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Newly created animal model of human postoperative junctional ectopic tachycardia
Jeffrey P Moak1, Marco A Mercader, Dingchao He
1Division of Cardiology, Children's National Medical Center, Washington, DC 20010, USA. jmoak@childrensnational.org
Insights
This study developed a new animal model for junctional ectopic tachycardia (JET) after heart surgery. The model mimics postoperative JET by inducing sinus node dysfunction and using specific interventions.
Area of Science:
- Cardiovascular Surgery
- Pediatric Cardiology
- Cardiac Electrophysiology
Background:
- Junctional ectopic tachycardia (JET) is a complication following pediatric open heart surgery.
- Risk factors for JET include young age, extended cardiopulmonary bypass, and inotropic agents.
- Postoperative JET typically arises early, linked to sinus node dysfunction and originating from the atrioventricular node or conduction system.
Purpose of the Study:
- To establish a reproducible animal model for studying postoperative junctional ectopic tachycardia.
- To investigate the mechanisms and triggers of experimental JET in a controlled setting.
Main Methods:
- Eleven juvenile pigs underwent open heart surgery with implanted atrial and ventricular electrodes.
- Sinus node dysfunction was induced via clamp crushing, radiofrequency ablation, or sinus node removal.
- Junctional ectopic tachycardia and fascicular tachycardia were initiated using slow atrioventricular nodal pathway ablation and/or digoxin administration.
Main Results:
- Successful induction of sinus node dysfunction was achieved in 8 out of 9 pigs.
- Junctional ectopic tachycardia (mean rate 171 ± 32 bpm) occurred in 8/9 pigs, and fascicular tachycardia (mean rate 187 ± 39 bpm) in 9/9 pigs.
- Conduction system origin was confirmed through His and right bundle recordings.
Conclusions:
- Experimental JET and fascicular tachycardia can be induced in the setting of sinus node dysfunction, prolonged cardiopulmonary bypass, and enhanced conduction system automaticity.
- Conduction system automaticity resulted from physical injury or augmented transient inward currents (isoproterenol, digoxin).
- This animal model provides a basis for evaluating novel treatments for postoperative JET.
Objective:
Junctional ectopic tachycardia complicates the postoperative recovery from open heart surgery in children. The reported risk factors include younger age, prolonged cardiopulmonary bypass times, and administration of inotropic agents. Junctional ectopic tachycardia occurs early after open heart surgery, in the setting of relative postoperative sinus node dysfunction, and exhibits QRS morphology consistent with an origin from the atrioventricular node or proximal conduction system. Our goal was to develop a reproducible animal model for postoperative junctional ectopic tachycardia.
Methods:
Eleven pigs, aged 2 to 4 months, underwent open heart surgery after induction of general anesthesia. Electrodes were sewn to the left atrium and right ventricle.
Results:
Sinus node dysfunction was created using clamp crushing without or with radiofrequency ablation (successful in 1 of 5 pigs) or sinus node removal (successful in 4 of 4). After prolonged cardiopulmonary bypass (>120 minutes) alone and with isoproterenol infusion, no spontaneous junctional ectopic tachycardia developed. Junctional ectopic tachycardia or fascicular tachycardia could be initiated after either slow atrioventricular nodal pathway ablation and/or digoxin administration. Junctional ectopic tachycardia occurred in 8 of 9 pigs (mean ventricular rate, 171 ± 32 bpm), and fascicular tachycardia occurred in 9 of 9 pigs (mean ventricular rate, 187 ± 39 bpm). His and right bundle recordings confirmed the conduction system origin.
Conclusions:
Experimental junctional ectopic tachycardia or fascicular tachycardia can occur in the intraoperative setting of sinus node dysfunction, prolonged cardiopulmonary bypass, and enhanced conduction system automaticity. Conduction system automaticity occurred after either physical injury (ablation or tricuspid valve stretch) or measures to augment the transient inward current of the conduction system (isoproterenol and digoxin). This animal model can serve as the basis to assess new treatments of postoperative junctional ectopic tachycardia.
