title: Electrical remodeling of the atria following loss of atrioventricular synchrony: a long-term study in humans.
abstract: BACKGROUND
  Evidence suggests that an increased incidence of atrial fibrillation occurs in patients undergoing single-chamber ventricular pacing (VVI) when compared with those undergoing single-chamber atrial pacing (AAI) or those having dual-chamber atrioventricular pacing (DDD). The mechanism for this is unknown. We hypothesized that long-term loss of atrioventricular (AV) synchrony leads to atrial electrical remodeling: a potential explanation for this difference.
  
  
  RESULTS
  The study was a prospective, randomized comparison between 18 patients paced in VVI mode and 12 patients paced in DDD mode for 3 months. Under autonomic blockade, effective refractory periods (ERPs) from the lateral right atrium (RA), RA appendage, RA septum, and coronary sinus-corrected sinus node recovery times (cSNRTs), as well as P-wave duration (PWD), and biatrial diameters were measured at baseline and 3 months. The VVI group was then programmed to DDD pacing and reevaluated after a further 3 months. After long-term VVI pacing, ERPs at all 4 atrial sites increased significantly in a nonuniform fashion in association with biatrial dilatation. PWD and cSNRTs also prolonged significantly. With the reestablishment of AV synchrony, ERPs, PWD, cSNRTs, and biatrial dimensions returned to baseline levels. In the 12 patients who underwent long-term DDD pacing from baseline, no significant changes in atrial electrophysiology or biatrial dimensions were demonstrated.
  
  
  CONCLUSIONS
  Long-term loss of AV synchrony induced by VVI pacing is associated with atrial electrical remodeling, which is reversible after the reestablishment of AV synchrony with DDD pacing. This process may be partly responsible for the higher incidence of atrial fibrillation in patients undergoing VVI pacing compared with AV sequential pacing.
authors.affiliation: Department of Cardiology, The Royal Melbourne Hospital and The Department of Medicine, University of Melbourne, Australia.
authors.forename: P B
authors.initials: PB
authors.lastname: Sparks
authors.forename: H G
authors.initials: HG
authors.lastname: Mond
authors.forename: J K
authors.initials: JK
authors.lastname: Vohra
authors.forename: S
authors.initials: S
authors.lastname: Jayaprakash
authors.forename: J M
authors.initials: JM
authors.lastname: Kalman
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000628:therapy*; D001283:Atrioventricular Node / Q000503:physiopathology*; D018592:Cross-Over Studies; D004452:Echocardiography; D005260:Female; D006327:Heart Block / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D010138:Pacemaker, Artificial