Methods for Determining the Refractory Period and Excitable Gap During Persistent Atrial Fibrillation in the Goat

Duytschaever, Mattias; Mast, F.; Killian, Matthijs; Blaauw, Yuri; Wijffels, Maurits C.E.F.; Allessie, Maurits A.

doi:10.1161/hc3401.093156

Cited by 43 publications

(56 citation statements)

References 30 publications

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“…Goats were instrumented as described previously. 9 Briefly, during general anesthesia, Teflon-felt plaques with multiple electrodes were sutured onto the free wall of each atrium, Bachmann's bundle, and the left ventricle. All leads were tunneled subcutaneously to the neck and exteriorized by four 30-pole connectors.…”

Section: Goat Model Of Atrial Fibrillationmentioning

confidence: 99%

“…RP AF was measured by slow, fixed-rate pacing (1 Hz), resulting in a series of single, randomly coupled, premature stimuli. 9 Local capture of AF was evidenced by radial spread of activation from the pacing site and a short delay between stimulus and response. For each coupling interval, the percentage of capture was determined.…”

Section: Electrophysiological Measurementsmentioning

confidence: 99%

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“Early” Class III Drugs for the Treatment of Atrial Fibrillation

et al. 2004

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Background-Currently available antiarrhythmic drugs are only moderately effective against atrial fibrillation (AF) and may cause ventricular proarrhythmia. AVE0118 is a blocker of atrium-specific early K ϩ currents (I Kur /I to ). Methods and Results-Effects of intravenous AVE0118 and dofetilide on atrial effective refractory period (AERP) and inducibility of AF were measured before and after 48-hours of AF-induced electrical remodeling in the goat. During persistent AF (53Ϯ19 days), the cardioversion efficacy and effects on atrial wavelength of AVE0118, dofetilide, and ibutilide were evaluated. QT durations were measured during atrial pacing and persistent AF. After 48 hours of AF, the effect of dofetilide on AERP was reduced, and induction of AF was not prevented. In contrast, the class III action of AVE0118 was enhanced, and AF inducibility decreased from 100% to 32% (PϽ0.001). At 1, 3, and 10 mg · kg Ϫ1 · h Ϫ1 , AVE0118 terminated persistent AF in 1 of 8, 3 of 8, and 5 of 8 goats, respectively. Dofetilide and ibutilide terminated AF in 1 of 5 and 2 of 7 goats. AVE0118 0.5, 1.5, and 5 mg/kg prolonged the AERP during AF and increased the fibrillation wavelength from 6.7Ϯ0.6 to 8.5Ϯ0.5, 9.7Ϯ0.5, and 11.2Ϯ0.9 cm (PϽ0.01). Whereas dofetilide and ibutilide prolonged QT duration, AVE0118 had no appreciable effect. Conclusions-AVE0118 markedly prolongs the AERP during AF without affecting QT duration. Cardioversion of AF was due to an Ϸ2-fold increase in fibrillation wavelength. Atrium-selective class III drugs like AVE0118 may be a promising new option for safe and effective cardioversion of AF.

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Section: Goat Model Of Atrial Fibrillationmentioning

confidence: 99%

Section: Electrophysiological Measurementsmentioning

confidence: 99%

“Early” Class III Drugs for the Treatment of Atrial Fibrillation

et al. 2004

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“…The use of a mapping technique to determine RP and EG was also introduced in a previous study. 8 CV was measured on the maps. Because the CV of the wavefront is greatly influenced by the curvature, 9 a plainly propagating wavefront was taken, and CV was measured in a peripheral lesion of the reentrant wavefronts that appear to be essential in maintaining AF.…”

Section: Electrophysiological Measurementsmentioning

confidence: 99%

Widening of the Excitable Gap and Enlargement of the Core of Reentry During Atrial Fibrillation With a Pure Sodium Channel Blocker in Canine Atria

et al. 2003

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Background-This study aimed to assess the effects of pilsicainide, a pure sodium channel blocker, on electrophysiological action and wavefront dynamics during atrial fibrillation (AF). Methods and Results-In a newly developed model of isolated, perfused, and superfused canine atria (nϭ12), the right and left endocardia were mapped simultaneously by use of a computerized mapping system. AF was induced with 1 to 5 mol/L acetylcholine. The antifibrillatory actions of pilsicainide on AF cycle length (AFCL), refractory period (RP), conduction velocity (CV), excitable gap (EG), and the core of the mother rotor were studied. The RP was defined as the shortest coupling interval that could capture the fibrillating atrium. The EG was estimated as the difference between the AFCL and RP. At baseline, multiple wavefronts were observed. After 2.5 g/mL infusion of pilsicainide, all preparations showed irregular activity, and AF was terminated in 2 preparations. The AFCL and RP were prolonged, and CV was decreased significantly. The EG was widened (147%; PϽ0.01), and the core perimeter was increased (100%; PϽ0.01). Increasing the dosage either terminated AF (6 preparations) or converted to organized activity (ie, atypical atrial flutter) (4 preparations). On the maps, all "unorganized" AFs were terminated with the excitation of the core of the mother rotor by an outside wavefront, whereas in preparations with atrial flutter, pilsicainide did not terminate its activity. Conclusions-Widening

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“…This generally slows down the resulting ventricular rate, which becomes irregularly irregular. The atrial cycle length also changes continuously and may not be the same between different atrial regions (Duytschaever et al, 2001). As electrophysiological remodeling of the atrial myocardium occurs early during AF, with changes in effective refractory period and excitability, the input signals arriving to the AV node may vary significantly.…”

Section: Activation Of the Atrioventricular Node In Atrial Fibrillationmentioning

confidence: 99%

Atrioventricular Conduction in Atrial Fibrillation: Pathophysiology and Clinical Implications

Róka¹

2012

Atrial Fibrillation - Basic Research and Clinical Applications

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Methods for Determining the Refractory Period and Excitable Gap During Persistent Atrial Fibrillation in the Goat

Cited by 43 publications

References 30 publications

“Early” Class III Drugs for the Treatment of Atrial Fibrillation

“Early” Class III Drugs for the Treatment of Atrial Fibrillation

Widening of the Excitable Gap and Enlargement of the Core of Reentry During Atrial Fibrillation With a Pure Sodium Channel Blocker in Canine Atria

Atrioventricular Conduction in Atrial Fibrillation: Pathophysiology and Clinical Implications

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