Pediatric Atrial Ectopic Tachycardia 

  • Author: Shubhayan Sanatani, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Mar 29, 2011
 

Background

Atrial ectopic tachycardia (AET) is a rare arrhythmia; however, it is the most common form of incessant supraventricular tachycardia (SVT) in children. Atrial ectopic tachycardia is believed to be secondary to increased automaticity of a nonsinus atrial focus or foci. This arrhythmia, which is also known as ectopic atrial tachycardia or automatic atrial tachycardia, has a high association with tachycardia-induced cardiomyopathy. Atrial ectopic tachycardia is often refractory to medical therapy and is not usually responsive to direct current (DC) cardioversion.

The diagnosis of atrial ectopic tachycardia is based on the presence of a narrow complex tachycardia (in the absence of aberrancy or preexisting bundle branch block) with visible P waves at an inappropriately rapid rate. The rates range from 120 to 300 beats per minute (bpm) and are typically higher than 200 bpm, although physiologic rates may be observed (see Electrocardiography).

Patients with atrial ectopic tachycardia may present with circulat ory collapse similar to patients with cardiomyopathy. Immediate rate control is desired in these cases. Three options are available for long-term treatment of patients with atrial ectopic tachycardia: medication to suppress the arrhythmia or control the ventricular response, catheter ablation, or, uncommonly, surgery (see Treatment and Management).

Go to Atrial Tachycardia and Multifocal Atrial Tachycardia for information on these topics.

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Pathophysiology

Spontaneous depolarization is a phenomenon of automatic myocardium. The sinus node is usually the pacemaker of the heart, because it has the most rapid spontaneous rate of firing. A small cluster of cells with abnormal automaticity is presumed to be responsible for atrial ectopic tachycardia. The conduction spreads from this cluster to the surrounding atrium and to the ventricles via the atrioventricular (AV) node. A conduction delay from atrium to ventricle often occurs, with most patients demonstrating first-degree AV block and some showing second-degree block.

Because atrial ectopic tachycardia is often incessant, tachycardia-induced cardiomyopathy is commonly observed. Although the exact underlying mechanism of the development of cardiac dysfunction in the setting of chronic arrhythmias is unknown, numerous reports have documented improved cardiac function following ventricular rate control and treatment of the arrhythmia.

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Etiology

Atrial ectopic tachycardia is usually idiopathic. Occasionally, mycoplasmal or viral infections, such as respiratory syncytial virus, may trigger this arrhythmia, although more complex atrial tachycardias, such as chaotic atrial tachycardia, are more frequently found in this scenario. Atrial tumors have been reported to be associated with atrial ectopic tachycardia. Reports of familial cases with an autosomal dominant inheritance are present in the literature.[1] This arrhythmia is also observed in patients who have congenital heart disease and have undergone surgical treatment of this congenital heart disease.

The adult form of atrial ectopic tachycardia may have a different etiology and natural history than the pediatric form.

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Epidemiology

Although the exact incidence is unknown and few large series have been reported, atrial ectopic tachycardia reportedly comprises 5-10% of pediatric SVTs. Although estimates of the incidence of pediatric SVTs widely vary, atrial ectopic tachycardia likely occurs with an incidence of approximately 1 case per 10,000 children.

Atrial ectopic tachycardia is predominantly observed in infants and children; this accounts for a peak of 11-16% of tachycardias for which a mechanism is determined in young childhood.

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Prognosis

Atrial ectopic tachycardia is generally well tolerated. Syncope is unusual, and cardiac arrest is rare, except when encountered as a complication of treatment. Tachycardia-induced cardiomyopathy is the most significant sequela of atrial ectopic tachycardia and may be insidious. The time to development depends on the rate and duration of the tachycardia; however, ventricular dilatation may be present on initial presentation. This can also be reversed with successful treatment of the arrhythmia.

Several reports have documented the spontaneous remission of atrial ectopic tachycardia in the pediatric population and in young adults.[2] This may occur in as many as one third of patients following withdrawal of medication. A review from Texas Children's Hospital suggests that children younger than 3 years have a better response to medication and a higher rate of spontaneous resolution of the arrhythmia.[3]

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Patient Education

For patient education information, see eMedicine's Heart Center, as well as Supraventricular Tachycardia.

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Contributor Information and Disclosures
Author

Shubhayan Sanatani, MD  Associate Professor, Department of Pediatrics, University of British Columbia Faculty of Medicine; Consulting Staff, Division of Pediatric Cardiology, British Columbia Children's Hospital, Canada

Shubhayan Sanatani, MD is a member of the following medical societies: British Columbia Medical Association, Canadian Cardiovascular Society, Canadian Heart Rhythm Society, Canadian Heart Rhythm Society, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Robert Murray Hamilton, MD, MSc, FRCPC  Section Head, Electrophysiology, Director, High-Risk Hereditary Heart Conditions Clinic, Labatt Family Heart Centre; Professor, Department of Pediatrics, Associate Scientist, Physiology and Experimental Medicine, The Hospital for Sick Children and Research Institute, University of Toronto Faculty of Medicine, Canada

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

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 College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital 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, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

References
  1. Dagres N, Gutersohn A, Wieneke H, Sack S, Erbel R. A new hereditary form of ectopic atrial tachycardia with autosomal dominant inheritance. Int J Cardiol. Feb 2004;93(2-3):311-3. [Medline].

  2. Bauersfeld U, Gow RM, Hamilton RM, Izukawa T. Treatment of atrial ectopic tachycardia in infants < 6 months old. Am Heart J. Jun 1995;129(6):1145-8. [Medline].

  3. Salerno JC, Kertesz NJ, Friedman RA, Fenrich AL Jr. Clinical course of atrial ectopic tachycardia is age-dependent: results and treatment in children or =3 years of age. J Am Coll Cardiol. Feb 4 2004;43(3):438-44. [Medline].

  4. Gelb BD, Garson A Jr. Noninvasive discrimination of right atrial ectopic tachycardia from sinus tachycardia in "dilated cardiomyopathy". Am Heart J. 1990;120:886-91. [Medline].

  5. Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol. Sep 5 2006;48(5):1010-7. [Medline].

  6. Higa S, Tai CT, Lin YJ, et al. Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation. Circulation. Jan 6 2004;109(1):84-91. [Medline]. [Full Text].

  7. Liew R, Catanchin A, Behr ER, Ward D. Use of non-contact mapping in the treatment of right atrial tachycardias in patients with and without congenital heart disease. Europace. Aug 2008;10(8):972-81. [Medline].

  8. Cummings RM, Mahle WT, Strieper MJ, Campbell RM, Costello L, Balfour V. Outcomes following electroanatomic mapping and ablation for the treatment of ectopic atrial tachycardia in the pediatric population. Pediatr Cardiol. Mar 2008;29(2):393-7. [Medline].

  9. Haas NA, Fox S, Skinner JR. Successful use of an intravenous infusion of flecainide and amiodarone for a refractory combination of postoperative junctional and ectopic tachycardias. Cardiol Young. Aug 2005;15(4):427-30. [Medline].

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