eMedicine Specialties > Radiology > Cardiac

Ebstein Anomaly

Author: Julia Gates, MD, Department of Radiology, Consulting Staff and Assistant Residency Program Director, Baystate Medical Center
Coauthor(s): George Hartnell, MB, Professor of Radiology, Tufts University School of Medicine, Director of Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
Contributor Information and Disclosures

Updated: Mar 6, 2008

Introduction

Background

Professor Wilhelm Ebstein (1836-1912), who was a professor of medicine in Gottingen, Germany, first described Ebstein anomaly in 1866.1,2,3 The condition accounts for less than 1% of congenital heart diseases and occurs in 1 in 210,000 live births.4 Ebstein anomaly occurs with equal frequency in male individuals and female individuals; severely affected neonates can present on the first day of life. The condition may completely escape detection, or patients may not become symptomatic until late in life. In some individuals, Ebstein anomaly is not diagnosed until the eighth decade of life.5 As many as one half of patients have an atrial septal defect (ASD), and as many as one quarter have an accessory conduction pathway.

Pathophysiology

Numerous abnormalities are associated with Ebstein anomaly, including the following:

  • Ventricular septal defect (VSD)6,7,8
  • Aortic coarctation9,10
  • Interatrial communication - ASD, especially secundum ASD, and patent foramen ovale7,8,11,12
  • Pulmonary atresia with an intact ventricular septum7,13
  • Partial atrioventricular canal8
  • Hypoplastic pulmonary arteries8
  • Patent ductus arteriosus8
  • Pulmonary stenosis14,7
  • Parachute mitral valve8
  • Cleft anterior leaflet of the mitral valve8
  • Mitral valve prolapse7,8
  • Left ventricular outflow obstruction11
  • Hypertensive pulmonary vascular disease11
  • Congenital deaf-mutism15
  • Corrected transposition of the great arteries16,17,18
  • Subaortic stenosis19
  • Tetralogy of Fallot20

Frequency

United States

Ebstein anomaly occurs in 1 of 210,000 live births.4

Mortality/Morbidity

Mortality depends on the severity of the lesion and other cardiac defects in each patient. Patients with severe disease may die in infancy if untreated, whereas patients with mild or moderate disease may not present until the eighth decade of life.

Sex

Ebstein anomaly occurs with equal frequency in male and female individual.

Age

Patients can present with Ebstein anomaly at any age.

Anatomy

The tricuspid valve is composed of 3 leaflets, including the anterior, posterior, and septal (also termed mural or medial) leaflets. In Ebstein anomaly, the leaflets are affected to various degrees. The septal leaflet is affected more than the posterior leaflet, which is affected more than the anterior leaflet.8 The septal and posterior leaflets are often displaced inferiorly toward the apex of the heart. The anterior tricuspid valve leaflet may be elongated,21 and it may adhere to the wall of the right ventricle.8,12 The septal and posterior leaflets are displaced inferiorly at least 20 mm or 8 mm/m2 in adults.12,21 This degree of inferior displacement of the septal leaflet is regarded as definitive.22

The leaflets may be tethered by muscular bands or by shortened chordae tendineae and shortened papillary muscles, or the leaflets may adhere directly to the ventricular wall.8 The valve annulus is not displaced; therefore, it is situated correctly between the atrium and ventricle. Similarly, the proximal attachment of the anterior leaflet to the annulus is normal.12 The mural leaflet always is present; if absent, the condition is termed unguarded tricuspid orifice rather than Ebstein anomaly.23

Because the annulus is sited anatomically as usual but because the septal and posterior valve attachments are displaced inferiorly, a region of upper right ventricle functionally becomes atrial; this is termed the atrialized portion of the right ventricle. As a result of its structural alteration, this region actually is thinned and hence prone to aneurysmal dilatation, particularly between the attachment of the posterior leaflet and the annulus.12 Furthermore, the right ventricle has a decreased number of myocardial fibers, which increases the risk of dilatation.23

Presentation

Clinical findings in Ebstein anomaly include the following:

  • Asymptomatic presentation
  • Dyspnea on exertion
  • Palpitations and/or ectopy
  • Exercise intolerance in patients
  • Atrial arrhythmias
  • Cyanosis
  • Paroxysmal supraventricular tachycardia
  • Atrial fibrillation - Paroxysmal or chronic
  • Atrial flutter - Paroxysmal or chronic
  • Accessory conduction pathways (Wolff-Parkinson-White syndrome, especially type B; Kent bundle; Mahaim fiber)
  • Cardiac conduction block - Arteriovenous block, left bundle-branch block, and right bundle branch block
  • Sinus node dysfunction
  • Congestive hepatosplenomegaly

Epstein anomaly classically falls into the gamut of chest radiograph findings termed cyanosis with decreased pulmonary vascularity, though chest radiographic findings are often characteristic (see Images 1-3).

