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Junctional Ectopic Tachycardia Treatment & Management

  • Author: M Silvana Horenstein, MD; Chief Editor: Stuart Berger, MD  more...
 
Updated: Feb 11, 2014
 

Medical Care

Congenital junctional ectopic tachycardia (JET) is usually initially treated with antiarrhythmic therapy, with the choice of medication guided by the degree of coexisting ventricular dysfunction. The most appropriate management of asymptomatic infants with "slow" JET (ie, 150 beats per minute [bpm]) is debatable. However, these asymptomatic patients should have close monitoring.

Numerous therapeutic options have been used for the treatment of postoperative JET, including the following:

  • Some propose that management of symptomatic infants with slow JET should consist of digoxin to control symptoms of cardiac failure and antiarrhythmic drugs to control the ventricular rate of the arrhythmia. However, caution should be used because development of ventricular fibrillation or faster tachycardia (≤400 bpm) during progressive digoxin loading has been described in patients with congenital JET and severe cardiac failure.
  • Propafenone has also been effective in preventing or controlling JET in some neonates, especially neonates with slower ventricular rates (approximately 170 bpm).
  • Amiodarone may successfully control ventricular rate. Furthermore, the combination of amiodarone and a class Ic antiarrhythmic drug can be used to reduce the dose of amiodarone. A multicenter study reported that success of intravenous amiodarone is dose-related.[9] However, so are its adverse effects. Therefore, the dose-related risks should be taken into account when treating children with incessant arrhythmias. It has been reported that prophylactic use of amiodarone being started in the operating room at the time of rewarming during cardiopulmonary bypass decreases the incidence of JET.[10]
  • True drug-refractory JET is very rare. Therefore, in patients who fail to respond to a single drug regimen, a second antiarrhythmic agent with different electrophysiological effects may be added.
  • Controlled hypothermia has been relatively effective in reducing JET rate in patients in the immediate postoperative period.[11, 12] These patients are often intubated and can be effectively paralyzed, sedated, and cooled. For refractory cases, adding procainamide has been effective.[13] Other traditional approaches include increase of ventricular preload and reduction of inotropic agents (which are also usually chronotropic) as much as possible.
  • The use of atrial or AV sequential pacing can help to restore AV sequence and cardiac output once the JET rate is reduced.
  • Multiple antiarrhythmic agents have been used and are considered somewhat effective in postoperative JET.
  • Occasionally, atrial high-rate pacing to the point of 2:1 AV block can provide a controlled ventricular response while continuing to suppress the JET focus. This finding suggests a relatively high insertion site of the JET focus into the AV conduction system.
  • Ventricular paired pacing, with or without additional atrial pacing, has been used in rare cases when patients have not responded to other therapies. This technique is potentially dangerous and requires essentially constant monitoring and adjustment by personnel who are extremely familiar with electrophysiologic procedures. During ventricular paired pacing, electrolytes and antiarrhythmic medications should be administered by constant infusions only.
  • A small-case series advocates for radiofrequency catheter ablation for JET if antiarrhythmic drug therapy has failed.[14] Success was safely achieved by plotting the entire His-bundle using a modern navigation system that would permit marking the spot of earliest retrograde conduction during tachycardia, and, later, empirically ablating that spot during sinus rhythm.
  • A study suggested that supplementation with magnesium sulfate during cardiopulmonary bypass reduces the incidence of postoperative JET.[15]
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Surgical Care

The primary functions of surgical care in postoperative JET are to correct major residual defects that may be contributing to morbidity, to ensure that atrial-based pacing can be achieved, and to provide extracorporeal life support (ie, extracorporeal membrane oxygenation [ECMO]) if required.

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Contributor Information and Disclosures
Author

M Silvana Horenstein, MD Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Robert Murray Hamilton, MD, MSc, FRCPC Electrophysiologist, Senior Associate Scientist, Physiology and Experimental Medicine, Labatt Family Heart Centre; Professor, Department of Pediatrics, University of Toronto Faculty of Medicine

Robert Murray Hamilton, MD, MSc, FRCPC is a member of the following medical societies: American Heart Association, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Medical Protective Association, Heart Rhythm Society, Canadian Cardiovascular Society, Cardiac Electrophysiology Society, Pediatric and Congenital Electrophysiology Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hugh D Allen, MD Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, Western Society for Pediatric Research, American College of Cardiology, American Heart Association, American Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD Medical Director of The Heart Center, Children's Hospital of Wisconsin; Associate Professor, Department of Pediatrics, Section of Pediatric Cardiology, Medical College of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

Charles I Berul, MD Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, Heart Rhythm Society, Cardiac Electrophysiology Society, Pediatric and Congenital Electrophysiology Society, American College of Cardiology, American Heart Association, Society for Pediatric Research

Disclosure: Received grant/research funds from Medtronic for consulting.

