title: Mechanism of spontaneous termination of functional reentry in isolated canine right atrium. Evidence for the presence of an excitable but nonexcited core.
abstract: BACKGROUND
  According to the spiral wave hypothesis of reentry, the core of functional reentry remains excitable but not excited. We sought to determine whether the core remains excitable and whether excitation of the core by an outside wave front leads to termination of the reentry in the atrium.
  
  
  RESULTS
  In nine isolated canine right endocardial atrial tissues (3.8 by 3.2 cm wide), reentry was induced by a premature point stimulus (S2). The isochronal activation maps and dynamics of the activation patterns were visualized with the use of 509 bipolar electrodes (1.6-mm resolution). The S2 applied after 8 regular beats induced reentry with a mean cycle length of 162 +/- 20 ms (15 episodes). Reentry had a large excitable gap (93 +/- 26 ms) as determined by early capture with twice the level of threshold stimuli. The central area (core) around which the wave fronts rotated had a mean surface area of 12 +/- 3 mm2. The electrograms located in the core of the reentry registered no or very low amplitude potentials. In 13 of 15 episodes, reentry terminated when an outside new wave front merged with the original wave front and excited the core. Core excitation caused disruption of the original wave front, and the newly formed wave front(s) vanished at the tissue border within 77 +/- 18 ms. In 2 episodes, reentry terminated abruptly when an outside new wave front propagating in a direction opposite to the reentrant wave front collided with the leading edge of the reentrant wave front.
  
  
  CONCLUSIONS
  Functional reentry in the atrium is compatible with a spiral wave of excitation with an excitable but nonexcited core and a large excitable gap. Reentry may be terminated either by direct excitation of the core that displaces the wave front to the tissue border or by collision with an outside new wave front.
authors.affiliation: Department of Medicine, UCLA School of Medicine, USA.
authors.forename: T
authors.initials: T
authors.lastname: Ikeda
authors.forename: T
authors.initials: T
authors.lastname: Uchida
authors.forename: D
authors.initials: D
authors.lastname: Hough
authors.forename: J J
authors.initials: JJ
authors.lastname: Lee
authors.forename: M C
authors.initials: MC
authors.lastname: Fishbein
authors.forename: W J
authors.initials: WJ
authors.lastname: Mandel
authors.forename: P S
authors.initials: PS
authors.lastname: Chen
authors.forename: H S
authors.initials: HS
authors.lastname: Karagueuzian
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D016280:Atrial Function, Right; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004594:Electrophysiology; D005260:Female; D006325:Heart Atria; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000473:pathology