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Updated: Dec 17, 2025
Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Reconsidering the multiple wavelet hypothesis of atrial fibrillation
Seungyup Lee1, Celeen M Khrestian1, Jayakumar Sahadevan2
1Department of Medicine, Case Western Reserve University, Cleveland, Ohio.
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.
