title: Intramural activation during early human ventricular fibrillation.
abstract: BACKGROUND
  We investigated patterns of intramural activation in early human ventricular fibrillation (VF) and hypothesized that intramural reentry colocalizes to sites with increased intramural fibrosis.
  
  
  RESULTS
  Thirteen human Langendorff hearts were used for this study. Twenty-five plunge needles (4 unipoles/needle) were used to map 100 intramural sites. For the global mapping component, 11 20-s episodes of early VF were studied in 6 hearts. Simultaneous activation of all 4 electrodes was the most common pattern observed in 48.7% of needles, followed by an endocardial-to-epicardial activation pattern (9.8% of needles) and epicardial-to-endocardial activation pattern (5.5% of needles); 19.3% of needles had nonuniform multidirectional patterns. In 2 orthogonal planes, 1 parallel and 1 perpendicular to the epicardium and endocardium, reentry was detected in 14.3% of beats at any 1 level, and 5.8% of these were transmural. Simultaneous mapping of the epicardium and endocardium in 5 hearts detected concurrently rotating rotors with similar chirality and cycle length, suggesting the presence of transmural scroll waves (n=6), which was confirmed by high-resolution fixed-space mapping in 2 of those hearts plus 1 additional heart. Transmural optical mapping in 1 additional heart confirmed simultaneous epicardial and endocardial activation. Histopathology revealed greater fibrosis at sites of reentry compared to areas without (53.3±11.9% versus 27.5±2.4%, P=0.02).
  
  
  CONCLUSIONS
  Intramural activation patterns suggest that early human VF does not organize as multiple reentrant wavefronts but is best explained by transmural scroll wave activation. Intramural reentry localizes to regions of greater intramural fibrosis.
authors.affiliation: The Hull Family Cardiac Fibrillation Management Laboratory, University Health Network, Toronto, Ontario, Canada.
authors.forename: Krishnakumar
authors.initials: K
authors.lastname: Nair
authors.forename: Karthikeyan
authors.initials: K
authors.lastname: Umapathy
authors.forename: Talha
authors.initials: T
authors.lastname: Farid
authors.forename: Stephane
authors.initials: S
authors.lastname: Masse
authors.forename: Erin
authors.initials: E
authors.lastname: Mueller
authors.forename: Radhika V
authors.initials: RV
authors.lastname: Sivanandan
authors.forename: Kwaku
authors.initials: K
authors.lastname: Poku
authors.forename: Vivek
authors.initials: V
authors.lastname: Rao
authors.forename: Vidhya
authors.initials: V
authors.lastname: Nair
authors.forename: Jagdish
authors.initials: J
authors.lastname: Butany
authors.forename: Raymond E
authors.initials: RE
authors.lastname: Ideker
authors.forename: Kumaraswamy
authors.initials: K
authors.lastname: Nanthakumar
mesh_terms: D000328:Adult; D000368:Aged; D009202:Cardiomyopathies / Q000601:surgery; D004566:Electrodes; D004699:Endocardium / Q000473:pathology / Q000503:physiopathology*; D056149:Epicardial Mapping; D005260:Female; D005355:Fibrosis; D006329:Heart Conduction System / Q000503:physiopathology*; D016027:Heart Transplantation; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D010496:Pericardium / Q000473:pathology / Q000503:physiopathology*; D014693:Ventricular Fibrillation / Q000503:physiopathology*