The Journal of Thoracic and Cardiovascular Surgery
Volume 130, Issue 6 , Pages 1542-1548, December 2005

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

      Affiliations

    • Division of Cardiology at Children's Medical Center at Dallas and the University of Texas Southwestern Medical Center, Dallas, Tex
    • Corresponding Author InformationAddress for reprints: Ilana Zeltser, MD, Children's Medical Center at Dallas, The University of Texas Southwestern, 1935 Motor St, Dallas, TX 75235
  • ,
  • J. William Gaynor, MD

      Affiliations

    • Divisions of Cardiothoracic Surgery,
  • ,
  • Matus Petko, MD

      Affiliations

    • Divisions of Cardiothoracic Surgery,
  • ,
  • Richard J. Myung, MD

      Affiliations

    • Divisions of Cardiothoracic Surgery,
  • ,
  • Mariusz Birbach, MD

      Affiliations

    • Divisions of Cardiothoracic Surgery,
  • ,
  • Robert Waibel

      Affiliations

    • Divisions of Cardiothoracic Surgery,
  • ,
  • Richard F. Ittenbach, PhD

      Affiliations

    • Biostatistic and Data Management Core,
  • ,
  • Ronn E. Tanel, MD

      Affiliations

    • Cardiology at The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, Pa
  • ,
  • Victoria L. Vetter, MD

      Affiliations

    • Cardiology at The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, Pa
  • ,
  • Larry A. Rhodes, MD

      Affiliations

    • Cardiology at The Children's Hospital of Philadelphia and the University of Pennsylvania School of Medicine, Philadelphia, Pa

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.

CTSNet classification:  21, 24

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

 

 This study was supported in part by a postdoctoral research fellowship award (I.Z.) from the American Heart Association (award ID no. 0325738U). Additional support for this project was provided through the Daniel M. Tabas Endowed Chair in Pediatric Cardiothoracic Surgery (J.W.G.).

PII: S0022-5223(05)01405-4

doi:10.1016/j.jtcvs.2005.08.034

The Journal of Thoracic and Cardiovascular Surgery
Volume 130, Issue 6 , Pages 1542-1548, December 2005