title: Inducibility of atrial fibrillation depends not on inflammation but on atrial structural remodeling in rat experimental autoimmune myocarditis.
abstract: BACKGROUND
  There is increasing evidence to support a link between inflammation and atrial fibrillation (AF). However, the role of inflammation on new-onset AF is still to be elucidated.
  
  
  METHODS
  Rats underwent induction of experimental autoimmune myocarditis (EAM). Atrial structural change was evaluated by echocardiography and histological analysis. Electrophysiological data and the in vivo atrial response to burst atrial pacing were evaluated in the acute (2 weeks after EAM induction) and chronic phases (8 weeks after induction). In addition, atrial pacing after 2, 4, and 6 h after lipopolysaccharide (LPS) infusion, when the expression of gap junctions was modified, were challenged with young healthy rats.
  
  
  RESULTS
  AF was induced in 11 of 15 chronic phase EAM rats but not in either acute phase EAM rats or LPS infusion rats (P<.01). Echocardiography showed dilatation of both atrium and ventricle and a decrease in the ejection fraction in the chronic phase. Histology revealed severe inflammatory lesions only in the acute phase. Interstitial atrial fibrosis as well as the area of atrial myocyte increased in the chronic phase but not in the acute phase.
  
  
  CONCLUSIONS
  AF could be induced in the chronic phase of myocarditis rats, but not in the acute phase of myocarditis rats or in rats with LPS infusion. Acute inflammation per se did not increase the occurrence of AF induction. Atrial structural remodeling caused by inflammation and hemodynamic effects is necessary to induce AF.
authors.affiliation: Division of Cardiology, Niigata University School of Medical and Dental Sciences, 1-757 Asahimachi, Niigata City, Niigata 951-8510, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Hoyano
authors.forename: Masahiro
authors.initials: M
authors.lastname: Ito
authors.forename: Shinpei
authors.initials: S
authors.lastname: Kimura
authors.forename: Komei
authors.initials: K
authors.lastname: Tanaka
authors.forename: Kazuki
authors.initials: K
authors.lastname: Okamura
authors.forename: Satoru
authors.initials: S
authors.lastname: Komura
authors.forename: Wataru
authors.initials: W
authors.lastname: Mitsuma
authors.forename: Satoru
authors.initials: S
authors.lastname: Hirono
authors.forename: Masaomi
authors.initials: M
authors.lastname: Chinushi
authors.forename: Makoto
authors.initials: M
authors.lastname: Kodama
authors.forename: Yoshifusa
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D001327:Autoimmune Diseases / Q000150:complications / Q000378:metabolism / Q000473:pathology; D015153:Blotting, Western; D002908:Chronic Disease; D018031:Connexin 43 / Q000096:biosynthesis; D017630:Connexins / Q000096:biosynthesis; D019560:Echocardiography, Three-Dimensional; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology*; D007249:Inflammation / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D008297:Male; D009205:Myocarditis / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D011917:Rats, Inbred Lew; D017208:Rats, Wistar; D000097003:Gap Junction alpha-5 Protein
chemical_list: D018031:Connexin 43; D017630:Connexins; D000097003:Gap Junction alpha-5 Protein