title: Development of a substrate of atrial fibrillation during chronic atrioventricular block in the goat.
abstract: BACKGROUND
  Atrial dilatation is an important risk factor for atrial fibrillation (AF). In the present study, we monitored the electrophysiological changes during progressive atrial dilatation in chronically instrumented goats.
  
  
  RESULTS
  In 8 goats, 2 screw-in leads with piezoelectric crystals were implanted transvenously in the right atrium. After 2 weeks, atrial diameter and effective refractory period were measured. AF paroxysms were induced by burst pacing to determine the baseline AF cycle length and stability of AF. After His-bundle ablation, the above measurements were repeated once a week. After 4 weeks of complete AV block, the free wall of the right atrium was mapped and the atrium was fixed in formalin for histological analysis. After His-bundle ablation, the ventricular rate decreased from 113.8+/-4.8 to 44.6+/-2.5 bpm. Right atrial diameter increased gradually by 13.5+/-3.9% during 4 weeks of AV block (P<0.01). The duration of induced AF paroxysms increased from 4.6 seconds to 6.4 minutes (P<0.05). Atrial effective refractory period and AF cycle length remained constant. Spontaneous paroxysms of AF were not observed. Atrial mapping during rapid pacing revealed that slow conduction (<30 cm/s) was present in 3.7+/-1.0% of the mapped area (control, 0.9+/-0.5%, P<0.05). Histological analysis showed hypertrophy without atrial fibrosis. Connexin40 and connexin43 expression was unchanged.
  
  
  CONCLUSIONS
  Chronic AV block in the goat leads to progressive atrial dilatation, prolongation of induced AF paroxysms, and local conduction delays. The increase in AF stability was not a result of a shortening of atrial refractoriness or atrial fibrosis.
authors.affiliation: Department of Physiology, University of Maastricht, The Netherlands.
authors.forename: Hans-Ruprecht
authors.initials: HR
authors.lastname: Neuberger
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schotten
authors.forename: Sander
authors.initials: S
authors.lastname: Verheule
authors.forename: Sabine
authors.initials: S
authors.lastname: Eijsbouts
authors.forename: Yuri
authors.initials: Y
authors.lastname: Blaauw
authors.forename: Arne
authors.initials: A
authors.lastname: van Hunnik
authors.forename: Maurits
authors.initials: M
authors.lastname: Allessie
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D009320:Atrial Natriuretic Factor / Q000097:blood; D002304:Cardiac Pacing, Artificial; D006332:Cardiomegaly / Q000209:etiology; D048429:Cell Size; D002908:Chronic Disease; D018031:Connexin 43 / Q000096:biosynthesis; D017630:Connexins / Q000096:biosynthesis; D005260:Female; D006041:Goats; D006327:Heart Block / Q000150:complications*; D006329:Heart Conduction System / Q000503:physiopathology; D006439:Hemodynamics; D006984:Hypertrophy; D032383:Myocytes, Cardiac / Q000473:pathology; D009431:Neural Conduction; D009638:Norepinephrine / Q000097:blood; D012032:Refractory Period, Electrophysiological; D000097003:Gap Junction alpha-5 Protein
chemical_list: D000450:Aldosterone; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor; D018031:Connexin 43; D017630:Connexins; D009638:Norepinephrine; D000097003:Gap Junction alpha-5 Protein