title: Structural atrial remodeling alters the substrate and spatiotemporal organization of atrial fibrillation: a comparison in canine models of structural and electrical atrial remodeling.
abstract: Several animal models of atrial fibrillation (AF) have been developed that demonstrate either atrial structural remodeling or atrial electrical remodeling, but the characteristics and spatiotemporal organization of the AF between the models have not been compared. Thirty-nine dogs were divided into five groups: rapid atrial pacing (RAP), chronic mitral regurgitation (MR), congestive heart failure (CHF), methylcholine (Meth), and control. Right and left atria (RA and LA, respectively) were simultaneously mapped during episodes of AF in each animal using high-density (240 electrodes) epicardial arrays. Multiple 30-s AF epochs were recorded in each dog. Fast Fourier transform was calculated every 1 s over a sliding 2-s window, and dominant frequency (DF) was determined. Stable, discrete, high-frequency areas were seen in none of the RAP or control dogs, four of nine MR dogs, four of six CHF dogs, and seven of nine Meth dogs in either the RA or LA or both. Average DFs in the Meth model were significantly greater than in all other models in both LA and RA except LA DFs in the RAP model. The RAP model was the only one with a consistent LA-to-RA DF gradient (9.5 +/- 0.2 vs. 8.3 +/- 0.3 Hz, P < 0.00005). The Meth model had a higher spatial and temporal variance of DFs and lower measured organization levels compared with the other AF models, and it was the only model to show a linear relationship between the highest DF and dispersion (R(2) = 0.86). These data indicate that structural remodeling of atria (models known to have predominantly altered conduction) leads to an AF characterized by a stable high-frequency area, whereas electrical remodeling of atria (models known to have predominantly shortened refractoriness without significant conduction abnormalities) leads to an AF characterized by multiple high-frequency areas and multiple wavelets.
authors.affiliation: Cardiac Electrophysiology, University of California-San Francisco, CA 94143-1354, USA.
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Everett
authors.forename: Emily E
authors.initials: EE
authors.lastname: Wilson
authors.forename: Sander
authors.initials: S
authors.lastname: Verheule
authors.forename: Jose M
authors.initials: JM
authors.lastname: Guerra
authors.forename: Scott
authors.initials: S
authors.lastname: Foreman
authors.forename: Jeffrey E
authors.initials: JE
authors.lastname: Olgin
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000473:pathology / Q000503:physiopathology; D001281:Atrial Fibrillation / Q000473:pathology* / Q000503:physiopathology*; D016279:Atrial Function, Left / Q000502:physiology; D016280:Atrial Function, Right / Q000502:physiology; D002794:Choline / Q000009:adverse effects / Q000031:analogs & derivatives; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D004594:Electrophysiology; D005583:Fourier Analysis; D006325:Heart Atria / Q000294:innervation* / Q000473:pathology / Q000503:physiopathology*; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000473:pathology / Q000503:physiopathology
chemical_list: C017506:methylcholine; D002794:Choline