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] 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.
[1] Ligation of the left atrial appendage may reduce AFib by alteration of the GP.
[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.