title: Transmural conduction is the predominant mechanism of breakthrough during atrial fibrillation: evidence from simultaneous endo-epicardial high-density activation mapping.
abstract: BACKGROUND
  Endo-epicardial dissociation (EED) of electric activations resulting in transmural conduction of fibrillation waves (breakthroughs) has been postulated to contribute to the complexity of the substrate of atrial fibrillation (AF). The aim of this study was to elucidate the correlation between EED and incidence of breakthrough and to test the plausibility of transmural conduction versus ectopic focal discharges as sources of breakthrough.
  
  
  RESULTS
  We analyzed high-resolution simultaneous endo-epicardial in vivo mapping data recorded in left atrial free walls of goats with acute AF, 3 weeks and 6 months of AF (all n=7). Waves were analyzed for number, size, and width and categorized according to their origin outside (peripheral wave) or within the mapping area (breakthrough). Breakthrough incidence was lowest (2.1±1.0%) in acute AF, higher (11.4±6.1%) after 3 weeks (P<0.01 versus acute AF) and highest (14.2±3.8%) after 6 months AF (P<0.001 versus acute AF) and similar in the epicardium and endocardium. Most of the breakthroughs (86%; n=564) could be explained by transmural conduction, whereas only 13% (n=85) could be explained by ectopic focal discharges. Transmural microreentry did not play a role as source of breakthrough.
  
  
  CONCLUSIONS
  This is the first study to present simultaneous endo-epicardial in vivo mapping data at sites of breakthrough events. Breakthrough incidence and degree of EED increased with increasing AF substrate complexity. In goat left atrial free walls, most of the breakthroughs can be explained by transmural conduction, whereas ectopic focal discharges play a limited role as source of breakthrough.
authors.affiliation: Department of Physiology, University Maastricht, Maastricht, The Netherlands.
authors.forename: Jens
authors.initials: J
authors.lastname: Eckstein
authors.forename: Stef
authors.initials: S
authors.lastname: Zeemering
authors.forename: Dominik
authors.initials: D
authors.lastname: Linz
authors.forename: Bart
authors.initials: B
authors.lastname: Maesen
authors.forename: Sander
authors.initials: S
authors.lastname: Verheule
authors.forename: Arne
authors.initials: A
authors.lastname: van Hunnik
authors.forename: Harry
authors.initials: H
authors.lastname: Crijns
authors.forename: Maurits A
authors.initials: MA
authors.lastname: Allessie
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schotten
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004699:Endocardium / Q000503:physiopathology; D056149:Epicardial Mapping / Q000379:methods*; D006041:Goats; D006325:Heart Atria / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*