title: Reverse structural and gap-junctional remodeling after prolonged atrial fibrillation in the goat.
abstract: BACKGROUND
  Prolonged atrial fibrillation (AF) results in electrical, structural, and gap-junctional remodeling. We examined the reversibility of the changes in (ultra)structure and gap junctions.
  
  
  RESULTS
  Four groups of goats were used: (1) sinus rhythm (SR), (2) 4 months' AF (4 mo AF), (3) 2 months' SR after 4 mo AF (2 mo post-AF), and (4) 4 months' SR after 4 mo AF (4 mo post-AF). Atria were characterized electrophysiologically, (ultra)structure was studied by light and electron microscopy, and structural and gap-junctional protein expression was studied by immunohistochemistry or Western blotting. The atrial effective refractory period had completely returned to normal values 2 mo post-AF. Induced AF episodes still lasted for minutes at 2 and 4 mo post-AF, compared with seconds in the SR group. Structural abnormalities were still present at 2 and 4 mo post-AF, although to a lesser extent. The increased atrial myocyte diameter was back to normal at 4 mo post-AF. The number of myocytes with severe myolysis had almost normalized 4 mo post-AF, whereas myocytes with mild myolysis remained significantly increased. Extracellular matrix area fraction after 4 mo AF was similar to SR. However, the extracellular matrix fraction per myocyte had increased after 4 mo AF and remained higher post-AF. Changes in expression of structural proteins were partially restored post-AF. The reduction of connexin 40 that was observed during AF was completely reversed at 4 mo post-AF.
  
  
  CONCLUSIONS
  Recovery from structural remodeling after 4 mo AF is a slow process and is still incomplete 4 mo post-AF. Several months post-AF, the duration of AF episodes is still prolonged (minutes).
authors.affiliation: Cardiovascular Research Institute Maastricht, The Netherlands. jannie.ausma@fys.unimaas.nl
authors.forename: Jannie
authors.initials: J
authors.lastname: Ausma
authors.forename: Huub M W
authors.initials: HM
authors.lastname: van der Velden
authors.forename: Marie-Hélène
authors.initials: MH
authors.lastname: Lenders
authors.forename: Erwin P
authors.initials: EP
authors.lastname: van Ankeren
authors.forename: Habo J
authors.initials: HJ
authors.lastname: Jongsma
authors.forename: Frans C S
authors.initials: FC
authors.lastname: Ramaekers
authors.forename: Marcel
authors.initials: M
authors.lastname: Borgers
authors.forename: Maurits A
authors.initials: MA
authors.lastname: Allessie
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology* / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D048429:Cell Size; D017630:Connexins / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D022062:Electrophysiologic Techniques, Cardiac; D017629:Gap Junctions / Q000648:ultrastructure*; D006003:Glycogen / Q000378:metabolism; D006041:Goats; D006325:Heart Atria / Q000473:pathology* / Q000503:physiopathology; D007150:Immunohistochemistry; D009206:Myocardium / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D020127:Recovery of Function; D012016:Reference Values; D012074:Remission Induction
chemical_list: D017630:Connexins; D006003:Glycogen