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Curr Opin Cardiol. 2006 Jan;21(1):51-4.

The intrinsic cardiac nervous system and atrial fibrillation.

Author information

1
Cardiac Arrhythmia Research Institute, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA. benjamin-scherlag@ouhsc.edu

Abstract

PURPOSE OF REVIEW:

Radiofrequency ablation techniques to cure cardiac arrhythmias have focused on destroying myocardial tissue involved in abnormal excitation or conduction. This review will address recent basic and clinical studies which suggest that targeting autonomic nerves and ganglia on the large vessels and the heart, within the pericardium, can result in cardiac arrhythmia suppression with little, if any, damage to healthy myocardium.

RECENT FINDINGS:

Basic reports have shown that electrical stimulation of autonomic nerves on the heart itself can facilitate the induction of atrial fibrillation. The initial investigations found that the lowest threshold for inducing atrial fibrillation was at the entrances of the pulmonary veins. Moreover, beta-blockade blunted this response whereas atropine abolished atrial fibrillation inducibility. Subsequent studies found that ganglionated plexi clustered at the pulmonary vein entrances (within fat pads) could be stimulated without atrial excitation. Now, premature beats induced in the pulmonary veins could be converted to atrial fibrillation with a significantly greater propensity than without ganglionated plexi stimulation. Furthermore, ablation of these ganglionated plexi abolished atrial fibrillation inducibility. Clinical studies have been forthcoming clearly implicating these intrinsic cardiac ganglia in clinical atrial fibrillation.

SUMMARY:

Previous ablation procedures have focused on destroying myocardial sites that participated in the initiation and perpetuation of various tachyarrhythmias. New basic and clinical findings may allow targeting autonomic elements at a few specific sites on the heart that are directly related to arrhythmia formation, thereby reducing extensive damage to healthy myocardium.

PMID:
16355030
[Indexed for MEDLINE]

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