title: Paroxysmal lone atrial fibrillation is associated with an abnormal atrial substrate: characterizing the "second factor".
abstract: OBJECTIVE
  The purpose of this study was to determine whether patients with paroxysmal "lone" atrial fibrillation (AF) have an abnormal atrial substrate.
  
  
  BACKGROUND
  While "AF begets AF," prompt termination to prevent electrical remodeling does not prevent disease progression.
  
  
  METHODS
  Twenty-five patients with paroxysmal lone AF, without arrhythmia in the week prior, and 25 reference patients with left-sided accessory pathways were studied. Multipolar catheters placed at the lateral right atrium (RA), crista terminalis, coronary sinus, septal RA, and sequentially within the left atrium (LA) determined the effective refractory period (ERP) at 10 sites, conduction time along linear catheters, and conduction characteristics at the crista terminalis. Bi-atrial electroanatomic maps were created to determine regional differences in conduction velocity and voltage.
  
  
  RESULTS
  Patients with AF demonstrated the following compared with reference patients: larger atrial volumes (RA: 94 +/- 18 ml vs. 69 +/- 9 ml, p = 0.003; LA: 99 +/- 19 ml vs. 77 +/- 17 ml, p = 0.006); longer ERP (at 600 ms: 255 +/- 25 ms vs. 222 +/- 16 ms, p < 0.001; at 450 ms: 234 +/- 20 ms vs. 212 +/- 14 ms, p = 0.004); longer conduction time along linear catheters (57 +/- 18 ms vs. 47 +/- 10 ms, p = 0.01); longer bi-atrial activation time (128 +/- 17 ms vs. 89 +/- 10 ms, p < 0.001); slower conduction velocity (RA: 1.3 +/- 0.3 mm/ms vs. 2.1 +/- 0.5 mm/ms; LA: 1.2 +/- 0.2 mm/ms vs. 2.2 +/- 0.4 mm/ms, p < 0.001); greater proportion of fractionated electrograms (27 +/- 8% vs. 8 +/- 5%, p < 0.001); longer corrected sinus node recovery time (265 +/- 57 ms vs. 185 +/- 60 ms, p = 0.002); and lower voltage (RA: 1.7 +/- 0.4 mV vs. 2.9 +/- 0.4 mV; LA: 1.7 +/- 0.7 mV vs. 3.3 +/- 0.7 mV, p < 0.001).
  
  
  CONCLUSIONS
  Patients with paroxysmal lone AF, remote from arrhythmia, demonstrate bi-atrial abnormalities characterized by structural change, conduction abnormalities, and sinus node dysfunction. These factors are likely contributors to the "second factor" that predisposes to the development and progression of AF.
authors.affiliation: Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, University of Adelaide, Adelaide, Australia.
authors.forename: Martin K
authors.initials: MK
authors.lastname: Stiles
authors.forename: Bobby
authors.initials: B
authors.lastname: John
authors.forename: Christopher X
authors.initials: CX
authors.lastname: Wong
authors.forename: Pawel
authors.initials: P
authors.lastname: Kuklik
authors.forename: Anthony G
authors.initials: AG
authors.lastname: Brooks
authors.forename: Dennis H
authors.initials: DH
authors.lastname: Lau
authors.forename: Hany
authors.initials: H
authors.lastname: Dimitri
authors.forename: Kurt C
authors.initials: KC
authors.lastname: Roberts-Thomson
authors.forename: Lauren
authors.initials: L
authors.lastname: Wilson
authors.forename: Paolo
authors.initials: P
authors.lastname: De Sciscio
authors.forename: Glenn D
authors.initials: GD
authors.lastname: Young
authors.forename: Prashanthan
authors.initials: P
authors.lastname: Sanders