Autonomics and Atrial Fibrillation | Ten Points to Remember
- Stavrakis S, Nakagawa H, Po SS, Scherlag BJ, Lazzara R, Jackman WM.
- The Role of the Autonomic Ganglia in Atrial Fibrillation. JACC Clin Electrophysiol 2015;1:1-13.
The following are 10 points to remember about this state-of-the-art review article on the role of the autonomic ganglia in atrial fibrillation (AF):
- The intrinsic cardiac autonomic system (CANS) is comprised of clusters of autonomic ganglia (“ganglionated plexi”[GP]) that are located on the epicardial aspect of the heart.
- The extrinsic CANS, made up of ganglia in the central nervous system and their axons destined for the heart, modulates sinoatrial and atrioventricular nodal function through the GPs.
- The four left atrial GPs include the superior left (located outside the left superior pulmonary vein [PV] near the roof), anterior right (adjacent to the anterior aspect of the right superior PV), and inferior left and right (located at the inferoposterior left atrium, below the ostia of the left inferior and right inferior PVs, respectively).
- In experimental models, GP stimulation results in rapid firing from the PVs, initiating AF, and GP ablation prevents AF induction.
- Low-level vagal stimulation suppresses GP activity, implying that the extrinsic CANS exerts a tonic inhibitory effect on the GPs. This effect may be attenuated with aging, which helps to explain the development of AF in older individuals (“hyperactive GP” hypothesis).
- High frequency stimulation in the vicinity of the GPs yields bradycardia due to atrioventricular nodal block (“vagal response”). However, this response is not sensitive in identifying the location of a GP.
- Given location of the GPs, the standard PV isolation lesion set likely modifies GP function to some degree.
- The outcome of patients undergoing PV isolation for paroxysmal AF is enhanced when GPs are formally targeted during ablation.
- Whether complete/durable denervation is achieved with endocardial left atrial ablation is unknown.
- A preliminary study in humans suggested that low-level vagal stimulation (via the tragus) slowed AF, and abbreviated its duration. Whether noninvasive neuromodulation has a durable effect in patients with AF is unknown.
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