Objective Investigating the long-term effect of ganglionated plexi (GP) ablation on atrial fibrillation (AF) after GP ablation.
Methods 13 dogs were randomly divided into sham-operated group and GP ablation group. All animals underwent a right thoracotomy at the 4th intercostal space. Induced AF and atrial effective refractory period (AERP) were measured by burst rapid pacing at right atrium. After anterior right GP and inferior right GP ablation, AF and AERP were measured again in the GP ablation group. The animals were allowed to recover for 8 weeks, after which, AF and AERP was measured again. The levels of atrial natriuretic peptide (ANP), TNF-a and interleukin (IL)-6 in blood and atrial tissues were examined. Immunocytochemical staining of cardiac nerves was performed in tissues from the dogs.
Results AF was easily induced in the GP ablation group after 8 weeks while AF was not observed in the sham-operated group, and immediately after GP ablation. AERP and dispersion of AERP (dAERP) were increased after GP ablation, while AERP recovered after 8 weeks. Compared with sham-operated group, the levels of ANP, TNF-a and IL-6 in the right atrium increased significantly 8 weeks after GP ablation (204.6±31.2 vs 299. 1±32. 5; 1.3±0.5 vs 4.7±0.7; 0.9±0.3 vs 1.8±0.5; p <0.05). In GP ablation group, the density of GAP43-positive, TH-positive and ChAT-positive nerves in the right atrium was 821±752, 481±627 and 629±644 per mm2, respectively, which was significantly (p<0.01) lower than the nerve density in sham-operated tissues (2590±841, 1752±605 and 3147±886 per mm2, respectively).
Conclusion Atrial substrate remodelling after GP ablation may be the mechanism of induced AF.
- Atrial fibrillation
- epicardial ganglionic plexi ablation
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