eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Endocardial Fibroelastosis: Differential Diagnoses & Workup

Author: Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK
Contributor Information and Disclosures

Updated: May 14, 2009

Differential Diagnoses

Anomalous Left Coronary Artery From the Pulmonary Artery
Mucopolysaccharidosis Type II
Cardiomyopathy, Dilated
Mucopolysaccharidosis Type III
Cardiomyopathy, Restrictive
Mucopolysaccharidosis Type IS
Carnitine Deficiency
Mucopolysaccharidosis Type IV
Glycogen-Storage Disease Type I
Mucopolysaccharidosis Type VI
Glycogen-Storage Disease Type II
Mucopolysaccharidosis Type VII
Hypoplastic Left Heart Syndrome
Myocarditis, Viral
Mucopolysaccharidosis Type IH
Neonatal Lupus and Cutaneous Lupus Erythematosus in Children

Other Problems to Be Considered

Congenital heart diseases (especially left ventricular [LV] outflow tract obstruction)
Other causes of nonimmune hydrops fetalis
Neonatal lupus erythematosus
Left ventricular noncompaction
Centronuclear myopathy

Workup

Laboratory Studies

Blood tests in endocardial fibroelastosis (EFE) include the following:

  • Serum electrolyte levels
  • BUN and creatinine levels
  • CBC count
  • Blood culture tests indicated for management of acute episodes
  • Autoantibody profile including anti-Ro and anti-La

Imaging Studies

  • Chest radiography

  • Chest radiograph, anteroposterior view, showing c...

    Chest radiograph, anteroposterior view, showing cardiomegaly and pulmonary venous congestion in a 6-month-old infant with endocardial fibroelastosis (EFE).

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    Chest radiograph, anteroposterior view, showing c...

    Chest radiograph, anteroposterior view, showing cardiomegaly and pulmonary venous congestion in a 6-month-old infant with endocardial fibroelastosis (EFE).


  • Chest radiograph, left lateral view, showing enla...

    Chest radiograph, left lateral view, showing enlarged heart in 6-month-old infant.

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    Chest radiograph, left lateral view, showing enla...

    Chest radiograph, left lateral view, showing enlarged heart in 6-month-old infant.

    • Cardiomegaly and cardiothoracic ratios exceed 0.65 in 50% of patients.
    • Cardiac enlargement (CE) is present in some patients at birth. In others, the heart size is normal during the first few weeks to the first few months of life, but CE subsequently develops.
    • The shape of the cardiac silhouette varies, although it is often globular.
    • Pulmonary venous congestion is common.
    • Left lower lobe atelectasis secondary to dilated left atrium (LA) is found in 25% of patients.
  • Echocardiography
    • LA and left ventricular (LV) dimensions are increased.
    • LV, septal, and posterior wall (PW) excursions are reduced.
    • The ejection fraction (EF) is reduced.
    • Mitral valve (MV) motion is abnormal.
    • Echogenicity along the endocardium of the LV (diagnostic clue) is dense.
    • Suggestive indicators include increased endocardial echo brightness and globular shape of the LV.
    • The echocardiograph may depict a normalization of the shortening fraction and the LV dimensions when the clinical condition improves following medical therapy.
    • A varying degree of mitral regurgitation is common.
  • Fetal echocardiography
    • This is a valuable tool for early identification, particularly of the secondary type.
    • One of the congenital malformations (eg, aortic stenosis) is often demonstrated at the initial study. The endocardial fibroelastosis becomes obvious in repeat studies.
  • Electron beam CT scanning: Recently, electron beam CT has been reported to be useful in the early diagnosis of endocardial fibroelastosis because of its demonstration of calcification and fibrosis of the ventricles, especially at the apex.
  • MRI: Reports highlight the role of MRI in identifying the presence of endocardial fibroelastosis.6,7 MRI that uses perfusion and myocardial delayed enhancement can be useful in establishing the diagnosis. Endocardial fibroelastosis gives the endocardial surface a rim of hypointense signal in the perfusion sequences and a rim of hyperintense signal in the myocardial delayed-enhancement sequences.

