title: Possible involvement of fibrocytes in atrial fibrosis in patients with chronic atrial fibrillation.
abstract: BACKGROUND
  Chronic atrial fibrillation (AF) is characterized by a remodeling process with prominent atrial fibrosis. Fibrocytes, a bone marrow-derived population of fibroblast-like cells, have been placed at the center of a number of fibrosing conditions. The purpose of this study was to evaluate the contribution of fibrocytes to atrial fibrosis in patients with chronic AF and the possible mechanisms.
  
  
  RESULTS
  We enrolled 22 consecutive valvular heart disease patients with chronic AF (>6 months: CAF group) and 15 valvular heart disease patients in sinus rhythm served as controls (SR group). Left atrial tissue samples were obtained during cardiac surgery. The infiltration of fibrocytes into the atrial interstitium was observed by confocal microscopy. The number of atrial fibrocytes was approximately three-fold higher in the CAF group compared with the SR controls, and positively correlated with both the atrial collagen volume fraction (r=0.713; P=0.0002) and the left atrial volume index (r=0.631; P=0.002). In the peripheral blood samples collected before the operation, approximately 2.5-fold higher percentage of circulating fibrocytes was identified in the CAF group. These fibrocytes showed a stronger proliferative capacity (≍2.5-fold) and higher level expression of collagen I and α-SMA (≍2-fold and 4-fold, respectively) compared with the SR controls.
  
  
  CONCLUSIONS
  The results suggested that fibrocytes may be involved in atrial fibrosis in chronic AF through enhanced profibrotic characteristics.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Medical School of Zhejiang University.
authors.forename: Xudong
authors.initials: X
authors.lastname: Xie
authors.forename: Yanrong
authors.initials: Y
authors.lastname: Liu
authors.forename: Shilong
authors.initials: S
authors.lastname: Gao
authors.forename: Bifeng
authors.initials: B
authors.lastname: Wu
authors.forename: Xiaosheng
authors.initials: X
authors.lastname: Hu
authors.forename: Junzhu
authors.initials: J
authors.lastname: Chen
mesh_terms: D000199:Actins / Q000096:biosynthesis*; D001281:Atrial Fibrillation / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D002908:Chronic Disease; D024042:Collagen Type I / Q000096:biosynthesis*; D005260:Female; D005355:Fibrosis; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology; D006349:Heart Valve Diseases / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D024042:Collagen Type I