Effect of Flecainide and Ibutilide Alone and in Combination to Terminate and Prevent Recurrence of Atrial Fibrillation

Figures

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  Figure 1.. Effect of flecainide (1.5 µmol/L) and ibutilide (20 nmol/L) alone and in combination on atrial and ventricular action potential waveforms. Cycle length, 500 ms. The data were obtained from right atrial preparations with a rim of the right ventricle.

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  Figure 2.. Effect of flecainide (1.5 µmol/L) and ibutilide (20 nmol/L) alone and in combination on atrial and ventricular action potential duration (APD70 in atria and APD90 in ventricles), effective refractory period (ERP), and postrepolarization refractoriness (PRR). N=5 for each condition. Cycle length, 500 ms. The data were obtained from right atrial preparations with a rim of the right ventricle. *<0.05 vs control. **P<0.01 vs control.

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  Figure 3.. Effect of flecainide, ibutilide, and their combination on the atrial and ventricular diastolic threshold of excitation (DTE). N=5 per each condition. Cycle length, 500 ms. The data were obtained from right atrial preparations with a rim of the right ventricle. *<0.05 vs control.

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  Figure 4.. Prevention and termination of acetylcholine (ACh)-mediated atrial fibrillation (AF) by flecainide (1.5 µmol/L), ibutilide (20 nmol/L), and their combination. N=10 for control and n=5 for each tested drug and the drug combination. The data were obtained from right atrial preparations with a rim of the right ventricle.

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  Figure 5.. An example of self-terminating atrial fibrillation (AF) episodes preceding the induction of a nonself-terminated AF (lasting >1 h) in the presence of acetylcholine (0.5 µmol/L). All AFs were induced by a single premature stimulation. Shown is a pseudo-ECG recording. The data were obtained from right atrial preparations with a rim of the right ventricle.

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  Figure 6.. Drug-induced cardioversion of atrial fibrillation (AF) and its mechanism. A, A typical example of AF cardioversion by the flecainide and ibutilide combination. AF cardioversion was preceded by the conversion of AF to atrial tachycardia. B, Apparent prime mechanism of AF termination with flecainide and ibutilide combination: rate-dependent depression of excitability. The recordings were simultaneously obtained following the termination of AF (in the presence of acetylcholine [ACh]+flecainide+ibutilide). The data were obtained from right atrial preparations with a rim of the right ventricle. AP indicates action potential.

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  Figure 7.. Representative midmyocardial (M) cell and epicardial (Epi) action potentials and pseudo-ECG recordings simultaneously obtained from a left ventricular wedge preparation under control conditions, after ibutilide (50 nmol/L), and following the addition of flecainide (1.5 µmol/L) to the perfusate containing ibutilide. Cycle length, 2000 ms.

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  Figure 8.. Effect of ibutilide (50 nmol/L) following by the combination of ibutilide (50 nmol/L) and flecainide (1.5 µmol/L) on repolarization and electrocardiographic parameters in left ventricular wedge preparations. The symbols in each graph are individual data points, and the horizontal lines indicate the mean values. N=5 for each. Cycle length, 2000 ms. Epi indicates epicardial region APD90; and midmyocardial action potential duration (M APD90), M cell region APD90. *P<0.05 vs control and vs ibutilide. **P<0.05 vs ibutilide.