Ganglionated plexi (GP) comprise the intrinsic cardiac autonomic 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]
There are intrinsic plexuses that form part of the autonomic nervous system (ANS), [4] the best known intrinsic plexus being the enteric nervous system. The GP are part of the cardiac intrinsic ANS. [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]
Ganglionated plexi (GP) comprise the intrinsic cardiac autonomic 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]
There are intrinsic plexuses that form part of the autonomic nervous system (ANS), [4] the best known intrinsic plexus being the enteric nervous system. The GP are part of the cardiac intrinsic ANS. [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]