title: Atrial protective effects of n-3 polyunsaturated fatty acids: a long-term study in ovine chronic heart failure.
abstract: BACKGROUND
  It has been suggested that omega-3 polyunsaturated fatty acids (n-3 PUFAs) may prevent the development of atrial fibrillation (AF).
  
  
  OBJECTIVE
  The purpose of this study was to evaluate the impact of these agents on development of the AF substrate in heart failure (HF).
  
  
  METHODS
  In this study, HF was induced by intracoronary doxorubicin infusions. Twenty-one sheep [7 with n-3 PUFAs treated HF (HF-PUFA), 7 with olive oil-treated HF controls (HF-CTL), 7 controls (CTL)] were studied. Open chest electrophysiologic study was performed with assessment of biatrial effective refractory period (ERP) and conduction. Cardiac function was monitored by magnetic resonance imaging. Atrial n-3 PUFAs levels were quantified using chromatography. Structural analysis was also performed.
  
  
  RESULTS
  Atrial n-3 PUFAs levels were twofold to threefold higher in the HF-PUFA group. n-3 PUFAs prevented the development of HF-related left atrial enlargement (P = .001) but not left ventricular/atrial dysfunction. Atrial ERP was significantly lower in the HF-PUFA group (P <.001), but ERP heterogeneity was unchanged. In addition, n-3 PUFAs suppressed atrial conduction abnormalities seen in HF of prolonged P-wave duration (P = .01) and slowed (P <.001) and heterogeneous (P <.05) conduction. The duration of induced AF episodes in HF-PUFA was shorter (P = .02), although AF inducibility was unaltered (P = NS). A 20% reduction of atrial interstitial fibrosis was seen in the HF-PUFA group (P <.05).
  
  
  CONCLUSIONS
  In this ovine HF study, chronic n-3 PUFAs use protected against adverse atrial remodeling by preventing atrial enlargement, fibrosis, and conduction abnormalities leading to shorter AF episodes despite lower ERP.
authors.affiliation: Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital, Adelaide, Australia.
authors.forename: Dennis H
authors.initials: DH
authors.lastname: Lau
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Psaltis
authors.forename: Angelo
authors.initials: A
authors.lastname: Carbone
authors.forename: Darren J
authors.initials: DJ
authors.lastname: Kelly
authors.forename: Lorraine
authors.initials: L
authors.lastname: Mackenzie
authors.forename: Michael
authors.initials: M
authors.lastname: Worthington
authors.forename: Robert G
authors.initials: RG
authors.lastname: Metcalf
authors.forename: Pawel
authors.initials: P
authors.lastname: Kuklik
authors.forename: Adam J
authors.initials: AJ
authors.lastname: Nelson
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Christopher X
authors.initials: CX
authors.lastname: Wong
authors.forename: Anthony G
authors.initials: AG
authors.lastname: Brooks
authors.forename: David A
authors.initials: DA
authors.lastname: Saint
authors.forename: Michael J
authors.initials: MJ
authors.lastname: James
authors.forename: James
authors.initials: J
authors.lastname: Edwards
authors.forename: Glenn D
authors.initials: GD
authors.lastname: Young
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Worthley
authors.forename: Prashanthan
authors.initials: P
authors.lastname: Sanders
mesh_terms: D000818:Animals; D016275:Atrial Function / Q000187:drug effects* / Q000502:physiology; D004195:Disease Models, Animal; D004562:Electrocardiography; D015525:Fatty Acids, Omega-3 / Q000008:administration & dosage* / Q000493:pharmacokinetics; D005500:Follow-Up Studies; D006325:Heart Atria / Q000187:drug effects*; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control*; D012756:Sheep; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015525:Fatty Acids, Omega-3