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Is the Atrial Neural Plexis A Therapeutic Target in Atrial Fibrillation?

Authors:

Eue-Keun Choi ,

Seoul National University Hospital, Seoul, KR
About Eue-Keun
M.D., Ph.D.
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Peng-Sheng Chen

Indiana University School of Medicine, Indianapolis, Indiana, US
About Peng-Sheng
M.D.
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Abstract

Circumferential pulmonary vein isolation is the mainstay of atrial fibrillation (AF) ablation, but alternative approaches and techniques have been developed to improve the outcomes. One of these additional ablation targets are ganglionated plexi of the intrinsic cardiac autonomic system that contain a variety of sympathetic and parasympathetic neurons that communicate with the extrinsic cardiac autonomic nervous system. The ganglionated plexi of the heart do not serve as a simple relay station but could modulate the autonomic interaction between the extrinsic and intrinsic cardiac autonomic system. Intrinsic cardiac autonomic nerve activity is an invariable trigger of paroxysmal atrial tachyarrhythmia, including atrial fibrillation. Although multiple studies have shown that ganglionated plexi play an important role in initiating atrial fibrillation, there is no consensus on a standardized protocol for selecting target sites and determining how ganglionated plexi ablation can best be accomplished. Recent clinical trials have demonstrated the feasibility and efficacy of ganglionated plexi ablation in addition to pulmonary vein isolation, but novel technologies and strategies are necessary to improve the current ablation techniques in managing patients with atrial fibrillation. This review focuses on the relationship between atrial ganglionated plexi and atrial fibrillation and the potential benefits and limitations of ganglionated plexi ablation in the management of atrial fibrillation.

How to Cite: 1. Choi E-K, Chen P-S. Is the Atrial Neural Plexis A Therapeutic Target in Atrial Fibrillation?. Methodist DeBakey Cardiovascular Journal. 2015;11(2):82-86. DOI: http://doi.org/10.14797/mdcj-11-2-82
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Published on 01 Apr 2015.
Peer Reviewed

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