The Reopened Ventricular Septal Defect

SJNCE the first open intracardiac repair of interventricular septal defects and tetralogy of Fallot,1 2 rapid progress has been made in operative technics and in extracorporeal perfusion technology. Operative risk has steadily declined, and recent communications indicate that in ventricular septal defects uncomplicated by pulmonary hypertention the mortality rate is approximately 2 per cent.3 5 In tetralogy of Fallot the mortality risk is in the vicinity of 12 to 16 per cent,6' 7 but this incidence is also diminish57 ingZ,.5 7 The results after successful closure of a ventricular septal defect and the correction of Fallot's tetralogy are gratifyin.4, 7, 8 Symptoms disappear or are markedly alleviated. The precordiumn becomes quiet, and the typical murmurs cease or are dramatically modified. Cyanosis disappears. Radiographically, there may be a reduction in heart size, and the plethora of the lung fields regresses. It soon became apparent, however, that the therapeutic benefits of complete closure were not always achieved because of disruption of the repair, and the technic was refined.9' 10 Although the first disruptions were reported in attempted closure of uncomplicated ventricular septal defects and continue to be described in more recent reports pertaining to the treatment of this lesion,1-13 it has been the experience in this laboratory that the per-