Abstract

Complex fractionated atrial electrograms (CFEs) have been described as a target during atrial fibrillation (AF) ablation, however, the mechanism leading to CFEs is poorly understood. We used noncontact mapping in a canine model of AF to determine the activation patterns in areas characterized by CFEs. Sustained AF was induced in 5 canines with 12 weeks of atrial tachy-pacing. A noncontact Multielctrode Array (MEA) was deployed in the left atrium (LA) and a contact bipolar CFE map was constructed. Areas of CFE were outlined on the map, and the MEA was then used to reconstruct wavefront propagation through CFE areas during 3 separate recording segments for each CFE site. There were 18 CFE regions identified (3.8/dog) and 54 noncontact CFE activation sequences studied. Activation patterns during the three recoding segments over time were consistent in 11/18 CFE regions (61%). The CFE regions were stereotypically located at the PV/LA junctions and the LA roof. Thirty-five CFE regions were characterized by wavefront collision, usually between circulating LA wavefronts and entry/exit from the PVs. Thirteen CFE regions were noted to be the central functional barrier of a rotor (Figure ) or partial rotor. Five regions were characterized by repeated conduction through a central isthmus with wavebreak. In this pacing-induced AF model, common causes of CFEs include collision between circulating LA wavefronts conduction through channels of functional block, the central vortex of a circulating rotor. The vast majority of these CFE regions were caused by heterogeneous anatomy and areas of functional block rather than true “drivers” of AF.

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