Ganglionated plexi (GP) comprise the intrinsic cardiacautonomic nervous system composed of autonomic ganglia of the heart atrium and ventricles.[1] The GP are embedded in the epicardial fat pads, consisting of only a few neurons or as many as 400 neurons.[1] GP has been shown to be a contributor to atrial fibrillation, such that ablation of the GP has been a strategy for treatment of atrial fibrillation.[1] Addition of GP ablation to pulmonary vein isolation has not improved outcomes,[2] but possibly other methods of GP ablation would be more successful.[3]
In animal models, cardiac overload leads to change in the electrophysiological properties of these neurons, leading to the suggestion that such changes might be relevant to the pathophysiology of heart failure.[5]
In humans, the ganglia are mostly associated with the posterior or superior aspect of the atria.[6] The ganglia mediate at least some of the effects of vagal nerve stimulation on the sinoatrial node, although don't seem to mediate atrioventricular node conduction.[7]
^Smith, R. B. (January 1971). "The occurrence and location of intrinsic cardiac ganglia and nerve plexuses in the human neonate". The Anatomical Record. 169 (1): 33–40. doi:10.1002/ar.1091690104.
^Aksu, Tolga; Gopinathannair, Rakesh; Gupta, Dhiraj; Pauza, Dainius H. (June 2021). "Intrinsic cardiac autonomic nervous system: What do clinical electrophysiologists need to know about the "heart brain"?". Journal of Cardiovascular Electrophysiology. 32 (6): 1737–1747. doi:10.1111/jce.15058.