title: Different structural remodelling in atrial fibrillation with different types of mitral valvular diseases.
abstract: OBJECTIVE
  The aim of this study was to determine the relationship between atrial structural remodelling and atrial fibrillation (AF) for different types of mitral valvular diseases (MVDs).
  
  
  RESULTS
  Left atrial appendages tissue samples were obtained from 24 patients with MVDs undergoing mitral valve replacement surgery. Masson's trichrome staining and immunohistochemical staining were performed to assess the extent of the fibrosis. Ultrastructural changes in left atrial appendages were examined by electron microscope. The degree of fibrosis showed significant increases in patients with AF compared with patients with sinus rhythm (SR) (P = 0.023). The collagen volume fraction (CVF) of fibrosis significantly increased in mitral stenosis and atrial fibrillation (MS-AF) compared with the mitral regurgitation and atrial fibrillation (MR-AF) group (P = 0.043). Collagen Type I levels were significantly increased in AF patients with mitral stenosis compared with AF patients with mitral regurgitation (P = 0.043). Different CVF of Matrix metalloproteinases-2 was present between the MS-SR group and the MS-AF group (P = 0.001). Electron microscopy revealed normally structured sarcomeres with a predominance of loosely packed cardiomyocytes in samples from patients with SR. Fibrotic bands, which tended to separate individual cardiomyocytes, were apparent in samples from patients with AF.
  
  
  CONCLUSIONS
  Atrial structural remodelling is associated with AF patients with MVDs. Different heart rhythm statuses with different types of MVDs are associated with variable atrial structural remodelling. Different atrial structural remodelling is a mechanism that may contribute to the increased risk of AF with MVDs.
authors.affiliation: Division of Thoracic and Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Qian
authors.forename: Jun
authors.initials: J
authors.lastname: Meng
authors.forename: Hong
authors.initials: H
authors.lastname: Tang
authors.forename: Guo
authors.initials: G
authors.lastname: Yang
authors.forename: Yiling
authors.initials: Y
authors.lastname: Deng
authors.forename: Dongming
authors.initials: D
authors.lastname: Wei
authors.forename: Bo
authors.initials: B
authors.lastname: Xiang
authors.forename: Xijun
authors.initials: X
authors.lastname: Xiao
mesh_terms: D000328:Adult; D020517:Atrial Appendage / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D001281:Atrial Fibrillation / Q000453:epidemiology / Q000473:pathology*; D001706:Biopsy; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D008854:Microscopy, Electron; D008875:Middle Aged; D008946:Mitral Valve Stenosis / Q000453:epidemiology / Q000473:pathology* / Q000601:surgery; D012307:Risk Factors; D013194:Staining and Labeling; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism
chemical_list: D024042:Collagen Type I; D024061:Collagen Type III; D019715:Tissue Inhibitor of Metalloproteinase-1; D019716:Tissue Inhibitor of Metalloproteinase-2; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9