title: Incidence, evolution, and spatial distribution of functional reentry during ventricular fibrillation in pigs.
abstract: Functional reentry has been hypothesized to be an underlying mechanism of ventricular fibrillation (VF); however, its contribution to activation patterns during fully developed VF is unclear. We applied new quantitative pattern analysis techniques to mapping data acquired from a 21 x 24 unipolar electrode array (2-mm spacing) located on the ventricular epicardium of 7 open-chest, unsupported pigs. Data epochs 4 seconds long beginning 1, 10, 20, 30, and 40 seconds after electrical induction were analyzed. Reentrant circuits were automatically identified and quantified. We found that 2.3% of activation pathways could unambiguously be classified as reentrant. From scaling analysis, an additional 28% of the pathways may also have been reentrant. Reentry was short-lived with 1.5+/-1.5 (mean+/-SD) complete cycles per circuit. The fraction of reentrant pathways, number of cycles per circuit, cycle duration, and area and perimeter of the cores all increased significantly as VF progressed. Core drift speed decreased significantly. Neither the orientation of the cores nor the direction of drift was well predicted by the epicardial fiber orientation (r2=0.108 and 0.138, respectively, by linear regression). Reentrant circuits were clustered in regions of the epicardium. We conclude the following: (1) Epicardial reentry is relatively uncommon and short-lived during VF, suggesting either that sustained reentry is transmural or that mechanisms governing sustained reentry are relatively unimportant to the dynamics of VF. (2) Reentrant circuits become more common, larger, and longer-lived as VF progresses, which may explain a recently observed increase in VF organization during the first minute of VF. (3) The conditions necessary to induce and sustain reentry are distributed nonuniformly.
authors.affiliation: Department of Biomedical Engineering, University of Alabama at Birmingham, 35294, USA. jmr@crml.uab.edu
authors.forename: J M
authors.initials: JM
authors.lastname: Rogers
authors.forename: J
authors.initials: J
authors.lastname: Huang
authors.forename: W M
authors.initials: WM
authors.lastname: Smith
authors.forename: R E
authors.initials: RE
authors.lastname: Ideker
mesh_terms: D000818:Animals; D006329:Heart Conduction System / Q000503:physiopathology*; D013552:Swine; D014693:Ventricular Fibrillation / Q000503:physiopathology*