Abstract
Atrial fibrillation (AF) is the most common type of cardiac arrhythmia and is associated with significant morbidity and mortality. The autonomic nervous system (ANS) plays an important role in the initiation and development of AF, causing alterations in atrial structure and electrophysiological defects. The intrinsic ANS of the heart consists of multiple ganglionated plexi (GP), commonly nestled in epicardial fat pads. These GPs contain both parasympathetic and sympathetic afferent and efferent neuronal circuits that control the electrophysiological properties of the myocardium. Pulmonary vein isolation and other cardiac catheter ablation targets including GP ablation can disrupt the fibers connecting GPs or directly damage the GPs, mediating the benefits of the ablation procedure. Ablation of GPs has been evaluated over the past decade as an adjunctive procedure for the treatment of patients suffering from AF. The success rate of GP ablation is strongly associated with specific ablation sites, surgical techniques, localization techniques, method of access and the incorporation of additional interventions. In this review, we present the current data on the clinical utility of GP ablation and its significance in AF elimination and the restoration of normal sinus rhythm in humans.
Highlights
Atrial Fibrillation presents clinically as chaotic electrical excitation that is detrimental to normal atrial contractility [1]
There appears to be an essential role for the right anterior ganglionated plexi (GP) which inhibits positive vagal responses and increases heart rate during pulmonary vein isolation (PVI) [90]. These findings demonstrate the importance of GP ablation of specific sites between the PVs and interatrial groove when targeting Atrial fibrillation (AF)
The ablation of GPs appears to be an efficacious technique for improving outcomes of patients with paroxysmal, persistent and long-standing persistent forms of AF
Summary
Atrial Fibrillation presents clinically as chaotic electrical excitation that is detrimental to normal atrial contractility [1]. The VOM extends from the coronary sinus, between the left PVs and left atrial appendage, traverses between the base of the left superior PV and pulmonary artery before attaching to the pericardium superiorly [67,68] In this general region the VOM, myocardial sleeve and autonomic ganglia are found, with the ganglia located in a fat pad between the left PVs and left atrial appendage [67,68,69] Studies have shown that the LOM may act as a conduit of sympathetic innervation between the ventricles and the left superior ganglia [67]. Previous studies have shown this GP to shorten the effective refractory period and increase the window of vulnerability to arrhythmias at all atrial and PV sites influenced by stimulation of the vagal trunk [73]. R + L PV isolation, lesion of LA isthmus, resection of LAA + connecting lesion of appendage base with LSPV
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