In infants, diagnosis is a dilemma because of their inability to articulate the chief complaint. Approximately one fifth of infants presenting with supraventricular tachycardia have structural heart disease, most often Ebstein anomaly.24 The probability of a structural abnormality is increased in patients with Wolf-Parkinson-White syndrome type B.24,25 Maternal use of lithium during pregnancy is thought to induce some accessory conduction pathways.7

Infants with severe Ebstein anomaly and marked cardiomegaly (see Image 2) may have further compromise due to excessive bilateral, pulmonary compression from the enlarged heart. Corrective surgery with cardiac reduction can help obviate ventilator dependence.8 Infants may benefit from inhaled nitric oxide therapy.26 Critically ill neonates can be given extracorporeal membrane oxygenation as a temporary measure.27

The severity of the abnormality can be assessed and graded 1-4 by calculating the ratio of the area of the right atrium and atrialized right ventricle to the area of the functional right ventricle and left heart chambers (on the 4-chamber view). The higher the grade, the worse the prognosis. This scheme was used in neonates in a retrospective study.14 When echocardiography is difficult, definition of the anatomy can be improved by using cardiac MRI and cine magnetic resonance angiography (MRA) when this is available.28,29,30

Related eMedicine topics:
Atrial Flutter
Tetralogy of Fallot

Related Medscape topics:
CME/CE Diagnosis and Management of Atrial Fibrillation: Focus on Guidelines
CME Supraventricular Tachycardia -- An Interactive Case

Preferred Examination

Chest radiography is the best initial study, though findings are often nonspecific.

Two-dimensional echocardiography is usually performed next and may be all that is required. Echocardiography can help confirm the diagnosis, assess the severity of the anatomic lesion, and determine the effects on cardiac function.

When available and of high quality, fast cardiac MRI with contrast-enhanced 3-dimensional (3D) MRA has the potential to replace cardiac catheterization for assessing pulmonary artery anatomy and for providing information that echocardiography cannot. MRI can depict anatomy and function with an unrestricted field of view; even the pulmonary arteries and tricuspid valve can be evaluated during a single study. Comprehensive imaging of this type provides a vehicle for surgical planning.31,32

Limitations of Techniques

Traditional imaging modalities have included chest radiography, echocardiography, and cardiac catheterization with right ventriculography.

Plain radiographic findings are nonspecific despite occasional pathognomonic appearances. Normal chest radiographic findings do not exclude the diagnosis.

Echocardiography is usually performed after chest radiography; however, if echocardiography is inadequate, MRI can be used to assess anatomy and function with an unrestricted field of view. Echocardiography can be limited by restricted acoustic access, especially in patients who are obese, who underwent surgery, or who cannot lie still. Echocardiography cannot be used to measure the size of the left and right pulmonary arteries.

MRI is not routinely performed because of its limited availability and expense; the limited availability of qualified personnel to perform the protocol, interpret the study, or both; the patient's inability to cooperate (eg, because of claustrophobia); unsuitability or contraindications (eg, clinically unstable condition, pacemaker, metal objects in an anatomic location where MRI is dangerous and therefore contraindicated); and physicians' unawareness of the uses of MRI.

Differential Diagnoses

Pulmonary Hypertension
Tetralogy of Fallot
Tricuspid Atresia
Ventricular Septal Defect

Other Problems to Be Considered

Patients who clinically present with tricuspid regurgitation and right-sided cardiac enlargement may have dysplasia of the tricuspid valve, an unguarded tricuspid orifice, tricuspid valve prolapse, arrhythmogenic right ventricular dysplasia, trauma, endocarditis, or dilatation of the tricuspid valve annulus secondary to pulmonary valve regurgitation.21,23,33 Acquired causes of tricuspid regurgitation and right-sided cardiac enlargement seen in adults also include carcinoid syndrome, pulmonary hypertension, and left heart failure, though the last 2 are unlikely to be mistaken for Ebstein anomaly on the basis of clinical or radiographic findings.

Ebstein anomaly classically falls into the gamut of chest radiographic findings termed cyanosis with decreased pulmonary vascularity, though chest radiographic findings often are characteristic (see Images 1-3).34 The differential diagnosis for this category includes Ebstein anomaly, tetralogy of Fallot, pulmonary atresia with VSD, pulmonary atresia with an intact ventricular septum, hypoplastic right ventricle and/or Uhl anomaly or parchment right ventricle, and tricuspid atresia with a restrictive VSD.

More on Ebstein Anomaly

Overview: Ebstein Anomaly
Imaging: Ebstein Anomaly
Follow-up: Ebstein Anomaly
Multimedia: Ebstein Anomaly
References
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References

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Further Reading

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Keywords

Ebstein's anomaly, arrhythmia, heart block, congenital heart disease, atrial septal defect, accessory conduction pathway, cardiac conduction block, ventricular septal defect, atrial fibrillation, heart disease, cardiovascular disease

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Contributor Information and Disclosures

Author

Julia Gates, MD, Department of Radiology, Consulting Staff and Assistant Residency Program Director, Baystate Medical Center
Julia Gates, MD is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Roentgen Ray Society, Association of University Radiologists, Massachusetts Medical Society, and Radiological Society of North America
Disclosure: Nothing to disclose.

Coauthor(s)

George Hartnell, MB, Professor of Radiology, Tufts University School of Medicine, Director of Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
George Hartnell, MB is a member of the following medical societies: American College of Cardiology, American College of Radiology, American Heart Association, Association of University Radiologists, British Institute of Radiology, British Medical Association, Massachusetts Medical Society, Radiological Society of North America, Royal College of Physicians, Royal College of Radiologists, and Society of Cardiovascular and Interventional Radiology
Disclosure: Nothing to disclose.

Medical Editor

S Bruce Greenberg, MD, Professor of Radiology, University of Arkansas for Medical Sciences; Consulting Staff, Department of Radiology, Arkansas Children's Hospital
S Bruce Greenberg, MD is a member of the following medical societies: Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

David S Levey, MD, PhD, Orthopedic/Spine MRI TeleRadiologist, Radsource, LLC
David S Levey, MD, PhD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, and Texas Medical Association
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Consulting Staff, Department of Radiology, Virginia Mason Medical Center
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

 
 
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