Atrial Fibrillation Begets Atrial Fibrillation

Abstract

Background-The mechanism(s) for acute changes in electrophysiological properties of the atria during rapid pacing induced atrial fibrillation (AF) is not completely understood. We sought to evaluate the contribution of the intrinsic cardiac autonomic nervous system in acute atrial electrical remodeling and AF induced by 6-hour rapid atrial pacing. Methods and Results-Continuous rapid pacing (1200 bpm, 2ϫ threshold [TH]) was performed at the left atrial appendage. Group 1 (nϭ7) underwent 6-hour pacing immediately followed by ganglionated plexi (GP) ablation; group 2 (nϭ7) underwent GP ablation immediately followed by 6-hour pacing; and group 3 (nϭ4) underwent administration of autonomic blockers, atropine (1 mg/kg), and propranolol (0.6 mg/kg) immediately followed by 6-hour pacing. The effective refractory period (ERP) and window of vulnerability (WOV, in milliseconds), ie, the difference between the longest and the shortest coupling interval of the premature stimulus that induced AF, were measured at 2ϫTH and 10ϫTH at the left atrium, right atrium, and pulmonary veins every hour before and after GP ablation or autonomic blockade. In group 1, ERP was markedly shortened in the first 2 hours and then stabilized both at 2ϫTH and 10ϫTH; however, WOV was progressively widened throughout the 6-hour period. After GP ablation, ERP was significantly longer than before ablation and AF could not be induced (WOVϭ0) at either 2ϫTH or 10ϫTH. In groups 2 and 3, rapid atrial pacing failed to shorten the ERP. AF could not be induced in 6 of 7 dogs in group 2 and all 4 dogs in group 3 during the 6-hour pacing period. Conclusion-The

EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication

“…495,496 Although AF can typically be reversed in its early stages, it becomes more difficult to eliminate over time due to such remodelling. 238,497 Dominant-frequency analysis points to an evolution of mechanisms in AF patients, with PV sources becoming less predominant as AF becomes more persistent and atrial remodelling progresses. 498 The data suggest that in patients with long-standing persistent AF, atrial remodelling augments the number of AF drivers and shifts their location away from the PV/ostial region.…”

Neuronal Na v 1.8 Channels as a Novel Therapeutic Target of Acute Atrial Fibrillation Prevention

“…RAP can shorten ERP and increase ERP dispersion and ΣWOV, which were all reversed after GP ablation. Implementing GP ablation or autonomic blockers (atropine or propranolol) followed by RAP can prevent induced spontaneous AF and atrial electrical remodeling 26, 27. In our study, administrating A‐803467 can effectively attenuate ERP shortening and suppress increased ERP dispersion and ΣWOV, indicating a pharmacological denervation effect by this selective Na v 1.8 blocker.…”

“…This could suggest that blocking Na v 1.8 could avoid functional substrate forming in PV myocardium, probably as a result of inhibiting GP function and atrial electrical remodeling. Although we could not deny the fact that sodium pentobarbital has been reported vagolytic and may increase the ERP value when applying,29, 30 the effect of A‐803467 on ERP in the present study is still established, since both groups were treated equally with the anesthetic to eliminate bias between groups, and the minimum dosage was used to reduce the possibility of unnecessary influence, as in our previously published studies 18, 26, 31, 32…”

Temporary Suppression of Cardiac Ganglionated Plexi Leads to Long‐Term Suppression of Atrial Fibrillation: Evidence of Early Autonomic Intervention to Break the Vicious Cycle of “AF Begets AF”

“…Lu et al found that either GP ablation or autonomic blockade reduced ERP dispersion and prevented ERP shortening and AF inducibility in a canine model of 6‐hour RAP, suggesting the presence of autonomic remodeling and its importance in facilitating atrial electrical remodeling in the acute stage 7. Direct neural recordings from the GP also revealed that as AF continued, the activity of the major LA GP increased progressively, which helped maintain short and dispersed ERPs to sustain AF.…”

“…In addition, autonomic remodeling plays an important role in the pathogenesis of AF. Several publications demonstrated that hyperactivity or imbalance of the cardiac autonomic nervous system (ANS) facilitates the initiation and maintenance of AF 4, 5, 6, 7, 8, 9, 10, 11. Hyperactivity of the cardiac ANS and AF also form a vicious cycle in which the former can initiate AF and the latter further enhance the activity of the cardiac ANS to perpetuate AF 7, 9…”