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Atrioventricular Nodal Reentry Tachycardia

  • Author: Brian Olshansky, MD; Chief Editor: Jeffrey N Rottman, MD  more...
 
Updated: Apr 08, 2015
 

Background

Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT). The substrate for AVNRT is the presence of dual AV nodal pathways. (See Etiology.)[1, 2]

Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term paroxysmal supraventricular tachycardia (or even the misleading term paroxysmal atrial tachycardia [PAT]) has been used to refer to these tachyarrhythmias. With improved knowledge of the electrophysiology of reentrant SVT, greater specificity in nomenclature, based on the mechanism of reentry, has been possible. Such improved classification aids in the choice of appropriate therapies. (See Etiology, Prognosis, Treatment, and Medication.)

AVNRT is usually well tolerated, often occurring in patients with no structural heart disease. (See Prognosis, Presentation, and Workup.)

Patient education

Patients should be instructed on vagal maneuvers (Valsalva, diving reflex). These are used to try to terminate an episode of AVNRT. Patients with hemodynamic compromise or syncope should be instructed on avoiding activities that could be dangerous to them or to others (eg, driving, swimming) while the risk of an episode remains. Ablation obviates the need for long-term restriction.

For patient education information, see the Heart Health Center, as well as Supraventricular Tachycardia.

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Etiology

The substrate for AVNRT is anatomic. AVNRT occurs in young, healthy patients but also in those with chronic heart disease.

In patients with atrioventricular (AV) nodal reentry, two pathways connect into the AV node and help form part of the reentrant circuit. In the majority of patients with AVNRT, antegrade conduction occurs over the slow pathway, and retrograde conduction occurs over the fast pathway during AVNRT. (See the image below.)

Electrophysiological mechanism of atrioventricular Electrophysiological mechanism of atrioventricular nodal reentry tachycardia.

In most patients with AVNRT, the tachycardia is initiated when an atrial premature complex is blocked in the fast pathway but can conduct via the slow pathway. Although many patients may have a dual pathway physiology, for AVNRT to occur, the fast pathway must have a longer refractory period antegrade than the slow conducting pathway.

In approximately 10% of patients, AVNRT is induced by premature ventricular stimulation. In addition to the typical mechanism of AV nodal reentry described above, atypical AV nodal reentry can occur in the opposite direction, with antegrade conduction in the fast pathway and retrograde conduction in the slow pathway. Less commonly, the reentrant circuit can be over 2 slow pathways, the so-called slow-slow AV nodal reentry. (See the images below.)

Atypical atrioventricular nodal reentry tachycardi Atypical atrioventricular nodal reentry tachycardia.
Typical atrioventricular nodal reentry tachycardia Typical atrioventricular nodal reentry tachycardia.
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Epidemiology

In the United States, AVNRT occurs in 60% of patients (with a female predominance) presenting with paroxysmal SVT. The prevalence of SVT in the general population is likely several cases per thousand persons. Internationally, the occurrence of AVNRT is similar to that in the United States.

AVNRT may occur in persons of any age. It is common in young adults, but some patients do not present until their seventh or eighth decade or later.

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Prognosis

The prognosis for patients with AVNRT is usually good in the absence of structural heart disease. Most patients respond acutely to vagal maneuvers or adenosine and long term to medications to prevent recurrence or to radiofrequency ablation, which is approximately 95% curative and has a low risk of complications. It is the preferred method of treatment for most patients.

One review of the literature concluded that cryoablation is safe and effective for AVNRT and is an option in patients for whom the avoidance of AV block is a priority, such as children and young adults.[3]

Complications of AVNRT include hemodynamic compromise, congestive heart failure, syncope, tachycardia-induced angina, cardiomyopathy, myocardial ischemia, and myocardial infarction.

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Contributor Information and Disclosures
Author

Brian Olshansky, MD Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, Heart Rhythm Society, Cardiac Electrophysiology Society, American Heart Association

Disclosure: Received honoraria from Guidant/Boston Scientific for speaking and teaching; Received honoraria from Medtronic for speaking and teaching; Received consulting fee from Guidant/Boston Scientific for consulting; Received consulting fee from BioControl for consulting; Received consulting fee from Boehringer Ingelheim for consulting; Received consulting fee from Amarin for review panel membership; Received consulting fee from sanofi aventis for review panel membership.

Coauthor(s)

Renee M Sullivan, MD, FACC Assistant Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Missouri Health System; Staff Physician, Electrophysiology, Harry S Truman Veterans Affairs Medical Center

Renee M Sullivan, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, Heart Rhythm Society, European Cardiac Arrhythmia Society, Group on Women in Medicine and Science

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

Marco A Barzallo, MD Consulting Staff, HeartCare Midwest, SC

Disclosure: Nothing to disclose.

Mukesh Garg, MD, MRCP Assistant Professor, Department of Internal Medicine, Section of Cardiology, Truman Medical Center, University of Missouri at Kansas City

Disclosure: Nothing to disclose.

Shamila Garg, MD

Disclosure: Nothing to disclose.

Marina Hannen, MD  Clinical Assistant Professor, Department of Cardiology, Section of Cardiovascular Diseases, University of Kansas Medical Center; Consulting Staff, Mid-American Cardiology Associates

Disclosure: Nothing to disclose.

Russell F Kelly MD, Assistant Professor, Department of Internal Medicine, Rush Medical College; Chairman of Adult Cardiology and Director of the Fellowship Program, Cook County Hospital

Russell F Kelly is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Annette Quick, MD, Medical Director, Cardiovascular Care Unit, Associate Professor, Department of Medicine, University of Missouri-Kansas City School of Medicine

Disclosure: Nothing to disclose.

Chirag M Sandesara, MD, FACC Virginia Cardiovascular Associates, Cardiac Rhythm Care

Chirag M Sandesara, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD   Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. Philadelphia, Pa: WB Saunders; 2004.

  2. Janse MJ, Anderson RH, McGuire MA, Ho SY. "AV nodal" reentry: Part I: "AV nodal" reentry revisited. J Cardiovasc Electrophysiol. 1993 Oct. 4(5):561-72. [Medline].

  3. Hanninen M, Yeung-Lai-Wah N, Massel D, Gula LJ, Skanes AC, Yee R, et al. Cryoablation versus RF ablation for AVNRT: A meta-analysis and systematic review. J Cardiovasc Electrophysiol. 2013 Dec. 24(12):1354-60. [Medline].

  4. Gursoy S, Steurer G, Brugada J, et al. Brief report: the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia. N Engl J Med. 1992 Sep 10. 327(11):772-4. [Medline].

  5. Fogoros RN. Electrophysiologic Testing (Practical Cardiac Diagnosis). 3rd ed. London, UK: Blackwell Science; 1999.

  6. Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry, by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med. 1992 Jul 30. 327(5):313-8. [Medline].

 
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Electrophysiological mechanism of atrioventricular nodal reentry tachycardia.
Atypical atrioventricular nodal reentry tachycardia.
Typical atrioventricular nodal reentry tachycardia.
 
 
 
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