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. 2020 Nov;17(11):1976-1983.
doi: 10.1016/j.hrthm.2020.06.017. Epub 2020 Jun 22.

Reconsidering the multiple wavelet hypothesis of atrial fibrillation

Affiliations

Reconsidering the multiple wavelet hypothesis of atrial fibrillation

Seungyup Lee et al. Heart Rhythm. 2020 Nov.

Abstract

Background: Moe and Abildskov proposed the multiple wavelet hypothesis of atrial fibrillation (AF) on the basis of observations in the canine vagal nerve stimulation (VNS) AF model. Data from mapping studies in an in vitro canine AF model by Allessie et al (Allessie MA, Lammers WJEP, Bonke FIM, Hollen SJ. Experimental evaluation of Moe's multiple wavelet hypothesis of atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology and Arrhythmias. Orlando, FL: Grune & Stratton; 1985:265-275.) were used to evaluate the Moe/Abildskov hypothesis, which revealed that a critical number of wavelets sustained AF.

Objective: The purpose of this study was to reassess VNS mapping data using the same methods used by Allessie to evaluate Moe's multiple wavelet hypothesis.

Methods: Using the canine VNS AF model in 6 dogs, 510 unipolar atrial electrograms were recorded simultaneously from both atria. Activation sequence maps were produced from sustained AF during VNS in each dog. Per Allessie, consecutive 10 ms activation windows were analyzed over a period of 300 ms. Repetitive activation analysis was applied to Moe's canine VNS AF model.

Results: The number of wavefronts in each AF episode was 0-8 in Allessie's studies measured by sequential atrial mapping and 0-10 in our biatrial simultaneous mapping studies. In both studies, an electrically silent period was observed in each atrium and was reactivated by wavefronts emanating from focal sources. Allessie postulated that an electrically silent atrium was reactivated by a wavefront propagating from the other atrium. However, in our biatrial simultaneous mapping studies, each electrically silent atrium was reactivated by a distinct focal source.

Conclusion: Data from both studies showed a similar number of wavefronts, similar AF activation patterns, and periods of electrical atrial silence reactivated by focal sources. Also, in our studies, independent focal sources initiated wavefronts reactivating the atria, thereby explaining the mechanism maintaining AF.

Keywords: Focal source; Mapping; Mechanism of atrial fibrillation; Reentry; Vagal nerve stimulation.

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Conflict of interest statement

Conflict of interest: None

Figures

Figure 1.
Figure 1.
30 consecutive 10 ms activation window from only the RA by Allessie et al. (panel A), and both atria from our mapping data (panel B, Dog #1). Panel A: During windows 18 and 19, electrically silent periods were observed in the RA and were reactivated by wavefront emanating from focal activation (window 20). Panel B: During windows 13 and 14, electrically silent periods were observed in both atria, and were reactivated by wavefronts emanating from focal sources in the posterior LA and RA. LA, left atrium; RA, right atrium.
Figure 2.
Figure 2.
A representative example of the same episode (fig. 1B) of sustained AF due to focal sources of different CL. Panel A: Activation sequence map of four consecutive beats during AF in both atria. Panel B: Bipolar AEGs from selected sites a - f recorded simultaneously during AF from a focal QS activation (site b) and five nearby sites (a, c, d, e, and f). Selected AEGs are shown along with burst symbols and propagation arrows illustrating activation in panel A. Panel C: Selected bipolar AEGs along with each unipolar component (QS morphology) of the bipolar AEG from focal QS activation (site b). See text for discussion.
Figure 3.
Figure 3.
DF analysis of 4 seconds of data from the same episode (fig. 1B and fig. 2). DF analysis demonstrated that a group of adjacent sites with a single DF peak at 8 Hz was present in a portion of the LA, confirming the presence of an area of repetitive activation patterns, which corresponded to 1:1 atrial activation. DF, dominant frequency; LA, left atrium
Figure 4.
Figure 4.
Spontaneous termination of the episode from fig. 2 after stopping VNS. Panel A: The last five consecutive 80 ms windows of activation sequence during AF followed by sinus rhythm. Panel B: Bipolar AEG from the same focal QS site b in fig. 2, along with each unipolar component. When all wavefronts emanating from focal sources became extinguished and there was no further focal activation, there was an electrically silent period of 477 ms in both atria, followed by sinus rhythm. AEG, atrial electrograms; VNS, vagal nerve stimulation

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References

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