ABSTRACT. To examine the possible mechanisms of ventricular dysrhythmias in the presence of right ventricular hypertension and following ventriculotomy, we instrumented 6-month-old puppies. There were four groups: 1) six animals served as controls (instrumentation only); 2) six animals underwent ventriculotomy only; 3) six animals underwent pulmonary artery banding with a pneumatic vessel occluder to produce right ventricular hypertension; 4) six animals had both ventriculotomy and right ventricular hypertension. Each week for 8 wk, 24-h electrocardiograms and electrophysiologic studies were performed with the animals awake and unsedated. We attempted to induce ventricular dysrhythmias with premature extrastimuli, rapid pacing, isoproterenol, and vagal stimulation. electrocardiogram, there were no chronic spontaneous ventricular dysrhythmias in any control or ventriculotomy animal, but were present in 5 of 6 right ventricular hypertension animals and 6 of 6 ventriculotomy and right ventricular hypertension animals. At electrophysiology study, no ventricular dysrhythmias were induced in the control or ventriculotomy animals but in the right ventricular hypertension group, 5 of 6 had accelerated ventricular escape and 2 of 6 had induced ventricular dysrhythmias; in the ventriculotomy and right ventricular hypertension group, 5 of 6 had accelerated ventricular escape and the same 5 of 6 had induced ventricular dysrhythmias including two with sustained ventricular tachycardia. In four animals, the coupling interval to the dysrhythmia was dependent upon the preceding cycle, a feature of triggered activity. In In a long term follow-up of patients who had had intracardiac repair of tetralogy of Fallot, 10.3% had premature ventricular contractions found on routine electrocardiogram taken more than 1 month postoperatively, and 38% of those with premature ventricular contractions died suddenly between 3 months and 10 years postoperatively. Of the patients with premature ventricular contractions, 88% had a postoperative right ventricular systolic pressure of 60 mm Hg or more, and all had a right ventricular end diastolic pressure of 8 mm Hg or more. All of the patients who died suddenly had prior premature ventricular contractions, a right ventricular systolic pressure of at least 70 mm Hg, and a right ventricular end diastolic pressure of at least 10 mm Hg (1 1). These data have been confirmed by other investigators, and have been extended to other patients with right ventricular outflow obstruction and interventricular communication (7,9,10). On the basis of these findings, we have hypothesized a relationship between elevated right ventricular systolic pressure and end diastolic pressure, ventricular dysrhythmias, and sudden death (1 3). This may not be the only mechanism for late sudden death after tetralogy repair. Some patients may die from late complete AV block (37). However, two of these patients that later died suddenly had complete information regarding hemodynamics, dysrhythmia, and electrophysiology. Because of...