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Stabilization of intrinsic cardiac neuronal processing mitigates neurally induced atrial arrhythmias
Author(s) -
Richer Louis Philippe,
Ardell Jeffrey L.,
Vinet Alain,
Kus Teresa,
Cardinal René,
Vermeulen Michel,
Armour John Andrew
Publication year - 2008
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.22.1_supplement.1230.7
Subject(s) - medicine , atrial fibrillation , cardiology , anesthesia , spinal cord , hexamethonium , cardiac electrophysiology , tachycardia , neuromodulation , electrophysiology , stimulation , psychiatry
Our objective was to determine whether neuronally‐induced atrial arrhythmias can be suppressed by stabilizing the intrinsic cardiac nervous system. In anaesthetized dogs, trains of 5 electrical stimuli (1 mA; 1 ms) were delivered immediately after the P wave of the ECG to mediastinal nerves associated with the superior vena cava. Regional atrial electrical events were monitored with 191 right and left atrial epicardial unipolar electrodes. Mediastinal nerve sites that reproducibly initiated atrial arrhythmias were identified. These sites were re‐stimulated following hexamethonium (1 mg/kg, iv) blockade or pre‐emptive spinal cord stimulation (SCS: the dorsal aspect of the T1–T3 spinal cord was stimulated electrically at 50 Hz; 0.2 ms; 90% of motor threshold) with parameters sufficient to reduce intrinsic cardiac neuronal activity by 70% for up to 1 hour. Stimulating select mediastinal nerves sites consistently elicited atrial tachyarrhythmias (85% of which progressed to atrial fibrillation, AF) with dispersion of epicardial breakthrough sites. Either hexamethonium or pre‐emptive SCS reduced the incidence of mediastinal nerve‐induced AF (to 11% and 40%, respectively) while increasing pacemaker stability. We conclude that excessive and heterogeneous activation of the intrinsic cardiac nervous system results in atrial arrhythmias. The anti‐arrhythmic effects of stabilizing intrinsic cardiac neuronal processing, via either pharmacological or electrical neuromodulation, indicates a potential novel therapeutic approach to atrial arrhythmia suppression. Supported by the CIHR, the Québec Heart & Stroke Foundation and the NIH.