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Spinal cord stimulation (SCS) stabilizes intrinsic cardiac neurons to reduce neurally induced atrial fibrillation
Author(s) -
Gibbons David D.,
Richer LouisPhilippe,
Southerland E. Marie,
Vinet Alain,
Kus Teresa,
Armour J. Andrew,
Ardell Jeffrey L.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.789.4
Subject(s) - medicine , stimulation , atrial fibrillation , cardiology , refractory period , neuromodulation , anesthesia , sinus rhythm , spinal cord , atrial flutter , tachycardia , psychiatry
Objective To determine the contribution of discrete neuronal inputs to the intrinsic cardiac nervous system for targeted reduction of the atrial arrhythmogenic substrate. Methods In 15 anesthetized dogs, trains of electrical stimuli (1 mA, 1ms) were delivered during the atrial refractory period to mediastinal nerves associated with the superior vena cava to induce atrial tachyarrhythmias. Neuronal activity was recorded in the right atrial ganglionated plexus (RAGP). For SCS, the dorsal aspect of the T 1 ‐T 3 spinal cord was stimulated electrically (50 Hz; 0.2 ms; 90% of motor threshold). Results Mediastinal nerve stimulation caused an abrupt increase in RAGP neuronal activity (~5 fold) that was maintained for the duration of transient neurally‐induced atrial fibrillation. SCS reduced basal neuronal activity and mitigated any mediastinal nerve‐induced increases in RAGP neuronal activity. Prior to SCS, mediastinal nerve stimulation evoked atrial fibrillation/atrial flutter (AF/Afl) from 95% of sites. After SCS, atrial rhythms induced by mediastinal nerve stimulation were 38% AF/Afl, 56% bradycardia/sinus rhythm, and 6% sinus tachycardia. SCS likewise reduced dispersion in early pacemaker breakthrough loci secondary to mediastinal nerve stimulation. Conclusions Neuromodulation with dorsal cranial thoracic SCS stabilizes elements within the intrinsic cardiac nervous system to reduce the atrial arrhythmogenic substrate to its excessive neural inputs. (Supported by HL71830)