Other Tests

  • Twenty-four–hour Holter ECG: This is useful in documenting ambient arrhythmias.
  • Electrocardiography
    • Tall R waves, deep Q waves, and T-wave inversion or flattening in the left precordial or inferior lead have been reported.
    • Findings depict LV hypertrophy in more than 75% of patients.
    • In the first few weeks of life, right axis deviation and isolated right ventricular hypertrophy are more common.
    • Pulmonary hypertension may develop in patients who survive for a long period and appears as biventricular hypertrophy on electrocardiography.
    • Patterns of left, right, or biatrial enlargement are evident in 50% of patients.
    • Conduction or rhythm abnormalities include Wolff-Parkinson-White syndrome, left bundle branch block, supraventricular and ventricular arrhythmias, and varying degrees of atrioventricular block.
    • Low-voltage tracings in the initial stage of heart failure and in the terminal phase are noted in 5% of patients.
    • Occasionally, an infarct pattern appears, pointing to extensive myocardial fibrosis and necrosis.

Procedures

  • Cardiac catheterization
    • Cardiac chambers and pulmonary arteries contain elevated pressures consistent with heart failure. Generally, systolic pulmonary artery pressure is not more than 50% of systemic pressure. Marked pulmonary hypertension may be seen in older children.
    • The constrictive type of endocardial fibroelastosis is rare and is associated with a left-sided atrioventricular obstructive pattern, with very high LA pressures from an early age. A diastolic gradient can be detected across the mitral valve (MV). Pulmonary artery pressure is elevated and often reaches systemic levels in this type of endocardial fibroelastosis.
    • Postcatheterization precautions include hemorrhage, vascular disruption after balloon dilation, pain, nausea and vomiting, and arterial or venous obstruction due to thrombosis or spasm.
    • Complications may include blood vessel rupture, tachyarrhythmias, bradyarrhythmias, and vascular occlusion.
  • Angiocardiographic findings
    • Marked dilation of the LV cavity
    • Reduced EF with little or no LV wall thickening
    • Dyskinetic LV contraction
    • Mitral regurgitation (common)
    • In the contracted type, dilated right ventricle, right atrium, and pulmonary artery with slow clearance of the contrast from the left side of the heart
  • Digital subtraction angiography: This may reveal an avascular rim between the opacified LV cavity and the ventricular walls perfused by the coronary arteries. The contrast void rim can be identified even in ordinary cineangiographic films.
  • Biopsy: In cases in which the diagnosis is unclear, myocardial biopsy can be helpful.

Histologic Findings

  • Endomyocardial biopsy reveals an invasion of the endocardium and subendocardium by fibroelastic tissue.
  • Abnormalities are largely confined to the endocardium, with marked hyperplasia of its constituents, especially collagen and elastic fibers; hence, the basic abnormality in endocardial fibroelastosis appears to involve the synthesis of abnormally large amounts of collagen and elastin rather than a qualitative change in the structure of elastic fibers.
  • Surface deposits of fibrin have also been detected using electron microscopy. The underlying myocardium generally appears normal.

More on Endocardial Fibroelastosis

Overview: Endocardial Fibroelastosis
Differential Diagnoses & Workup: Endocardial Fibroelastosis
Treatment & Medication: Endocardial Fibroelastosis
Follow-up: Endocardial Fibroelastosis
Multimedia: Endocardial Fibroelastosis
References
Further Reading
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Further Reading

The American Dietetic Association has released and revised a heart failure evidence-based nutrition practice guideline.

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Keywords

endocardial fibroelastosis, EFE, elastic tissue hyperplasia, endocardial dysplasia, endocardial sclerosis, fetal endocarditis, fetal endomyocardial fibrosis, subendocardial sclerosis, endocardial fibroelastosis, thickening of the ventricular endocardium, unexplained heart failure, congenital heart diseases, aortic stenosis, atresia, primary EFE, secondary EFE, primary endocardial fibroelastosis, secondary endocardial fibroelastosis, acute congestive cardiac failure, congestive cardiac failure, CCF, cardiogenic shock, sudden death in infancy, nonimmune hydrops fetalis, hypoplastic left heart syndrome, coarctation of the aorta, ventricular septal defect, carnitine deficiency, treatment, diagnosis

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Contributor Information and Disclosures

Author

Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK
Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH is a member of the following medical societies: British Cardiac Society and Royal College of Physicians and Surgeons of Glasgow
Disclosure: Nothing to disclose.

Medical Editor

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA, Professor, Departments of Pediatrics (Cardiology), Cardiovascular Sciences, and Molecular and Human Genetics, Baylor College of Medicine; Chief of Pediatric Cardiology, Foundation Chair in Pediatric Cardiac Research, Texas Children's Hospital
Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Cardiology, American College of Sports Medicine, American Heart Association, American Medical Association, American Society of Human Genetics, Cardiac Electrophysiology Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Julian M Stewart, MD, PhD, Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College
Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

CME Editor

Gilbert Z Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center
Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
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.

 
 
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