Spontaneous atrial fibrillation occurrence following transesophageal atrial burst pacing in rats

Animal models play a crucial role in elucidating the complex pathophysiology of atrial fibrillation (AF) and in identifying and testing novel antiarrhythmic strategies. We aimed to develop and characterize a new experimental rat model of AF, induced by long-term transesophageal atrial electrical stimulation, and to investigate whether the "AF begets AF" concept applies to small rodent hearts.

Twelve adult male Wistar rats were randomized into two groups: Sham (n = 5) and AF (n = 7). All rats were implanted at the beginning of the study with ECG radiotelemetry devices and underwent continuous ECG monitoring throughout the study. To induce AF, the rats in the AF group underwent atrial pacing for 10 consecutive days (15 successive cycles of stimulation/day, 20 s each, with a free interval of 5 min between cycles; 4,000 stimuli/min, stimulus duration 6 ms, voltage 3 V above the diastolic threshold). A similar procedure was applied to the Sham group, but without performing the actual electrical stimulation. The number and duration of spontaneous AF episodes were evaluated based on continuous ECG monitoring prior to, during, and for one week after transesophageal atrial pacing. The inducibility of AF and the occurrence and duration of spontaneous AF episodes were evaluated and compared between the two groups.

Atrial fibrillation was induced in 85.7% of the rats subjected to atrial electrical pacing (Figure, A), with an average global inducibility of 44.0% ± 16.9% and a mean AF duration of 123.2 ± 96.3 s. No induced or spontaneous AF episodes were recorded in any of the Sham animals. In the AF group, none of the animals presented spontaneous AF before transesophageal atrial pacing. However, in the AF rats, after atrial electrical stimulation initiation, the number of atrial premature beats significantly increased (21.3 ± 6.8 / 24-h post-stimulation vs. 7.3 ± 6.5 / 24-h at baseline; p< 0.01; Figure, B), and all rats presented spontaneous AF episodes (Figure, C). At the end of the study, AF rats presented a total number of 23.9 ± 2.3 AF episodes / 24-h (Figure, D), with a mean AF burden of 337.7 ± 25.06 s / 24-h.

Our data demonstrate that, despite the small size of the atria, the "AF begets AF" concept is applicable in small rodents. The study presents a novel rat model of AF, in which spontaneous AF occurs following long-term atrial electrical stimulation. Given that the model is relatively rapid and easy to implement, it provides a setup for further investigation of AF pathophysiology, and for identifying and testing novel therapeutic strategies for AF.Figure 1