Endocardial stimulation of efferent parasympathetic nerves to the atrioventricular node in humans: Optimal stimulation sites and the effects of digoxin

Citation
Kj. Quan et al., Endocardial stimulation of efferent parasympathetic nerves to the atrioventricular node in humans: Optimal stimulation sites and the effects of digoxin, J INTERV C, 5(2), 2001, pp. 145-152
Citations number
25
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF INTERVENTIONAL CARDIAC ELECTROPHYSIOLOGY
ISSN journal
1383875X → ACNP
Volume
5
Issue
2
Year of publication
2001
Pages
145 - 152
Database
ISI
SICI code
1383-875X(2001)5:2<145:ESOEPN>2.0.ZU;2-I
Abstract
The purposes of this study were to identify optimal sites of stimulation of efferent parasympathetic nerve fibers to the human atrioventricular node v ia an endocardial catheter and to investigate the interaction between digox in and vagal activation at the end organ. Methods: The ventricular rate was measured during atrial fibrillation, prio r to and during parasympathetic nerve stimulation, in 8 patients taking dig oxin and in 10 controls. High frequency electrical stimuli were delivered v ia an hexapolar or quadripolar electrode catheter, placed at the posterosep tal right atrium near the atrioventricular node (n = 18 patients) or in the coronary sinus (n = 12 of 18 patients). In 4 patients, stimulation was rep eated after intravenous administration of 1 to 2 mg of atropine. Results: Nerve stimulation prolonged the R-R interval in all patients. Stim ulation close to the posteroseptal right atrium led to maximal atrioventric ular nodal slowing. The mean R-R intervals at baseline and during parasympa thetic nerve stimulation (60 mA) from the posteroseptal right atrium and th e proximal coronary sinus were 581 +/- 79 ms, 2440 +/- 466, and 900 +/- 228 ms respectively (p = 0.0001). The response to nerve stimulation was greate r in patients taking digoxin than in patients not taking the drug (p=0.02). Junctional rhythm occurred during nerve stimulation in 8/8 patients taking digoxin and 0/10 not taking the drug (p = 0.0001). The response to stimula tion was eliminated after atropine (p = 0.01). Conclusions: Parasympathetic nerves to the atrioventricular node were stimu lated from the proximal coronary sinus as well as the posteroseptal right a trium. Stimulation at the posteroseptal right atrium resulted in the greate st response, and digoxin enhanced this response. The augmented response sug gests that an interaction may exist between parasympathetic stimulation and digoxin at the end organ.