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Junctional Ectopic Tachycardia Medication

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

Medication Summary

The mechanism of junctional ectopic tachycardia (JET) is not well understood, and identifying a specific pharmacologic agent to target the disorder is difficult. Because some experimental forms of junctional tachycardia exhibit a triggered mechanism induced by digoxin toxicity, avoiding digoxin seems reasonable. Nevertheless, digoxin is frequently used in the treatment of JET without apparent adverse effect but with questionable efficacy. Ventricular dysfunction is often prominent in patients with postoperative and congenital JET; thus, calcium channel blockers are usually avoided because of their negative inotropic effects. One case report has documented use of calcium channel blockers with apparent effectiveness. Drugs effective against automatic tachycardias appear to be effective in the treatment of congenital and postoperative JET.

Congenital JET has been successfully controlled with amiodarone, propafenone, or cautious combinations of both medications. Postoperative JET has been successfully controlled with amiodarone, propafenone, procainamide, or moricizine (discontinued from the market in July 2007). Propranolol or sotalol have also been used in the therapy of these rhythm disorders.

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Antiarrhythmic agents

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Amiodarone (Cordarone)

 

May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.

Before administration, control the ventricular rate and CHF (if present) with digoxin.

Propafenone (Rythmol)

 

Treats life-threatening arrhythmias. Possibly works by reducing spontaneous automaticity and prolonging refractory period.

Moricizine (Ethmozine)

 

Discontinued in July 2007 because of diminished market demand. Class I antiarrhythmic agent. Significantly prolongs conduction within the atrium, AV node, and ventricular myocardium without affecting their refractory periods. No direct effect on sinus node function.

Procainamide (Procan, Pronestyl)

 

Class IA antiarrhythmic used for PVCs, ventricular tachycardias, and supraventricular tachycardias. Increases refractory period of the atria and ventricles. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Propranolol (Inderal)

 

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

Sotalol (Betapace)

 

Class III antiarrhythmic agent, which blocks potassium channels, prolongs action potential duration (APD), and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.

Atenolol (Tenormin)

 

Selectively blocks beta1-receptors with little or no effect on beta2 types.

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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
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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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