Abstract Body: Background: Abnormal sinoatrial node (SAN) function results from etiologies such as ischemia, cardiomyopathy, congenital abnormalities, or autonomic dysfunction. These irregularities may result in SAN dysfunction (SND) causing bradycardia and cardiac insufficiency. Treatment involves correction of underlying etiologies and pacemaker implantation. A large animal SND model would enable broader investigation into arrhythmia mechanisms and alternative treatment modalities that are currently lacking.
Methods: Nine Yucatan miniswine (31±3 kg) received ablation of right atrial early activation sites to establish SND. Atria were electroanatomically mapped (Abbott EnSite Precision) during sinus rhythm to construct endocardial geometry and localize early activation sites. An irrigated Tacticath or non-irrigated Safire catheter was used for RF ablation to abolish SAN activity and establish SND. Pacemakers were implanted to monitor rhythm and provide 50 bpm backup VVI pacing.
Results: Normal sinus rates ranged from 60 to 150 bpm with normally distributed circadian variation. Ablation power was 30 to 65 W with temperature cutoff ≤60°C. Subjects underwent a mean of 30±4 ablations (total time: 1401±209 sec). Successful SAN ablation and formation of SND was confirmed by: sinus pauses/asystole (with retrograde P waves after junctional escape or paced beats), or tachy/brady syndrome (alternating fast/slow rates). Five subjects exhibited SND within two weeks post-ablation, with a slower ambulatory ventricular rate (86±19 bpm) compared to subjects in sinus rhythm (123±16 bpm). One subject was lost due to perforation and tamponade during ablation. Three subjects in sinus rhythm received repeat ablation procedures, with two achieving SND and one remaining in sinus rhythm. SND persisted for at least four months.
Conclusion: We established a long-term, porcine model of SND by ablation of SAN and right atrial early activation sites. SND presented as sinus asystole or tachy/brady syndrome and was achieved in 78% of subjects. This model serves as a valuable research tool for further investigations into SND-related arrhythmia mechanisms and for developing alternative treatments such as biological pacemaking.