title: Effect of different pacing protocols on the induction of atrial fibrillation in a transvenously paced sheep model.
abstract: In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). This atrial electrical remodeling resulted in an increased vulnerability to atrial fibrillation (AF). These experimental findings formed the rationale for a stringent pursuit of sinus rhythm in patients with AF, since this would prevent or reverse atrial remodeling. This study tested the hypothesis that a reduction of arrhythmia burden would lead to a decreased vulnerability for AF. Different rapid atrial pacing protocols in a sheep model were used. During 15 weeks, 13 animals were continuously rapid paced and 7 animals were intermittently burst-paced, resulting in rapid atrial activation during 100% versus 33 +/- 4% of the time, respectively. In the continuously paced group, 77% of the animals developed sustained AF (i.e., > 1 hour) versus only 29% in the burst-paced group (P < 0.05). However, there was no difference in mean AERP shortening over time, nor maximal AERP shortening per animal, between both protocols. Minimal AERP was 103 +/- 5 ms in the continuously paced group and 107 +/- 5 in the burst-paced group (P = NS). Significant changes could be identified in effect on P wave duration, AVN function, and atrial dilation. Conduction slowing was more pronounced in the continuously paced group with a maximal P wave duration of 136 +/- 4 ms in this group versus 116 +/- 5 in the burst-paced group (P < 0.05). In the continuously paced group, the right atrial area significantly increased from 2.5 +/- 0.1 cm2 at baseline to 4.2 +/- 0.2 cm2. In the burst-paced group there was no significant atrial dilatation (from 2.6 +/- 0.1 to 2.8 +/- 0.1 cm2). In conclusion, limiting atrial arrhythmia burden slowed the development of sustained AF in this sheep model. This was not mediated by a decreased influence on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions.
authors.affiliation: Department of Cardiology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium.
authors.forename: R
authors.initials: R
authors.lastname: Willems
authors.forename: H
authors.initials: H
authors.lastname: Ector
authors.forename: P
authors.initials: P
authors.lastname: Holemans
authors.forename: F
authors.initials: F
authors.lastname: Van De Werf
authors.forename: H
authors.initials: H
authors.lastname: Heidbüchel
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D001281:Atrial Fibrillation / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004594:Electrophysiology; D005260:Female; D006439:Hemodynamics; D012756:Sheep; D014680:Veins