title: Left atrial remodeling in patients with atrial septal defects.
abstract: BACKGROUND
  Information regarding left atrial (LA) substrate in conditions predisposing to atrial fibrillation (AF) is limited.
  
  
  OBJECTIVE
  This study sought to characterize the left atrial remodeling that results from chronic atrial stretch caused by atrial septal defect (ASD).
  
  
  METHODS
  Eleven patients with hemodynamically significant ASDs and 12 control subjects were studied. The following were evaluated using multipolar catheters: effective refractory period (ERP) at 7 sites, P-wave duration (PWD), conduction time, and inducibility of AF. LA electroanatomic maps were created to determine atrial activation, and regional conduction and voltage abnormalities.
  
  
  RESULTS
  Patients with ASDs showed significant LA enlargement (P <0.001), unchanged or prolonged atrial ERPs, increase in LA conduction times (P = 0.03), prolonged PWD (P <0.001), regional conduction slowing (P <0.001), greater number of double potentials or fractionated electrograms (P <0.0001), reduced atrial voltage (P <0.001), and more frequent electrical scar (P = 0.005) compared with control subjects. In addition, patients with ASDs showed a greater propensity for sustained AF with single extrastimuli (4 of 11 vs. 0 of 12, P = 0.04).
  
  
  CONCLUSIONS
  ASDs are associated with chronic left atrial stretch, which results in remodeling characterized by LA enlargement, loss of myocardium, and electrical scar that results in widespread conduction abnormalities but with no change or an increase in ERP. These abnormalities were associated with a greater propensity for sustained AF.
authors.affiliation: Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.
authors.forename: Kurt C
authors.initials: KC
authors.lastname: Roberts-Thomson
authors.forename: Bobby
authors.initials: B
authors.lastname: John
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Worthley
authors.forename: Anthony G
authors.initials: AG
authors.lastname: Brooks
authors.forename: Martin K
authors.initials: MK
authors.lastname: Stiles
authors.forename: Dennis H
authors.initials: DH
authors.lastname: Lau
authors.forename: Pawel
authors.initials: P
authors.lastname: Kuklik
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Shipp
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Kalman
authors.forename: Prashanthan
authors.initials: P
authors.lastname: Sanders
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000209:etiology; D016279:Atrial Function, Left / Q000502:physiology*; D005260:Female; D006325:Heart Atria / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D006344:Heart Septal Defects, Atrial / Q000150:complications / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged