Susceptibility to @entity955 and XXXX in the @entity3153 : role of the accessory pathway.

@entity1 @entity1165 @entity2224 @entity955 @entity299 @entity4032 @entity3153 @entity943
Clinical and electrophysiologic characteristics associated with spontaneous and inducible @entity955 and @entity1165 were assessed in 20 consecutive @entity1 with @entity3153 undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. @entity1 with spontaneous @entity955 were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 +/- 26 vs 303 +/- 109 msec). However, @entity1 with and without spontaneous @entity955 did not differ with respect to prevalence of structural @entity299 (3 of 11 vs 2 of 9), intra-atrial conduction time (34 +/- 10 vs 32 +/- 10 msec), or interatrial conduction time (86 +/- 21 vs 88 +/- 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to @entity955 . Among the 20 @entity1 , 10 to 35 beats of nonsustained @entity1165 (seven @entity1 ) or @entity2224 (three @entity1 ) were induced at electrophysiologic study with one to three programmed extrastimuli. Clinically, a @entity943 ( @entity2224 during @entity955 ) had occurred in only one of these @entity1 . The discordance of these observations was significant (p less than 0.01). @entity1 with and without inducible @entity943 were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 @entity1 . During a mean follow-up of 27 months, @entity955 recurred in two @entity1 with failed ablation procedures and in one @entity1 with @entity4032 (despite accessory pathway division) (p = 0.019 vs pre-ablation). @entity943 remained inducible in two @entity1 in whom accessory pathway ablation failed (p = 0.01 vs initial study). However, spontaneous @entity1165 did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible @entity955 and @entity1165 in @entity1 with @entity3153 and no @entity299 depends primarily on the existence of a functional accessory pathway. These susceptibilities are eliminated by interruption of accessory pathway conduction. @entity1165 remain infrequent spontaneous events in the @entity3153 . Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.
