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J Thorac Cardiovasc Surg 2005;130:1542-1548
© 2005 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease

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

Ilana Zeltser, MD a , * , J. William Gaynor, MD b , Matus Petko, MD b , Richard J. Myung, MD b , Mariusz Birbach, MD b , Robert Waibel b , Richard F. Ittenbach, PhD c , Ronn E. Tanel, MD d , Victoria L. Vetter, MD d , Larry A. Rhodes, MD d

a Division of Cardiology at Children's Medical Center at Dallas and the University of Texas Southwestern Medical Center, Dallas, Tex
b Divisions of Cardiothoracic Surgery,
c Biostatistic and Data Management Core,
d Cardiology at The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, Pa

* Address for reprints: Ilana Zeltser, MD, Children's Medical Center at Dallas, The University of Texas Southwestern, 1935 Motor St, Dallas, TX 75235 (Email: Ilana.zeltser{at}childrens.com).

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.

Abbreviations and Acronyms AA = atrial arrhythmia; ECG = electrocardiogram; OR = odds ratio; PAB = pulmonary artery band; PR = pulmonary regurgitation; PV = pulmonary valvotomy; RV = right ventricular; SCD = sudden cardiac death; TOF = tetralogy of Fallot; VF = ventricular fibrillation; VT = ventricular tachycardia




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