The roles of chronic pressure and volume overload states in induction of arrhythmias: an animal model of physiologic sequelae after repair of tetralogy of Fallot.
OBJECTIVE
Sudden death occurs in as many as 8% of patients after repair of tetralogy of Fallot and has been attributed to arrhythmias. The purpose of this study was to establish an animal model to evaluate the individual contribution of different physiologic sequelae after tetralogy of Fallot repair in the development of late-onset arrhythmias.


METHODS
Forty-nine piglets were divided into 5 groups: (1) pulmonary artery band; (2) pulmonary valvotomy; (3) pulmonary artery band plus pulmonary valvotomy; (4) infundibular scar; and (5) age-matched control animals. Baseline and follow-up electrocardiograms were obtained and recorded, as well as changes in QRS duration. A total of 45 animals underwent hemodynamic evaluation and programmed electrical stimulation at 5.6 months postoperatively.


RESULTS
Sustained ventricular tachyarrhythmias (ventricular tachycardia/ventricular fibrillation) were induced in 31.1%, and atrial arrhythmias were induced in 33.3%. The pulmonary valvotomy group was 30 times more likely to evidence arrhythmias than control animals for sustained ventricular tachycardia/ventricular fibrillation, as well as atrial arrhythmias (P = .01). The pulmonary artery band group was 15 times more likely to evidence atrial arrhythmias than control animals (P = .02). Prolonged QRS duration was predictive of inducibility of both atrial arrhythmias (P < .01) and sustained ventricular tachycardia/ventricular fibrillation (P = .01). Mean right atrial (P = .01) and capillary wedge (P = .01) pressures predicted atrial arrhythmia inducibility. Right ventricular end-diastolic pressure predicted atrial arrhythmia (P= .01) and sustained ventricular tachycardia/ventricular fibrillation inducibility (P = .05). Right ventricular systolic pressure did not predict inducibility of either atrial arrhythmias (P = .10) or sustained ventricular tachycardia/ventricular fibrillation (P = .94).


CONCLUSIONS
Chronic right ventricular volume overload resulted in an increased incidence of inducible ventricular and atrial arrhythmias.
Zeltser
Ilana
I
Division of Cardiology at Children's Medical Center at Dallas and the University of Texas Southwestern Medical Center, Dallas, Tex 75235, USA. Ilana.zeltser@childrens.com
Gaynor
J William
JW
Petko
Matus
M
Myung
Richard J
RJ
Birbach
Mariusz
M
Waibel
Robert
R
Ittenbach
Richard F
RF
Tanel
Ronn E
RE
Vetter
Victoria L
VL
Rhodes
Larry A
LA
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D002921:Cicatrix / Q000150:complications; D004108:Dilatation, Pathologic / Q000150:complications; D004195:Disease Models, Animal; D006331:Heart Diseases / Q000150:complications; D006352:Heart Ventricles / Q000473:pathology; D006976:Hypertension, Pulmonary / Q000150:complications; D017380:Hypertrophy, Right Ventricular / Q000150:complications; D011183:Postoperative Complications / Q000209:etiology*; D013552:Swine; D013771:Tetralogy of Fallot / Q000503:physiopathology* / Q000601:surgery*