title: Association of echocardiographic atrial size and atrial fibrosis in a sequential model of congestive heart failure and atrial fibrillation.
abstract: BACKGROUND
  Cardioversion (CV) success of atrial fibrillation (AF) inversely correlates to the size of the left atrium (LA). Atrial fibrillation and its most important risk factor, congestive heart failure (CHF), both induce atrial structural enlargement and fibrosis. To investigate the effect of AF and CHF on atrial dilatation and fibrosis, and to estimate whether echocardiographically determined atrial size may be used as a marker for atrial fibrosis.
  
  
  METHODS
  In six dogs, pacemakers were implanted followed by HIS bundle ablation. After 4 weeks of rapid ventricular stimulation (185 bpm) for CHF induction, additional rapid atrial stimulation (500 bpm) was maintained for 7 weeks to induce AF. Serial determinations of echocardiographic atrial size were performed. Seven dogs with sinus rhythm served as histological controls. Postmortem tissue was obtained to determine the degree and composition of atrial fibrosis.
  
  
  RESULTS
  While the ejection fraction of the AF/CHF dogs decreased significantly from 57+/-5% to 19+/-7% (P<.01), an increased degree of atrial fibrosis was found (right atrium [RA], 4.9+/-2.0% to 19.9+/-5.4%; LA, 4.4+/-1.6% to 22.2+/-3.2%; P<.01), accompanied by a significant increase of atrial volumes (LA: 21+/-4 to 44+/-4 mm3; P<.01; RA: 10+/-3 to 18+/-6 mm3; P<.05) and LA diameters (34+/-4 to 43+/-2 mm, P<.05). Atrial fibrosis and size significantly correlated.
  
  
  CONCLUSIONS
  Atrial fibrillation/CHF leads to a significant atrial fibrosis and dilation. The increased echocardiographic size correlates to the degree of atrial fibrosis and may be used as clinical marker for atrial fibrosis. The fibrosis accompanying atrial dilatation may also explain why LA size, as determined by echocardiography, is a strong predictor of CV success.
authors.affiliation: Department of Cardiology, RWTH Aachen University, Aachen, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Knackstedt
authors.forename: Felix
authors.initials: F
authors.lastname: Gramley
authors.forename: Thomas
authors.initials: T
authors.lastname: Schimpf
authors.forename: Karl
authors.initials: K
authors.lastname: Mischke
authors.forename: Markus
authors.initials: M
authors.lastname: Zarse
authors.forename: Jurgita
authors.initials: J
authors.lastname: Plisiene
authors.forename: Michael
authors.initials: M
authors.lastname: Schmid
authors.forename: Johann
authors.initials: J
authors.lastname: Lorenzen
authors.forename: Dirk
authors.initials: D
authors.lastname: Frechen
authors.forename: Philipp
authors.initials: P
authors.lastname: Neef
authors.forename: Peter
authors.initials: P
authors.lastname: Hanrath
authors.forename: Malte
authors.initials: M
authors.lastname: Kelm
authors.forename: Patrick
authors.initials: P
authors.lastname: Schauerte
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology / Q000473:pathology*; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D005355:Fibrosis; D006325:Heart Atria / Q000473:pathology*; D006333:Heart Failure / Q000150:complications / Q000473:pathology*; D013318:Stroke Volume