Circulation, Vol 56, 566-571, Copyright © 1977 by American Heart Association
PC Gillette, MA Yeoman, CE Mullins and DG McNamara
In order to try to determine the mechanism of sudded death in patients
after surgical repair of tetralogy of Fallot, electrocardiographic,
intracardiac electrophysiologic, and clinical data of 51 children who had
postoperative intracardiac electrophysiologic studies were reviewed.
Ninety-four percent had developed right bundle branch block (RBBB) and 16
percent had additional left anterior hemiblock (LAH). Two had had transient
complete A-V block (CAVB) and one had permanent CAVB. Six had a first
degree A-V block and nine had premature ventricular contractions (PVC).
Nine patients were found to have prolonged intra- atrial conduction times,
four prolonged A-V nodal conduction, four prolonged His-Purkinje
conduction, and five prolonged corrected sinus node recovery times.
Patients with first degree A-V block or LAH did not have an increased
incidence of abnormalities on electrophysiologic study. No patient with
RBBB and LAH developed complete A-V block or died. Three of the nine
patients with PVCs died, one of intractable ventricular fibrillation and
two suddenly, presumably of dysrhythmia. All three had significant
congestive heart failure. Although late complete A-V block occurs and
should be watched for, ventricular dysrhythmias in patients with PVCs may
be the cause of most sudden deaths after tetralogy repair. We currently are
treating all of our postoperative tetralogy patients who have PVCs with
quinidine or propranolol.
ARTICLES
Sudden death after repair of tetralogy of Fallot. Electrocardiographic and electrophysiologic abnormalities
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