Unravelling the Paradoxical Effects of Ganglia Ablation
In 1973, Lazzara et al1 described 2 clusters of nerve bodies called ganglionated plexi (GP) adjacent to the sinus node and AV junction; high-frequency electric stimulation, which did not excite the underlying atrium, induced heart rate or AV conduction slowing, respectively. We are indebted to Randall et al2 who spent the next several decades delineating the anatomy and physiology of the intrinsic cardiac autonomic nervous system consisting of GP located at several sites in the atria and ventricles. Carrying on the legacy of Dr Randall,2 Armour and Ardell3,4 produced numerous publications and books, providing a hierarchical construct of the neural innervation of the heart, starting at the nuclei and axonal fields in the brain (extrinsic autonomic nervous system) followed by the spinal cord (intrathoracic) ganglia and axons and their connections to the intrinsic cardiac autonomic system with its GP and their axons of passage. The last part of this interconnected chain (the atrial neural network) was delineated anatomically by Armour et al5 and Pauza et al6 and functionally by Hou et al.7
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The overall function of the intrinsic autonomic nervous system consisting of the GP and the atrial neural network was summarized by Ardell,8 “… the intrinsic cardiac nerve plexus (GP and neural network) acts as more than a simple relay station for extrinsic autonomic projections to the heart…modulating…extrinsic and local cardio-cardiac reflexes. The intrinsic cardiac nerve plexus contains a heterogeneous population of cell types, including parasympathetic and sympathetic efferent neurons as well as afferent neurons.” Furthermore, as pointed out by Ardell,8 these afferent neurons participate in reflex loops between and within the various levels of the extrinsic, intrathoracic, and intrinsic systems, yet each level when disconnected from the other would retain independent functionality.