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Intra-Atrial Conduction Delay Revealed by Multisite Incremental Atrial Pacing is an Independent Marker of Remodeling in Human Atrial Fibrillation

OBJECTIVES: This study sought to characterize direction-dependent and coupling interval–dependent changes in left atrial conduction and electrogram morphology in uniformly classified patients with paroxysmal atrial fibrillation (AF) and normal bipolar voltage mapping. BACKGROUND: Although AF classif...

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Detalles Bibliográficos
Autores principales: Williams, Steven E., Linton, Nick W.F., Harrison, James, Chubb, Henry, Whitaker, John, Gill, Jaswinder, Rinaldi, Christopher A., Razavi, Reza, Niederer, Steven, Wright, Matthew, O'Neill, Mark
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Inc 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5612260/
https://www.ncbi.nlm.nih.gov/pubmed/28966986
http://dx.doi.org/10.1016/j.jacep.2017.02.012
Descripción
Sumario:OBJECTIVES: This study sought to characterize direction-dependent and coupling interval–dependent changes in left atrial conduction and electrogram morphology in uniformly classified patients with paroxysmal atrial fibrillation (AF) and normal bipolar voltage mapping. BACKGROUND: Although AF classifications are based on arrhythmia duration, the clinical course, and treatment response vary between patients within these groups. Electrophysiological mechanisms responsible for this variability are incompletely described. METHODS: Intracardiac contact mapping during incremental atrial pacing was used to characterize atrial conduction, activation dispersion, and electrogram morphology in 15 consecutive paroxysmal AF patients undergoing first-time pulmonary vein isolation. Outcome measures were vulnerability to AF induction at electrophysiology study and 2-year follow-up for arrhythmia recurrence. RESULTS: Conduction delay showed a bimodal distribution, occurring at either long (high right atrium pacing: 326 ± 13 ms; coronary sinus pacing: 319 ± 16 ms) or short (high right atrium pacing: 275 ± 11 ms; coronary sinus pacing: 271 ± 11 ms) extrastimulus coupling intervals. Arrhythmia recurrence was found only in patients with conduction delay at long extrastimulus coupling intervals, and patients with inducible AF were characterized by increased activation dispersion (activation dispersion time: 168 ± 29 ms vs. 136 ± 11 ms). Electrogram voltage and duration varied throughout the left atrium, between patients, and with pacing site but were not correlated with AF vulnerability or arrhythmia recurrence. CONCLUSIONS: Within the single clinical entity of paroxysmal AF, incremental atrial pacing identified a spectrum of activation patterns correlating with AF vulnerability and arrhythmia recurrence. In contrast, electrogram morphology (characterized by electrogram voltage and duration) was highly variable and not associated with AF vulnerability or recurrence. An improved understanding of the electrical phenotype in AF could lead to improved mechanistic classifications.