title: Left Atrial Size and Function in a Canine Model of Chronic Atrial Fibrillation and Heart Failure.
abstract: BACKGROUND
  Our aim was to assess how atrial fibrillation (AF) induction, chronicity, and RR interval irregularity affect left atrial (LA) function and size in the setting of underlying heart failure (HF), and to determine whether AF effects can be mitigated by vagal nerve stimulation (VNS).
  
  
  METHODS
  HF was induced by 4-weeks of rapid ventricular pacing in 24 dogs. Subsequently, AF was induced and maintained by atrial pacing at 600 bpm. Dogs were randomized into control (n = 9) and VNS (n = 15) groups. In the VNS group, atrioventricular node fat pad stimulation (310 μs, 20 Hz, 3-7 mA) was delivered continuously for 6 months. LA volume and LA strain data were calculated from bi-weekly echocardiograms.
  
  
  RESULTS
  RR intervals decreased with HF in both groups (p = 0.001), and decreased further during AF in control group (p = 0.014), with a non-significant increase in the VNS group during AF. LA size increased with HF (p<0.0001), with no additional increase during AF. LA strain decreased with HF (p = 0.025) and further decreased after induction of AF (p = 0.0001). LA strain decreased less (p = 0.001) in the VNS than in the control group. Beat-by-beat analysis showed a curvilinear increase of LA strain with longer preceding RR interval, (r = 0.45, p <0.0001) with LA strain 1.1% higher (p = 0.02) in the VNS-treated animals, independent of preceding RR interval duration. The curvilinear relationship between ratio of preceding and pre-preceding RR intervals, and subsequent LA strain was weaker, (r = 0.28, p = 0.001). However, VNS-treated animals again had higher LA strain (by 2.2%, p = 0.002) independently of the ratio of preceding and pre-preceding RR intervals.
  
  
  CONCLUSIONS
  In the underlying presence of pacing-induced HF, AF decreased LA strain, with little impact on LA size. LA strain depends on the preceding RR interval duration.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Adam
authors.initials: A
authors.lastname: Goldberg
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Kenya
authors.initials: K
authors.lastname: Kusunose
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Salima
authors.initials: S
authors.lastname: Qamruddin
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: L Leonardo
authors.initials: LL
authors.lastname: Rodriguez
authors.affiliation: Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Todor N
authors.initials: TN
authors.lastname: Mazgalev
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Brian P
authors.initials: BP
authors.lastname: Griffin
authors.affiliation: Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: David R
authors.initials: DR
authors.lastname: Van Wagoner
authors.affiliation: Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Youhua
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
authors.forename: Zoran B
authors.initials: ZB
authors.lastname: Popović
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology*; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D006325:Heart Atria / Q000473:pathology*; D006333:Heart Failure / Q000473:pathology*