@entity11808 for treatment of XXXX associated with the @entity3153 .

@entity1 @entity1165 @entity1163 @entity11808 @entity955 @entity16992 @entity4710 @entity3153
Thirty-three @entity1 with @entity4710 associated with the @entity3153 were treated with @entity11808 for 26 months (mean). @entity11808 at a mean dosage of 187 mg/day abolished or markedly decreased episodes of palpitations in 24 of 33 (73%), and no @entity1 had @entity1163 or required cardioversion while receiving the drug. @entity11808 was well tolerated and was discontinued in only 2 @entity1 because of side effects (6%). Only 1 @entity1 (3%) had a proarrhythmic effect while taking @entity11808 ( @entity1165 ). Fourteen of 16 @entity1 (88%) with @entity955 continue receiving @entity11808 . Episodes of palpitations have been abolished or markedly decreased and no @entity1 has had @entity1163 or required cardioversion. All 14 of these @entity1 had either anterograde block in the accessory pathway during @entity955 or greater than or equal to 75 ms increase in the shortest R to R interval formed by 2 preexcited QRS complexes. @entity11808 prolonged refractory periods of the atrial (p = 0.064) and ventricular (p = 0.061) muscle. It prolonged the cycle length at which 1:1 conduction of the accessory pathway in both the anterograde and retrograde directions occurred (both, p less than 0.001). Induction of @entity16992 ( @entity16992 ) was prevented in 36% of @entity1 at repeat electrophysiologic study. The @entity16992 cycle length increased 112 ms (mean, p less than 0.001) in those @entity1 in whom @entity16992 was still inducible. The loss of delta waves recorded with the 12-lead scalar electrocardiogram during @entity11808 therapy was a significant predictor of anterograde accessory pathway block (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
