title: Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation.
abstract: The purpose of the present study was to evaluate the effect of angiotensin II type 1 receptor (AT1R) antagonist on chronic structural remodeling in atrial fibrillation (AF).
  
  
  BACKGROUND
  We previously reported that an AT1R antagonist, candesartan, prevents acute electrical remodeling in a rapid pacing model. However, the effect of candesartan on chronic structural remodeling in AF is unclear.
  
  
  METHODS
  Sustained AF was induced in 20 dogs (10 in a control group and 10 in a candesartan group) by rapid pacing of the right atrium (RA) at 400 beats/min for five weeks. Candesartan was administered orally (10 mg/kg/day) for one week before rapid pacing and was continued for five weeks. The AF duration, atrial effective refractory period (AERP) at four sites in the RA, and intra-atrial conduction time (CT) from the RA appendage to the other three sites were measured every week.
  
  
  RESULTS
  The mean AF duration in the control group after five weeks was significantly longer than that with candesartan (1,333 +/- 725 vs. 411 +/- 301 s, p < 0.01). The degree of AERP shortening after five weeks was not significantly different between the two groups. The CT from the RA appendage to the low RA after five weeks with candesartan was significantly shorter than that in the control (43 +/- 14 vs. 68 +/- 10 ms, p < 0.05). The candesartan group had a significantly lower percentage of interstitial fibrosis than the control group (7 +/- 2% vs. 16 +/- 1% at the RA appendage, p < 0.001).
  
  
  CONCLUSIONS
  Candesartan can prevent the promotion of AF by suppressing the development of structural remodeling.
authors.affiliation: Department of Cardiology, School of Medicine, Fukuoka University, Fukuoka, Japan. kxk@fukuoka-u.ac.jp
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kumagai
authors.forename: Hideko
authors.initials: H
authors.lastname: Nakashima
authors.forename: Hidenori
authors.initials: H
authors.lastname: Urata
authors.forename: Naoki
authors.initials: N
authors.lastname: Gondo
authors.forename: Kikuo
authors.initials: K
authors.lastname: Arakawa
authors.forename: Keijiro
authors.initials: K
authors.lastname: Saku
mesh_terms: D057911:Angiotensin Receptor Antagonists; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D001562:Benzimidazoles / Q000494:pharmacology / Q000627:therapeutic use*; D001713:Biphenyl Compounds; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects; D002908:Chronic Disease; D004195:Disease Models, Animal; D004285:Dogs; D004594:Electrophysiology; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D008297:Male; D011897:Random Allocation; D011945:Receptors, Angiotensin / Q000627:therapeutic use*; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use*; D013997:Time Factors; D020257:Ventricular Remodeling / Q000187:drug effects* / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D011945:Receptors, Angiotensin; D013777:Tetrazoles; C081643:candesartan