Triggered firing in pulmonary veins initiated by in vitro autonomic nerve stimulation

2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design

“…113 Other studies have shown that synergic actions of both the sympathetic and parasympathetic neurotransmitters promote rapid PV firing in an experimental system. 114 Another study demonstrated that stimulation of the right anterior GP converts isolated premature depolarization from the RSPV into AF-inducing premature depolarizations, 115 indicating a link between GP activity and AF inducibility. The authors proposed a model of a highly integrated atrial neural network in which a GP hyperactive state could release a gradient of locally excessive concentrations of neurotransmitters that initiate AF, whereas activation of the axons can “retrogradely” excite the GP at a distance to cause the release of neurotransmitters to induce AF.…”

“…125 Another issue is reinnervation of the ANS during follow-up. 108,114 Whether reinnervation causes recurrent AF postablation remains uncertain. One study has reported that reinnervation of the ANS in patients after RF ablation is not directly related to AF recurrence.…”

“…103,105,114,116,124,355,576,577,578,579,580,581,582 Because the GP are consistently located within areas of highly fractionated atrial potentials (FAPs), also referred to as CFAEs, 103,105,114,116,124,355,576,577,578,579,580,581,582,583,584 it is useful to begin with a fractionation map of the LA and PVs during AF. The LA FAPs are usually located in four areas: (1) LAA ridge FAP area (between LAA and left PVs); (2) superior left FAP area; (3) inferoposterior FAP area; and (4) anterior right FAP area (Figure 4).…”

Neural mechanisms of atrial fibrillation

“…Prior studies demonstrated that the cardiac ANS plays a critical role in the dynamics of AF initiation and maintenance. [2][3][4] Hyperactivity of the intrinsic cardiac ANS causes the release of excessive amount of acetylcholine and catecholamines and may lead to rapid firing from pulmonary veins (PVs) or non-PV sites. 4 Clinically, alterations of autonomic tone, involving the sympathetic and parasympathetic nervous systems, are implicated in initiating paroxysmal AF.…”

“…[2][3][4] Hyperactivity of the intrinsic cardiac ANS causes the release of excessive amount of acetylcholine and catecholamines and may lead to rapid firing from pulmonary veins (PVs) or non-PV sites. 4 Clinically, alterations of autonomic tone, involving the sympathetic and parasympathetic nervous systems, are implicated in initiating paroxysmal AF. 5 Tan et al 6 reported that sympathetic and parasympathetic nerves are located closely together within the human pulmonary veins (PVs).…”