Ventricular Dysrhythmias after Congenital Heart Surgery: a Canine Model

Abstract

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...

Right Ventricular Myocardial Responses to Chronic Pulmonary Regurgitation in Lambs: Disturbances of Activation and Conduction

“…Our observations also help to delineate the contribution made by PR to arrhythmia. Although a previous animal model of chronic RV outflow tract obstruction and ventriculotomy (34) suggested that triggered mechanisms may be the predominant mechanism of tachycardia in patients after congenital heart surgery, the presence of frequent and complex automatic ventricular activity failed to predict clinically important ventricular arrhythmia or sudden death in at least two large clinical studies (4,35). Our data emphasize the potential contribution of chronic PR to the development of reentry arrhythmia.…”

Delayed enhancement imaging in a contemporary patient cohort following correction of tetralogy of Fallot

“…[5][6][7][8][9] Former studies suggest that fibrosis could be the cause of right ventricular dysfunction and arrhythmias, 10,11 and myocardial fibrosis has been demonstrated in patients after repair and in animal models of tetralogy of Fallot. 12,13 Delayed enhancement cardiac MRI has been established as a reliable tool to visualise myocardial necrosis and scar in clinical practice with modern phasesensitive inversion recovery sequences providing consistently high-quality images for both ventricles. 14 The aim of this study was to reliably detect or exclude myocardial scars of the right and left ventricles after complete repair of tetralogy of Fallot using phase-sensitive inversion recovery delayed enhancement imaging.…”

Magnetocardiographic and Magnetic Resonance Imaging for Noninvasive Localization of Ventricular Arrhythmia Origin in a Model of Nonischemic Cardiomyopathy

“…[9][10][11][12][13][14][15][16] Several potential substrates and possible mechanisms for ventricular arrhythmia exist, such as hypertrophy, dilatation, delayed intraventricular conduction due to bundle branch block, and surgical scars. 11,13,[17][18][19][20][21][22][23][24][25][26][27][28][29][30][31] VEBs and nonsustained ventricular tachycardia occur in up to 50% of patients 9,12,15,16,[32][33][34][35] and a correlation with prognosis has been implied in some, [10][11][12][13][14][15]32 but not in other reports. 16,19,33 Ventricular arrhythmias have been approached by invasive electrophysiological techniques with [25][26][27]36,37 or wi...…”