Surgical treatment of ventricular tachycardia after surgical repair of tetralogy of Fallot. Relation between intraoperative mapping and histological findings.

Abstract

BACKGROUND The mechanism of ventricular tachycardia (VT) after correction of tetralogy of Fallot (TF) is poorly understood. The purpose of this study was to examine the histopathology of the arrhythmogenic area detected by intraoperative mapping. METHODS AND RESULTS The patients were three men who underwent radical surgery for TF at age 3, 3, or 5 years, respectively. VT developed at 8, 9, or 11 years, respectively, after surgery, and shock developed during VT in every case. The ECG revealed monomorphic VT in two cases and polymorphic VT in one case. Induction of VT resulted in a wide left-axis deviation-pattern QRS with cycle lengths varying between 260 and 330 milliseconds. The VT origin was identified at the right ventricular outflow tract (RVOT). A radical operation was performed with the patient under cardiopulmonary bypass. On epicardial mapping, delayed activation of the RVOT was recorded during sinus rhythm, and clockwise circus movement of the macroreentry current during VT on the right ventricular free wall was documented in each case. The VTs were treated successfully by surgical resection and cryoablation of the myocardium. In every patient, histology of the myocardial specimens showed degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets. These lesions corresponded anatomically to the area of myocardium in which delayed activation was evident during epicardial mapping. CONCLUSIONS The results of this study indicate that patients with VT after radical correction of the TF have abnormal histopathological findings at the site of the prior right ventriculotomy scar. These lesions were noted within the region of delayed activation found during epicardial mapping and were found to be a part of the reentrant circuit.