title: Mechanism of spontaneous termination of stable atrial flutter in the canine sterile pericarditis model.
abstract: BACKGROUND
  We tested the hypotheses that spontaneous termination of stable atrial flutter is directly related to spontaneous beat-to-beat cycle length oscillations and that block of the circulating reentrant wave front occurs in an area of slow conduction.
  
  
  RESULTS
  We studied 30 episodes of spontaneous termination of stable atrial flutter induced by atrial stimulation in 11 conscious, nonsedated dogs with sterile pericarditis. Additionally, in 5 dogs, 14 episodes of spontaneous termination of stable atrial flutter were studied with a multisite mapping system to record simultaneously from 190 right atrial electrodes. In the conscious-state studies, atrial flutter cycle length oscillations began 6 +/- 1 (mean +/- SEM) beats before termination in 26 episodes, stable atrial flutter evolved into atrial fibrillation in 3 episodes, and no cycle length change occurred before termination in 1 episode. In the open-chest studies, in all instances, spontaneous oscillations began 7 +/- 1 beats before termination. The only consistent oscillation pattern occurred for the last two beats: a long cycle length (149 +/- 9 milliseconds) followed by a much shorter cycle length (110 +/- 6 milliseconds) (P < .01). Activation maps demonstrated that all cycle length oscillations were explained by changes of conduction in an area(s) of slow conduction in the reentrant circuit. In two instances, the last (short) cycle length was associated with disappearance of an area of slow conduction. In all episodes, the last circulating reentrant wave front blocked in an area of slow conduction in the reentrant circuit. Although not tested, during the last beat, the very early arrival of the circulating reentrant wave front at an area of slow conduction suggests an important role for refractoriness, with head and tail interactions, resulting in block.
  
  
  CONCLUSIONS
  Spontaneous termination of stable atrial flutter in the sterile pericarditis model (1) is preceded by beat-to-beat cycle length oscillations that result from changes in conduction in areas of slow conduction in the reentrant circuit and (2) results from block of the circulating reentrant wave front in an area of slow conduction.
authors.affiliation: Department of Medicine, Case Western Reserve University/University Hospitals of Cleveland, Ohio 44106.
authors.forename: J
authors.initials: J
authors.lastname: Ortiz
authors.forename: M
authors.initials: M
authors.lastname: Igarashi
authors.forename: H X
authors.initials: HX
authors.lastname: Gonzalez
authors.forename: K
authors.initials: K
authors.lastname: Laurita
authors.forename: Y
authors.initials: Y
authors.lastname: Rudy
authors.forename: A L
authors.initials: AL
authors.lastname: Waldo
mesh_terms: D000818:Animals; D001282:Atrial Flutter / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004562:Electrocardiography; D006327:Heart Block / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D010493:Pericarditis / Q000209:etiology / Q000503:physiopathology*