Ganglionated plexi (GP, also called Ganlionic plexi) comprise the intrinsic cardiac autonomic nervous system composed of autonomic ganglia of the heart atrium and ventricles. [1] Cholinergic neurons throughout the GPs project to all areas of the heart, [2] The GP are embedded in the epicardial fat pads, consisting of only a few neurons or as many as 400 neurons. [1]
Post ganglionic neurons from the vagal nerve pathways are components of the Ligament of Marshall, forming part of the "intrinsic" heart nervous system. [3] Vagus nerve stimulation has been shown to inhibit the activity of the GP, possibly through nerves that express Nav1.8 (a sodium channel subtype that is necessary for action potentials in these nerves), [4] but combining GP ablation with pulonary vein isolation may be a superior option. [5]
GP are spatially close to the pulmonary veins, so pulmonary vein isolation necessarily affects the GP. [6] [7] GP has been shown to be a contributor to atrial fibrillation (AFib), such that ablation of the GP has been a strategy for treatment of AFib. [1] GP ablation alone has been shown to eliminate AFib in approximately three-quarter of AFib patients. [1]
Ligation of the left atrial appendage may reduce AFib by alteration of the GP. [8]
There are intrinsic plexi that form part of the autonomic nervous system (ANS), [9] the best known intrinsic plexus being the enteric nervous system. The GP are part of the cardiac intrinsic ANS. [10]
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. [11]
In humans, the ganglia are mostly associated with the posterior or superior aspect of the atria. [12] 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. [13]