Ganglionated plexi

Ganglionated plexi (GP) 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] Vagus nerve stimulation has been shown to inhibit the activity of the GP, possibly through Nav1.8.^[3]

GP are spatially close to the pulmonary veins, so pulmonary vein isolation necessarily affects the GP.^[4][5] 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] Pulsed field ablation has shown to be an AFib ablation strategy which effectively destroys the GP.^[6] 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.^[7]

There are intrinsic plexuses that form part of the autonomic nervous system (ANS),^[8] the best known intrinsic plexus being the enteric nervous system. The GP are part of the cardiac intrinsic ANS.^[9]

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.^[10]

In humans, the ganglia are mostly associated with the posterior or superior aspect of the atria.^[11] 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.^[12]