Why the study?
Does cervical vagal trunk stimulation alter electrical conduction between the left superior pulmonary vein and left atria and increase atrial fibrillation inducibility in dogs?
Does cervical vagal trunk stimulation alter electrical conduction between the left superior pulmonary vein and left atria and increase atrial fibrillation inducibility in dogs?
Cervical vagal trunk stimulation in dogs increases ERP heterogeneity and alters conduction between the left superior pulmonary vein and left atrium, providing a substrate for atrial fibrillation initiation and maintenance.
Should not change clinical practice; leaves open vagal modulation of AF substrate in humans.
Objective: The effect of cervical vagal trunk stimulation on conduction between left superior pulmonary vein and left atria and atria fibrillation have not been systematically studied. We attempted to investigate the electrical conduction between LA and LSPV in dogs with cervical vagal trunk stimulation and evaluate the possible underline substrates for local reentry and initiation and maintenance of AF. Methods: 12 mongrel dogs (18-25 kg) underwent cervical vagal trunk stimulation at high-frequency (60 ms, 1-4V) to produce sinus arrest lasting >2 seconds,complete atrioventricular AV blocking or the sinus rate decreasing more than 50%. Left lateral thoracotomy was performed and the heart was exposed in a pericardial cradle. The HRA, LAA, PV-LAJ, LSPVm and LSPVd was locally stimulated (100 ms, 2-8V). ERP of HRA, LAA, PV-LAJ and within LSPV, ERP heterogeneity within LSPV and conduction between left superior pulmonary vein and left atria and atrial fibrillation inducing rate with vagal response was analyzed. Results: 1. During cervical vagal stimulation, the heart rate was reduced significantly from baseline 156±34 bpm to 75±34 bpm (p< 0.05, n=12), ERP of HRA, LAA, PV-LAJ, LSPVm and LSPVd sites was shortened locally in all animals, ERP hetero-geneity (COV-ERP ) was increased from baseline 3±3% to 30±13% (on average, p< 0.05; n=12) and inducibility of AF was increased from baseline 49.9% to 70.9% with S1S1stimulation (100 ms, 2-8V) and from baseline 3.7% to 43.5% with S1S2 (5 ms decremented stepwise S1S2 300/200 ms, 2-8V, n=12; 2. LA and PV potentials at LA, PV-LAJ, LSPVm and LSPVd was overlapped during sinus rate and separated remarkably by stimulating at distal part of LSPV (n=9); 3. Unidirectional and bi-directional conduction(n=9), bi-directional decremented conduction (n=6), delayed conduction from LSPVp to LSPVd (n=12) and slow conduction from stimulating signal to local tissue potential (n=9) before onset of AF were recorded by pacing from both LSPV and LA. Conclusion: Our study strongly suggested that fast ectopic beating, abnormal vagal nerve activation as well as remodeling conduction between left superior pulmonary vein and left atria might are the common underline substrates for local reentry and AF initiation and maintenance.
No takes yet. Share an insight, caveat, or question.
Song et al. (2008) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: