Loeffler Endocarditis Workup

  • Author: Sohail A Hassan, MD; Chief Editor: Richard A Lange, MD   more...
 
Updated: Dec 6, 2011
 

Laboratory Studies

  • CBC counts should be performed to look for the presence of eosinophils. Peripheral eosinophilia should not be considered mandatory for the diagnosis of Loeffler endocarditis, as described by Priglinger et al.[12]
  • Cytogenetics, fluorescent in situ hybridization (FISH), and molecular analysis show the presence of the FIP1L1-PDGFRA fusion gene as demonstrated by Cools et al and Rotoli et al.[18, 20]
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Imaging Studies

  • ECG, echocardiography, Doppler studies using echocardiogram, cardiac catheterization, endomyocardial biopsy, and CT scan or MRI of the chest may all be useful in diagnosis, as for cardiomyopathy of any cause.
  • The echocardiographic hallmark of Loeffler endocarditis includes a restrictive pattern of filling with relatively preserved left ventricular systolic function, as reported by Parillo et al.[27, 28]
    • Localized thickening of the basal posterior wall of the left ventricular free wall and restricted motion of the posterior leaflet of the mitral valve are seen, as reported by Spyrou et al and Child et al.[29, 30]
    • Apical thrombus in the left ventricle also has been reported.
    • Regurgitant AV valve lesions are often present.
    • Recurrent thrombosis of the prosthetic mitral valve in the setting of rising eosinophilia is reported by Watanabe et al.[31]
    • Three echocardiographic features of amyloidosis, another cause of restrictive cardiomyopathy, include thickened interatrial septum; thickening of the cardiac valves; and granular, sparkling texture of the myocardium. All may be present in amyloidosis but not in Loeffler endocarditis.
  • Echocardiographic Doppler findings are of restrictive cardiomyopathy, including decreased right ventricular and left ventricular velocities with inspiration and inspiratory augmentation of hepatic-vein diastolic flow reversal.
  • Cardiac catheterization reveals markedly elevated ventricular filling pressures and the presence of mitral or tricuspid regurgitation.
  • On left ventriculography, a characteristic feature is preserved left ventricular systolic function with obliteration of the left ventricular apex, as reported by Weller and associates.[23]
  • The hemodynamic picture on cardiac pressure tracings reveals a restrictive picture due to dense endocardial scarring and a reduction in left ventricular cavity caused by an organized thrombus, as reported by Weller et al and Parillo et al.[23, 27] The hemodynamic picture may include elevation of left ventricular end diastolic pressure, often greater than 5 mm Hg over right ventricular end diastolic pressure; however the pressures may be identical at times.
  • Cardiac MRI findings of endomyocardial fibrosis include right ventricular diastolic dysfunction, mild systolic dysfunction, and extensive subendocardial delayed contrast enhancement.[32]
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Other Tests

ECG shows nonspecific ST-segment and T-wave abnormalities as reported by Spyrou et al and Arnold et al.[29, 33]

Arrhythmia, especially atrial fibrillation, and conduction system defects, particularly right-bundle branch block, may be present, as reported by Fawzy et al.[34] For related information, see Medscape's Atrial Fibrillation and Cardiac Rhythm Management Resource Centers.

Nonspecific findings may include pseudo infarction patterns of left-axis deviation.

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Procedures

Percutaneous endomyocardial biopsy often confirms diagnosis. As endomyocardial involvement may be patchy, a false-negative biopsy result also is possible, as reported by Felice and colleagues.[35]

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Histologic Findings

Histologic specimens of the myocardial biopsy reveal thick and deep layers of loosely arranged collagen tissue, which, although localized primarily to the endocardium, may have strands extending into the underlying myocardium. Although peripheral eosinophilia is characteristic of Loeffler endocarditis, eosinophilic infiltration of the tissues and arteries is less common, possibly because of the infrequency of biopsy.

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Contributor Information and Disclosures
Author

Sohail A Hassan, MD  Cardiologist and Cardiac Electrophysiologist, Eastside Cardiovascular Medicine; Director or Electrophysiology at St John Macomb Hospital; Assistant Professor of Medicine, Wayne State University School of Medicine

Sohail A Hassan, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Heart Rhythm Society, and Michigan State Medical Society

Disclosure: Medtronic, St Jude''s Medical, Boston Scientific Honoraria Speaking and teaching; Zoll, Sanofi Aventis Honoraria Speaking and teaching

Coauthor(s)

Viqar Maria, MD  Resident Physician, Department of Internal Medicine, St John Hospital and Medical Center

Viqar Maria, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Henry Kim, MD, MPH  Fellowship Director, Department of Cardiology, Henry Ford Hospital

Henry Kim, MD, MPH is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Hanumant Deshmukh, MD †  Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science

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

Marschall S Runge, MD, PhD  Charles and Anne Sanders Distinguished Professor of Medicine, Chairman, Department of Medicine, Vice Dean for Clinical Affairs, University of North Carolina at Chapel Hill School of Medicine

Marschall S Runge, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Association of Professors of Cardiology, Association of Professors of Medicine, Southern Society for Clinical Investigation, and Texas Medical Association

Disclosure: Pfizer Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Orthoclinica Diagnostica Consulting fee Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD  Professor and Executive Vice Chairman, Department of Medicine, Director, Office of Educational Programs, University of Texas Health Science Center at San Antonio

Richard A Lange, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, and Association of Subspecialty Professors

Disclosure: Nothing to disclose.

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Pathogenesis of Loeffler syndrome.
Myocardial as well as valvular involvement with Loffler endocarditis. This image shows dense fibrosis of ventricle in a postmortem dissected heart.
 
 
 
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