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, J. William Gaynor, Matus Petko, Richard J. Myung, Mariusz Birbach, Robert Waibel, Richard F. Ittenbach, Ronn E. Tanel, Victoria L. Vetter, Larry A. Rhodes

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1542-1548
Number of pages7
JournalJournal of Thoracic and Cardiovascular Surgery
Volume130
Issue number6
DOIs
StatePublished - Dec 2005

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Tetralogy of Fallot
Cardiac Arrhythmias
Animal Models
Pressure
Ventricular Fibrillation
Ventricular Tachycardia
Pulmonary Artery
Lung
Blood Pressure
Atrial Pressure
Ventricular Pressure
Sudden Death
Tachycardia
Electric Stimulation
Cicatrix
Electrocardiography
Hemodynamics

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

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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. / Zeltser, Ilana; Gaynor, J. William; Petko, Matus; Myung, Richard J.; Birbach, Mariusz; Waibel, Robert; Ittenbach, Richard F.; Tanel, Ronn E.; Vetter, Victoria L.; Rhodes, Larry A.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 130, No. 6, 12.2005, p. 1542-1548.

Research output: Contribution to journalArticle

Zeltser, Ilana ; Gaynor, J. William ; Petko, Matus ; Myung, Richard J. ; Birbach, Mariusz ; Waibel, Robert ; Ittenbach, Richard F. ; Tanel, Ronn E. ; Vetter, Victoria L. ; Rhodes, Larry A. / 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. In: Journal of Thoracic and Cardiovascular Surgery. 2005 ; Vol. 130, No. 6. pp. 1542-1548.
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abstract = "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.",
author = "Ilana Zeltser and Gaynor, {J. William} and Matus Petko and Myung, {Richard J.} and Mariusz Birbach and Robert Waibel and Ittenbach, {Richard F.} and Tanel, {Ronn E.} and Vetter, {Victoria L.} and Rhodes, {Larry A.}",
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T1 - The roles of chronic pressure and volume overload states in induction of arrhythmias

T2 - An animal model of physiologic sequelae after repair of tetralogy of Fallot

AU - Zeltser, Ilana

AU - Gaynor, J. William

AU - Petko, Matus

AU - Myung, Richard J.

AU - Birbach, Mariusz

AU - Waibel, Robert

AU - Ittenbach, Richard F.

AU - Tanel, Ronn E.

AU - Vetter, Victoria L.

AU - Rhodes, Larry A.

PY - 2005/12

Y1 - 2005/12

N2 - 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.

AB - 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.

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