Frequency-Dependent Breakdown of Wave Propagation Into Fibrillatory Conduction Across the Pectinate Muscle Network in the Isolated Sheep Right Atrium

O. Berenfeld, A. Zaitsev, S. Mironov, A. Pertsov, J. Jalife
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引用次数: 204

Abstract

Atrial fibrillation (AF) may result from stationary reentry in the left atrium (LA), with fibrillatory conduction toward the right atrium (RA). We hypothesize that periodic input to the RA at an exceedingly high frequency results in disorganized wave propagation, compatible with fibrillatory conduction. Simultaneous endocardial and epicardial optical mapping (di-4-ANEPPS) was performed in isolated, coronary-perfused sheep RA. Rhythmic pacing of Bachmann’s bundle allowed well-controlled and realistic conditions for LA-driven RA. Pacing at increasingly higher frequencies (2.0 to 6.0 Hz) led to increasing delays in activation distal to major branching sites of the crista terminalis and pectinate bundles, culminating in spatially distributed intermittent blockade at or above ≈6.5 Hz. At this “breakdown frequency,” the direction of RA propagation became completely variable from beat to beat and thus transformed into fibrillatory conduction. Such frequency-dependent changes were independent of action potential duration. Rather, the spatial boundaries between proximal and distal frequencies correlated well with branch sites of the pectinate musculature. Thus, there exists a breakdown frequency in the sheep RA below which activity is periodic throughout the atrium and above which it is fibrillation-like. The data are consistent with the ideas that during AF, high-frequency activation initiated in the LA undergoes fibrillatory conduction toward the RA, and that sink-to-source effect at branch points of the crista terminalis and pectinate muscles is important in determining the complexity of the arrhythmia.
在离体绵羊右心房中,波传播进入纤维性传导的频率依赖性击穿
心房颤动(AF)可能是由左心房静止再入(LA)引起的,心房颤动向右心房传导(RA)。我们假设,以极高的频率周期性输入RA导致无组织波传播,与纤颤传导兼容。在离体、冠状动脉灌注的绵羊RA中同时进行心内膜和心外膜光学测图(di-4-ANEPPS)。巴赫曼的束有节奏的起搏允许很好地控制和现实的条件为la驱动的RA。频率越来越高(2.0 ~ 6.0 Hz)的起搏导致终端嵴和果突束远端主要分支部位的激活延迟增加,最终在≈6.5 Hz或更高频率时出现空间分布的间歇性阻断。在这个“击穿频率”下,RA的传播方向在每一次搏动之间变得完全可变,从而转化为纤颤传导。这种频率依赖性变化与动作电位持续时间无关。相反,近端和远端频率之间的空间边界与果突肌肉组织的分支位置密切相关。因此,绵羊类风湿性关节炎存在一个击穿频率,低于该频率,整个心房的活动是周期性的,高于该频率,则呈纤颤样。这些数据与以下观点一致:在房颤期间,LA启动的高频激活向RA进行纤颤传导,终端嵴和突起肌分支点的汇源效应是决定心律失常复杂性的重要因素。
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