline). Sotalolprolonged ERP in parallel to APD (from 119 ± 8 ms to 139 ± 8 ms, p < 0.05).Flecainide induced PRR by prolonging ERP more than APD90 (from 134 ± 9ms to 197 ± 28 ms, p < 0.05 vs. baseline and vs. sotalol). Conclusions Flecainideand sotalol prolong the atrial action potential during atrial fibrillationin humans. In addition, flecainide induces atrial PRR. These electrophysiologicaleffects may reduce AF recurrences and prevent their persistence.Drs. Kirchhof, Engelen and Breithardt areMembers of the Kompetenznetz Vorhofflimmern