References
  1. Dodge-Khatami A, Miller OI, Anderson RH, et al. Surgical substrates of postoperative junctional ectopic tachycardia in congenital heart defects. J Thorac Cardiovasc Surg. 2002 Apr. 123(4):624-30. [Medline].

  2. Zampi JD, Hirsch JC, Gurney JG, Donohue JE, Yu S, LaPage MJ, et al. Junctional ectopic tachycardia after infant heart surgery: incidence and outcomes. Pediatr Cardiol. 2012 Dec. 33(8):1362-9. [Medline].

  3. Liu CF, Ip JE, Lin AC, Lerman BB. Mechanistic Heterogeneity of Junctional Ectopic Tachycardia in Adults. Pacing Clin Electrophysiol. 2011 Sep 28. [Medline].

  4. Hoffman TM, Bush DM, Wernovsky G, et al. Postoperative junctional ectopic tachycardia in children: incidence, risk factors, and treatment. Ann Thorac Surg. 2002 Nov. 74(5):1607-11. [Medline].

  5. Andreasen JB, Johnsen SP, Ravn HB. Junctional ectopic tachycardia after surgery for congenital heart disease in children. Intensive Care Med. 2008 May. 34(5):895-902. [Medline].

  6. Zhao H, Cuneo BF, Strasburger JF, Huhta JC, Gotteiner NL, Wakai RT. Electrophysiological characteristics of fetal atrioventricular block. J Am Coll Cardiol. 2008 Jan 1. 51(1):77-84. [Medline].

  7. Borgman KY, Smith AH, Owen JP, Fish FA, Kannankeril PJ. A genetic contribution to risk for postoperative junctional ectopic tachycardia in children undergoing surgery for congenital heart disease. Heart Rhythm. 2011 Dec. 8(12):1900-4. [Medline]. [Full Text].

  8. Imamura M, Dossey AM, Garcia X, Shinkawa T, Jaquiss RD. Prophylactic amiodarone reduces junctional ectopic tachycardia after tetralogy of Fallot repair. J Thorac Cardiovasc Surg. 2011 Oct 27. [Medline].

  9. Saul JP, Scott WA, Brown S, et al. Intravenous amiodarone for incessant tachyarrhythmias in children: a randomized, double-blind, antiarrhythmic drug trial. Circulation. 2005 Nov 29. 112(22):3470-7. [Medline].

  10. Imamura M, Dossey AM, Garcia X, Shinkawa T, Jaquiss RD. Prophylactic amiodarone reduces junctional ectopic tachycardia after tetralogy of Fallot repair. J Thorac Cardiovasc Surg. 2012 Jan. 143(1):152-6. [Medline].

  11. Guccione P, Di Carlo D, Papa M, et al. [Hypothermia treatment of junctional ectopic tachycardia after surgical repair of congenital heart defects]. G Ital Cardiol. 1990 May. 20(5):415-8. [Medline].

  12. Pfammatter JP, Paul T, Ziemer G, Kallfelz HC. Successful management of junctional tachycardia by hypothermia after cardiac operations in infants. Ann Thorac Surg. 1995 Sep. 60(3):556-60. [Medline].

  13. Walsh EP, Saul JP, Sholler GF, et al. Evaluation of a staged treatment protocol for rapid automatic junctional tachycardia after operation for congenital heart disease. J Am Coll Cardiol. 1997 Apr. 29(5):1046-53. [Medline].

  14. Wu MH, Lin JL, Chang YC. Catheter ablation of junctional ectopic tachycardia by guarded low dose radiofrequency energy application. Pacing Clin Electrophysiol. 1996 Nov. 19(11 Pt 1):1655-8. [Medline].

  15. Manrique AM, Arroyo M, Lin Y, El Khoudary SR, Colvin E, Lichtenstein S, et al. Magnesium supplementation during cardiopulmonary bypass to prevent junctional ectopic tachycardia after pediatric cardiac surgery: a randomized controlled study. J Thorac Cardiovasc Surg. 2010 Jan. 139(1):162-169.e2. [Medline].

  16. Emmel M, Sreeram N, Brockmeier K. Catheter ablation of junctional ectopic tachycardia in children, with preservation of atrioventricular conduction. Z Kardiol. 2005 Apr. 94(4):280-6. [Medline].

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Lead II rhythm strip of a surface ECG from a patient with postoperative JET. Atrial activity (P) is marked with blue lines and ventricular depolarization (QRS) is marked in red. Note the narrow QRS complexes due to their origin at the AV junction. Also note the dissociation between atrial and ventricular depolarizations where some of the QRS complexes seem to "follow" the P waves. However, this is not possible because the PR intervals are exceedingly short to allow conduction. In addition, some of the P waves fall after the QRS.
 
 
 
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