Effect of different pacing protocols on the induction of atrial fibrillation in a transvenously paced sheep model

In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). Th is atrial electrical remodeling resulted in an increased vulnerability to a trial fibrillation (AF). These experimental findings formed the rationale f or a stringent pursuit of sinus rhythm in patients with AF, since this woul d prevent or reverse atrial remodeling. This study tested the hypothesis th at 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 w ere 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 on ly 29% in the burst-paced group (P < 0.05). However, there was no differenc e 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 c hanges 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 v ersus 216 +/- 5 in the burst-paced group (P < 0.05). In the continuously pa ced group, the right atrial area significantly increased from 2.5 +/- 0.1 c m(2) at baseline to 4.2 +/- 0.2 cm(2). In the burst-paced group there was n o significant atrial dilatation (from 2.6 +/- 0.2 to 2.8 +/- 0.1 cm(2)). In conclusion, limiting atrial arrhythmia burden slowed the development of su stained AF in this sheep model. This was not mediated by a decreased influe nce on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions.