To examine the possible mechanisms of ventricular dysrhythmias in the presence of right ventricular hypertension and following ventriculotomy we instrumented 6-month-oldpuppies. 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 awakeand 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 Hgventriculotomy 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 ± 7right 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 ventricularhypertension 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 ventricularhypertension animals and 6 of 6 ventriculotomy and right ventricular hypertension animals. At electrophysiology study no ventricular dysrhythmias were induced in the control orventriculotomy animals but in the right ventricular hypertension group 5 o 6had acceleratedventricular escape and 2 of 6 had induced ventricular dysrhythmias inthe ventriculotomy and right ventricular hypertension group 5 of 6 had accelerated ventricular escape and thesame 5 of 6 had induced ventricular dysrhythmias including two with sustained ventriculartachycardia. In four animals the coupling interval to the dysrhythmiawas 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 intraventricularconduction spontaneous and induced dysrhythmias. Ventriculotomymay be additive in prolongation of conduction and production of dysrhythmias. The mechanismforthe dysrhythmias may involve triggered activity. © 1984 International Pediatrics Research Foundation, Inc.
CITATION STYLE
Garson, A. (1984). Ventricular dysrhythmias after congenital heart surgery: A canine model. Pediatric Research, 18(11), 1112–1120. https://doi.org/10.1203/00006450-198411000-00012
Mendeley helps you to discover research relevant for your work.