Department of Medicine, Case Western Reserve University, Cleveland, Ohio.
Department of Medicine, Case Western Reserve University, Cleveland, Ohio; Division of Cardiovascular Medicine, University Hospitals Cleveland Medical Center, Cleveland, Ohio.
Heart Rhythm. 2020 Nov;17(11):1976-1983. doi: 10.1016/j.hrthm.2020.06.017. Epub 2020 Jun 22.
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.
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.
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.
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.
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.
Moe 和 Abildskov 在犬类迷走神经刺激（VNS）房颤（AF）模型的观察基础上提出了房颤的多子波假说。Allessie 等人在犬类体外 AF 模型的映射研究中的数据（Allessie MA、Lammers WJEP、Bonke FIM、Hollen SJ. 对房颤的 Moe 多子波假说的实验评估。在：Zipes DP、Jalife J，eds. 心脏电生理学和心律失常。奥兰多，FL：Grune & Stratton；1985:265-275.）被用于评估 Moe/Abildskov 假说，该假说表明维持 AF 需要一定数量的子波。
本研究旨在使用 Allessie 评估 Moe 多子波假说所使用的相同方法重新评估 VNS 映射数据。
在 6 只犬的 VNS AF 模型中，同时从左右心房记录 510 个单极心房电图。在每只犬的 VNS 期间记录持续 AF 的激活序列图。按照 Allessie 的方法，对连续 10 ms 的激活窗口进行 300 ms 的分析。重复性激活分析应用于 Moe 的犬 VNS AF 模型。
Allessie 的研究中，通过顺序心房映射测量，每个 AF 发作中的子波数为 0-8，而我们的双心房同时映射研究中的子波数为 0-10。在两项研究中，每个心房都观察到一个电静止期，并由起源于局灶源的子波重新激活。Allessie 假设电静止的心房是由来自另一个心房的子波传播激活的。然而，在我们的双心房同时映射研究中，每个电静止的心房都是由一个独特的局灶源重新激活的。
两项研究的数据都显示了相似的子波数、相似的 AF 激活模式以及由局灶源重新激活的电静止心房的时期。此外，在我们的研究中，独立的局灶源启动子波，重新激活心房，从而解释了维持 AF 的机制。
