Abstract 15820: Vagal Nerve Stimulation Modifies Intrinsic Cardiac Local Circuit Neurons in the Suppression of Atrial Arrhythmias
Background: Burst electrical stimuli delivered to intra-pericardial mediastinal nerves (MNS) reproducibly evoke atrial fibrillation (AF), an effect dependent upon heterogeneous activation of the intrinsic cardiac nervous system (ICNS). The objective of this study was to determine whether enhanced vagal inputs to subpopulations of intrinsic cardiac (IC) neurons alters MNS-induced neuronal imbalance within the ICNS thereby impacting the susceptibility to atrial fibrillation (AF).
Methods: Activity of multiple IC neurons within the right atrial ganglionated plexus was identified simultaneously in anesthetized canines using a 16-channel linear microelectrode array. Cardiac transducing IC neurons responding to: (1) cardiac touch; (2) occlusion of the inferior vena cava or thoracic aorta; versus (3) autonomic (stellate or vagal) stimulation were characterized and their activation during neurally induced atrial arrhythmias assessed in the absence or presence of pre-emptive vagal nerve stimulation (VNS; 15 Hz, 500 usec, 1.2x bradycardia threshold, for 3 min). AF was induced by burst electrical stimuli delivered to mediastinal nerves during the atrial refractory period.
Results: In response to mediastinal nerve stimulation, most IC neurons became excessively activated (0.28±0.07 baseline to 1.11±0.14 impulses/min during MNS, p<0.05); such network behavior preceding and persisting throughout AF. Chi-square analysis indicated that the sensitivity of IC neurons that responded to MNS was reflective of an increased responsiveness to cardiac afferent inputs (p<0.05). Conversely, IC responsiveness to either vagal or stellate ganglion inputs was similar when comparing MNS sensitive versus MNS insensitive neurons. MNS induced network imbalance in IC network interactions was suppressed by VNS therapy (0.15±0.09 baseline to 0.38±0.15 impulses/sec during MNS; p=0.18) concomitant with a reduction in the potential for MNS-induced AF induction (81% AF untreated; 31% AF post VNS).
Conclusion: Excessive, stochastic interconnectivity among IC local circuit neurons in the induction of AF can be obtunded by VNS resulting in the suppression of AF inducibility.
- Atrial arrhythmias
- Autonomic nervous system
- Reflexes, cardiovascular
- Systems physiology
- Arrhythmias, treatment of
- © 2013 by American Heart Association, Inc.