{'fraction_non_alphanumeric': 0.035506778566817304, 'fraction_numerical': 0.028728211749515817, 'mean_word_length': 5.593617021276596, 'pattern_counts': {'":': 0, '<': 4, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Ventricular Dysrhythmias after Congenital Heart Surgery: a Canine Model

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. The following “chronic” data were obtained in week 8 (p value for overall analysis of variance; values are mean ± SD): heart rate – 126 ± 16 beats/min (no significant difference between groups; all animals); right ventricular systolic pressure: control 26 ± 6 mm Hg, ventriculotomy 30 ± 3, right ventricular hypertension 65 ± 5, ventriculotomy and right ventricular hypertension 75 ± 18 (p < 0.001); right ventricular end diastolic: control 4 ± 1 mm Hg, ventriculotomy 4 ± 3, right ventricular hypertension 11 ± 5, ventriculotomy and right ventricular hypertension 16 ± 7 (p < 0.001); QRS duration: control 22 ± 5 ms, ventriculotomy 33 ± 7, right ventricular hypertension 44 ± 6, ventriculotomy and right ventricular hypertension 49 ± 4 (p < 0.01); right ventricular apex-base interval with ventricular pacing: control 20 ± 3 ms, ventriculotomy 34 ± 9, right ventricular hypertension 30 ± 5, ventriculotomy and right ventricular hypertension 31 ± 6 (p < 0.01). On 24-h 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 conclusion, in the dog with an otherwise normal right ventricle, ventriculotomy has no lasting dysrhythmogenic effect. Chronic right ventricle hypertrophy and dilation are associated with prolonged intraventricular conduction, spontaneous and induced dysrhythmias. Ventriculotomy may be additive in prolongation of conduction and production of dysrhythmias. The mechanism for the dysrhythmias may involve triggered activity.