Histopathologic correlates of inducible XXXX in two experimental @entity235 models of @entity583 .

@entity1164 @entity1165 @entity235 @entity1188 @entity453 @entity3980 @entity583
@entity1165 are the leading cause of @entity1164 . Determination of the substrates conducive to the initiation of @entity1165 remains an important clinical goal. The purpose of this study was to correlate electrophysiologic and histopathologic parameters conducive to the initiation of sustained @entity1165 using programmed electrical stimulation in two @entity235 models of @entity583 . Histopathologic correlates included: @entity1188 pattern (heterogeneous vs. homogeneous morphology), distribution (viable epicardial or endocardial rim), and size. Twenty-one adult @entity235 were randomly divided into two groups: (1) 12 @entity235 underwent two-stage, 2-hour occlusion of the proximal @entity453 ( @entity3980 ); and (2) nine animals had permanent, complete occlusion of the @entity3980 with latex embolization. Using programmed ventricular pacing with two premature ventricular extrastimuli, initiation of @entity1165 was attempted at both 1 and 2 weeks after @entity1188 with the chest closed and opened each time. Electrophysiologic evaluation of the @entity1188 type correlated significantly with the histologic morphology of the @entity1188 (p less than 0.001), the presence of a viable epicardial rim was an extremely important discriminating variable for ability to induce sustained @entity1165 (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). @entity1188 size alone was only marginally related to @entity1165 inducibility (p = 0.08). Non-uniform @entity1188 were more conducive to the initiation of sustained @entity1165 (p = 0.025). The presence of a large, non-uniform @entity1188 was the best overall discrimination variable for inducibility (p = 0.0002). Thus, in these experimental models, specific @entity1188 correlate significantly with susceptibility to inducible sustained @entity1165 .
