title: Histological evidence of inflammatory reaction associated with fibrosis in the atrial and ventricular walls in a case-control study of patients with history of atrial fibrillation.
abstract: OBJECTIVE
  Chronic inflammation in the atrial myocardium was shown to play an important role in the development of atrial fibrosis in patients with atrial fibrillation (AF). However, it is not clear to what extent atrial inflammatory reaction associated with AF extends on the ventricular myocardium. Our aim was to assess the extent of fibrosis and lymphomononuclear infiltration in human ventricular myocardium and explore its association with AF.
  
  
  RESULTS
  Medical records from consecutive autopsies were checked for presence of AF. Heart specimens from 30 patients died from cardiovascular causes (64 ± 12 years, 17 men) were collected in three equal groups: no AF, paroxysmal AF, and permanent AF. Tissue samples were taken from the Bachmann's bundle, crista terminalis, posterior left atrium, left ventricle and right ventricle free walls and stained with Masson's trichrome for analysis of fibrosis extent. Immunohistochemistry was performed using antibodies against CD3- and CD45-antigens and quantified as number of antigen-positive cells per 1 mm2. Fibrosis extent, CD3+ and CD45+ cell counts were elevated in AF patients at all sites (P < 0.001 for all). Fibrosis extent demonstrated correlation with both CD3+ and CD45+ cell counts in the right (r = 0.781, P < 0.001 for CD45+ and r = 0.720, P < 0.001 for CD3+) and the left (r = 0.515, P = 0.004 for CD45+ and r = 0.573, P = 0.001 for CD3+) ventricles. Neither fibrosis nor inflammatory cell count showed association with either age or comorbidities.
  
  
  CONCLUSIONS
  Histological signs of chronic inflammation affecting ventricular myocardium are strongly associated with AF and demonstrate significant correlation with fibrosis extent that cannot be explained by cardiovascular comorbidities otherwise.
authors.affiliation: Federal Almazov North-West Medical Research Centre, 2 Akkuratova street, St. Petersburg 197341, Russia.
authors.forename: Lubov B
authors.initials: LB
authors.lastname: Mitrofanova
authors.affiliation: Federal Almazov North-West Medical Research Centre, 2 Akkuratova street, St. Petersburg 197341, Russia.
authors.forename: Victoria
authors.initials: V
authors.lastname: Orshanskaya
authors.affiliation: Royal Brompton Hospital and Imperial College, Sydney Street, London, SW3 6NP UK.
authors.forename: Siew Yen
authors.initials: SY
authors.lastname: Ho
authors.affiliation: Department of Cardiology, Clinical Sciences, Lund University and Arrhythmia Clinic, Skåne University Hospital, 22185 Lund, Sweden pyotr.platonov@med.lu.se.
authors.forename: Pyotr G
authors.initials: PG
authors.lastname: Platonov
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001281:Atrial Fibrillation / Q000473:pathology* / Q000503:physiopathology; D001344:Autopsy; D015415:Biomarkers / Q000032:analysis; D001706:Biopsy; D017252:CD3 Complex / Q000032:analysis; D016022:Case-Control Studies; D005260:Female; D005355:Fibrosis; D006325:Heart Atria / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D006352:Heart Ventricles / Q000737:chemistry / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry; D017493:Leukocyte Common Antigens / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000473:pathology* / Q000503:physiopathology; D011379:Prognosis; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers; D017252:CD3 Complex; D017493:Leukocyte Common Antigens; C516769:PTPRC protein, human
keywords: Atrial fibrillation; Fibrosis; Inflammation; Structural remodelling; Ventricles