title: Amyloid deposition as a cause of atrial remodelling in persistent valvular atrial fibrillation.
abstract: OBJECTIVE
  The spectrum of histological alterations, namely atrial amyloidosis, in the right and left atria of patients with chronic persistent atrial fibrillation (AF) and rheumatic heart disease is not completely known.
  
  
  RESULTS
  One hundred and twenty-eight atrial appendages (66 left and 62 right), obtained from 72 patients with rheumatic valve disease and chronic AF undergoing cardiac surgery for valve replacement or repair and AF treatment were histologically evaluated for the presence of amyloid deposits. One hundred and four specimens of left and right auricles from 52 patients in sinus rhythm with severe chronic heart failure undergoing heart transplant were also analyzed (controls). Amyloid was found in 33 (46%) valvular patients with chronic persistent AF and in 6 (12%) controls. Amyloid was related to the presence and duration of AF, was more frequently found in left atrial samples and was independent of age. On stepwise logistic regression analysis, AF duration and female gender were independently related to amyloid deposition.
  
  
  CONCLUSIONS
  Patients with long-standing AF and rheumatic heart disease have a very high prevalence of atrial amyloidosis. Amyloid deposition is more frequent in left than in right atrial appendage and correlates with AF duration and female gender. Amyloid deposition could constitute an additional histological feature in the structural remodeling of atria during long-standing AF, at least in rheumatic valve disease. Persistence of AF might play a pivotal role in promoting amyloid deposition.
authors.affiliation: Department of Pathology, University of Bologna, Azienda Ospedaliera S. Orsola-Malpighi of Bologna, via Massarenti 9, 40138 Bologna, Italy. oleone@orsola-malpighi.med.unibo.it
authors.forename: O
authors.initials: O
authors.lastname: Leone
authors.forename: G
authors.initials: G
authors.lastname: Boriani
authors.forename: B
authors.initials: B
authors.lastname: Chiappini
authors.forename: D
authors.initials: D
authors.lastname: Pacini
authors.forename: G
authors.initials: G
authors.lastname: Cenacchi
authors.forename: S
authors.initials: S
authors.lastname: Martin Suarez
authors.forename: C
authors.initials: C
authors.lastname: Rapezzi
authors.forename: M L
authors.initials: ML
authors.lastname: Bacchi Reggiani
authors.forename: G
authors.initials: G
authors.lastname: Marinelli
mesh_terms: D000368:Aged; D000682:Amyloid / Q000032:analysis; D000686:Amyloidosis / Q000150:complications / Q000473:pathology*; D001281:Atrial Fibrillation / Q000209:etiology / Q000473:pathology*; D016275:Atrial Function / Q000502:physiology; D009202:Cardiomyopathies / Q000150:complications / Q000473:pathology*; D004452:Echocardiography / Q000379:methods; D005260:Female; D006325:Heart Atria / Q000473:pathology; D006349:Heart Valve Diseases / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D012214:Rheumatic Heart Disease / Q000473:pathology
chemical_list: D000682:Amyloid