title: The effects of remodeling with heart failure on mode of initiation of ventricular fibrillation and its spatiotemporal organization.
abstract: OBJECTIVE
  The effect of the heart failure substrate on the initiation of ventricular fibrillation (VF) and its resulting mechanism is not known. The objective of this study was to determine the effects of substrate on VF initiation and its spatiotemporal organization in the heart failure model.
  
  
  METHODS
  Optical action potentials were recorded from LV wedge preparations either from structurally normal hearts (control, n = 11) or from congestive heart failure (CHF; n = 7), at the epicardial surface, endocardial surface which included a papillary muscle, and a transmural cross section. Action potential duration (APD(80)) was determined, and VF was initiated. A fast Fourier transform was calculated, and the dominant frequency (DF) was determined.
  
  
  RESULTS
  The CHF group showed increased VF vulnerability (69 vs 26 %, p < 0.03), and every mapped surface showed an APD(80) gradient which included islands of higher APDs on the transmural surface (M cells) which was not observed in controls. VF in the CHF group was characterized by stable, discrete, high-DF areas that correlated to either foci or spiral waves located on the transmural surface at the site of the papillary muscle. Overall, the top 10 % of DFs correlated to an APD of 101 ms while the bottom 10 % of DFs correlated to an APD of 126 ms (p < 0.01).
  
  
  CONCLUSIONS
  In the CHF model, APD gradients correlated with an increased vulnerability to VF, and the highest stable DFs were located on the transmural surface which was not seen in controls. This indicates that the CHF substrate creates unique APD and DF characteristics.
authors.affiliation: Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N. Capitol, Ste. E400E, Indianapolis, IN, 46202, USA, theveret@iu.edu.
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Everett
authors.forename: George S
authors.initials: GS
authors.lastname: Hulley
authors.forename: Ken W
authors.initials: KW
authors.lastname: Lee
authors.forename: Roger
authors.initials: R
authors.lastname: Chang
authors.forename: Emily E
authors.initials: EE
authors.lastname: Wilson
authors.forename: Jeffrey E
authors.initials: JE
authors.lastname: Olgin
mesh_terms: D000818:Animals; D018780:Body Surface Potential Mapping / Q000379:methods; D004285:Dogs; D006329:Heart Conduction System / Q000503:physiopathology*; D006333:Heart Failure / Q000150:complications* / Q000503:physiopathology*; D008955:Models, Cardiovascular; D062211:Spatio-Temporal Analysis; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000503:physiopathology*; D020257:Ventricular Remodeling