Neural substrate of posterior left atrium: A novel modulation for inducibility and remodeling of atrial fibrillation in canine.

ABSTRACT:

Background

The neural mechanism of posterior left atrium (PLA) for genesis of atrial fibrillation has not been completely elucidated. We sought to assess the contribution of PLA denervation on atrial fibrillation (AF) inducibility and atrial remodeling.

Methods and results

After left thoracotomy in anesthetized dogs (n = 32), electrode catheters were attached to the PLA, left atrial roof, left pulmonary vein and left atrial appendage. Experiment 1 (n = 16): Vagal stimulation (VS group, n = 8) led to more pronounced ERP shortening in PLA than in other sites (CTL:71±7 ms vs VS: 52±6 ms, P<0.05;). Compared with control group (CTL group, n = 8), atropine alone or with propranolol applied to PLA greatly inhibited VS-induced ERP shortening, ERP dispersion increase, and AF inducibility in the left atrium (P<0.05); but ERP was not significantly different between atropine alone and DB conditions (Atro:85±8 ms vs DB:90±9ms, P>0.05). In addition, domain frequency (DF) of VS-induced AF waveform was not affected by atropine alone, while selective double autonomic blockade at PLA significantly decreased DF at all sites (P<0.05). Experiment 2 (n = 16): In group 1 (n = 8), ERP was markedly shortened in the first 2 hours (11-19% decrease) and then stabilized; however, WOV was progressively widened throughout the 6 hours rapid atrial pacing (BS: 51±9ms vs 6th hour: 161±30ms, P<0.05). After drug application, ERP was increased in all sites of atria, the ERP dispersion was significantly decreased (Atro: 2.36±0.02 vs 6th hour: 5.09±0.07, P<0.05) and AF could be induced in only 1 of 8 dogs. In group 2 (n = 8), 6 hours rapid atrial pacing failed to shorten the ERP and increased ERP dispersion, and only 2 episodes of AF could be induced (WOV = 0).

Conclusion

Local denervation of PLA, as predominant atrial autonomic profile, greatly inhibits AF inducibility and atrial remodeling.

SUBMITTER: Qin M 

PROVIDER: S-EPMC5419517 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature