@entity854 of right ventricular depolarization after repair of tetralogy of Fallot: a basis for XXXX .

@entity1 @entity296 @entity1165 @entity944 @entity854 @entity943
@entity943 is common after repair of tetralogy of Fallot (TF) and may cause @entity944 . To explore the mechanisms, ambulatory electrocardiographic monitoring and electrophysiologic studies were undertaken, without the use of provocative tests, in 22 @entity1 5 to 24 years (mean 13) after repair. His-Purkinje and right ventricular (RV) apical activation times were measured to assess conduction. Endocardial mapping of the right ventricle was performed, with additional recordings from the left ventricle in 10 @entity1 , to detect abnormalities of local depolarization and repolarization. Local RV electrograms were fractionated or delayed in 12 @entity1 (55%) at 1 or more RV sites (septum in 7 @entity1 , outflow in 7, free wall in 2 and apex 1 @entity1 ), reflecting disordered depolarization, but left ventricular recordings were normal in all. @entity943 out of hospital was more common (p less than 0.05) and more severe (p less than 0.01) in the @entity1 with @entity854 than in those with normal electrographic findings. In contrast, there was no association between @entity943 and conduction disturbances. Abnormalities of RV repolarization, consisting of low-frequency signals after the T wave, were observed in 17 @entity1 (77%), but were not associated with @entity943 . Thus, @entity943 during daily life was associated with fractionated depolarization at multiple sites in the right ventricle. This suggests that there are widespread areas of RV @entity296 that provide substrates for @entity1165 .
