Ventricular arrhythmia is common after repair of tetralogy of Fallot (TF) and may cause sudden death. To explore the mechanisms, ambulatory electrocardiographic monitoring and electrophysiologic studies were undertaken, without the use of provocative tests, in 22 patients 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 patients, to detect abnormalities of local depolarization and repolarization. Local RV electrograms were fractionated or delayed in 12 patients (55%) at 1 or more RV sites (septum in 7 patients, outflow in 7, free wall in 2 and apex 1 patient), reflecting disordered depolarization, but left ventricular recordings were normal in all. Ventricular arrhythmia out of hospital was more common (p less than 0.05) and more severe (p less than 0.01) in the patients with depolarization abnormalities than in those with normal electrographic findings. In contrast, there was no association between ventricular arrhythmia and conduction disturbances. Abnormalities of RV repolarization, consisting of low-frequency signals after the T wave, were observed in 17 patients (77%), but were not associated with arrhythmia. Thus, ventricular arrhythmia during daily life was associated with fractionated depolarization at multiple sites in the right ventricle. This suggests that there are widespread areas of RV myocardial damage that provide substrates for ventricular tachycardia.