title: Atrial amyloidosis: an arrhythmogenic substrate for persistent atrial fibrillation.
abstract: BACKGROUND
  Structural changes, like atrial fibrosis, may increase the likelihood of atrial fibrillation (AF) occurring in response to triggering events. The influence of isolated atrial amyloidosis (IAA) is largely unknown.
  
  
  RESULTS
  Right atrial appendages (1 or 2 entire cross sections) were obtained from 245 patients undergoing open-heart surgery. Atrial amyloid was identified by Congo red staining and classified by immunohistochemistry. Amyloid was found in 40 (16.3%) of 245 patients, and all deposits were immunoreactive for atrial natriuretic peptide (ANP). Thirty-eight (15.5%) patients suffered from persistent AF. The presence of amyloid correlated with age and P-wave duration and was related to sex, valve diseases, and the presence of AF (P<0.01). The association between atrial amyloid, AF, and P-wave duration was independent of age and sex. According to multiple logistic regression analysis, amyloid was the only age- and sex-independent predictor for the presence of AF. Atrial fibrosis was not a predictor for AF, and the amount of amyloid correlated inversely with the degree of interstitial fibrosis (P=0.001; r=-0.55).
  
  
  CONCLUSIONS
  Our study provides evidence that IAA affects atrial conduction and increases the risk of AF. The occurrence of IAA depends on age leading to the formation of an amyloid nidus. The progression and consequences of IAA are then influenced by pathological conditions, such as valve diseases, that increase synthesis and secretion of ANP. The inverse correlation between IAA and atrial fibrosis suggests that these patients may not benefit from treatment with ACE inhibitors to reduce the amount of atrial fibrosis.
authors.affiliation: Department of Pathology, Otto-von-Guericke-University, Magdeburg, Germany. christoph.roecken@medizin.uni-magdeburg.de
authors.forename: Christoph
authors.initials: C
authors.lastname: Röcken
authors.forename: Brigitte
authors.initials: B
authors.lastname: Peters
authors.forename: Gina
authors.initials: G
authors.lastname: Juenemann
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Saeger
authors.forename: Helmut U
authors.initials: HU
authors.lastname: Klein
authors.forename: Christof
authors.initials: C
authors.lastname: Huth
authors.forename: Albert
authors.initials: A
authors.lastname: Roessner
authors.forename: Andreas
authors.initials: A
authors.lastname: Goette
mesh_terms: D000328:Adult; D000368:Aged; D000686:Amyloidosis / Q000150:complications* / Q000209:etiology / Q000473:pathology; D020517:Atrial Appendage / Q000737:chemistry / Q000473:pathology; D001281:Atrial Fibrillation / Q000209:etiology*; D009320:Atrial Natriuretic Factor / Q000032:analysis / Q000276:immunology / Q000502:physiology; D005260:Female; D005355:Fibrosis; D006325:Heart Atria / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D013997:Time Factors
chemical_list: D009320:Atrial Natriuretic Factor