Reconsidering the multiple wavelet hypothesis of atrial fibrillation

被引:29
作者
Lee, Seungyup [1 ]
Khrestian, Celeen M. [1 ]
Sahadevan, Jayakumar [1 ,2 ]
Waldo, Albert L. [1 ,2 ]
机构
[1] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA
[2] Univ Hosp Cleveland, Div Cardiovasc Med, Med Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA
基金
美国国家卫生研究院;
关键词
Focal source; Mapping; Mechanism of atrial fibrillation; Reentry; Vagal nerve stimulation; PERSISTENT; ABLATION; MECHANISM;
D O I
10.1016/j.hrthm.2020.06.017
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:1976 / 1983
页数:8
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