Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Loeffler Endocarditis Medication

  • Author: Sohail A Hassan, MD; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Feb 17, 2015
 

Medication Summary

Symptomatic relief is achieved by routine cardiac therapy including diuretics, digitalis, afterload reduction, and anticoagulation.

Early phases of the disease have been treated, with varying degrees of success, with immune suppressants, including steroids and interferon therapy, and cytotoxic medications, particularly hydroxyurea.

Corticosteroids appear to be beneficial in acute myocarditis, together with cytotoxic drugs, including hydroxyurea, and may prolong survival substantially. Interferon therapy has also been reported as having some success.

Next

Tyrosine kinase inhibitors

Class Summary

These agents inhibit tyrosine kinase, which, in turn, inhibit activation of intracellular pathways that can promote deregulated cell proliferation.

Imatinib (Gleevec)

 

Small molecule that selectively inhibits the tyrosine kinase activity of c-kit, bcr-abl, and PDGFR.

Previous
Next

Antineoplastic agents, antimetabolite

Class Summary

These agents inhibit cell growth and proliferation.

Hydroxyurea (Hydrea)/Hydroxycarbamide

 

Inhibitor of deoxynucleotide synthesis and DOC for inducing hematologic remission in CML. Less leukemogenic than alkylating agents such as busulfan, melphalan, or chlorambucil.

Myelosuppressive effects last a few days to a week and are easier to control than those of alkylating agents. Hydroxyurea can be given as a single daily dose or divided bid or tid at higher dose ranges.

Previous
Next

Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Methylprednisolone (Adlone, Solu-Medrol, Depo-Medrol, Medrol)

 

Immune-modifying agents that can be used, with varying degrees of success, in early stage of Loeffler endocarditis. Monitoring of liver function tests and eosinophil count may help to observe long-term response.

Previous
Next

Diuretics

Class Summary

These agents provide relief of congestive heart failure symptoms.

Bumetanide (Bumex)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle. Does not appear to act in distal renal tubule.

Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until satisfactory effect achieved.

Previous
Next

Cardiac glycosides

Class Summary

These agents are used for treatment of systolic dysfunction in congestive heart failure.

Digoxin (Lanoxin)

 

Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Previous
Next

Angiotensin-converting enzyme inhibitors

Class Summary

These agents are used to treat congestive heart failure and reduce afterload.

Enalapril (Vasotec)

 

Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.

Previous
Next

Anti-interleukin-5 monoclonal antibodies

Class Summary

These agents inhibit the production, activation, and maturation of eosinophils.[46]

Mepolizumab

 

Received orphan drug status for first-line treatment in patients with hypereosinophilic syndrome in the US and the EU in 2004. Interleukin-5 stimulates the production, activation, and maturation of eosinophils. Since mepolizumab inhibits interleukin-5 and has a long terminal half-life, treatment with mepolizumab causes a sustained reduction in the numbers of circulating eosinophils. Thus, mepolizumab may be a useful therapeutic agent for the treatment of conditions characterized by increased levels of eosinophils.

A phase III, compassionate use trial of mepolizumab (NCT00244686) in patients with hypereosinophilic syndrome was ongoing in October 2007 in the US. Patients who have significant clinical disease but are unresponsive to traditional treatment and those who have demonstrated clinical benefit from previous anti-IL-5 treatment are eligible to take part in the trial.

Mepolizumab is also in phase I/II clinical development for the treatment of eosinophilic esophagitis.

A phase I/II trial (NCT00358449) began in August 2006 in the US, Australia, the UK, and Canada, and will enroll approximately 72 pediatric patients with eosinophilic esophagitis. The randomized, parallel-group clinical trial will evaluate the safety, tolerability, pharmacokinetics, and pharmacodynamics of intravenous mepolizumab for 12 weeks. In September 2006, GSK completed enrollment in a phase I/II study of mepolizumab for the treatment of eosinophilic esophagitis in 10 adult patients in Switzerland (NCT00274703). The randomized, double-blind, placebo-controlled study will evaluate the pharmacokinetics, pharmacodynamics, safety, and tolerability of IV mepolizumab.

A phase I/II trial of mepolizumab in 4 patients with eosinophilic esophagitis conducted by Cincinnati Children's Hospital found the monoclonal antibody was safe and effective. Brigham and Women's Hospital, in association with GSK, is conducting a phase I/II trial of mepolizumab, in the US, in patients with Churg-Strauss Syndrome (CSS). The trial, which started in September 2007, will evaluate the potential of mepolizumab to reduce the need for corticosteroid therapy in patients with CSS (NCT00527566). CSS, otherwise known as allergic granulomatosis, is defined by patients with asthma, eosinophilia, and vasculitis.

Previous
Next

Interferons

Class Summary

These agents are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Alpha, beta, and gamma interferons may be given topically, systemically, and intralesionally.

Interferon alfa-2b (Intron A)

 

Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles. Butterfield et al reported use of interferon alpha in treatment of HES with some success.

Interferon alfa 2a (Roferon A)

 

Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles. Butterfield et al reported use of interferon alpha in treatment of HES with some success.

Previous
 
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, Michigan State Medical Society, Heart Rhythm Society

Disclosure: Received honoraria from Medtronic, for speaking and teaching; Received honoraria from Zoll for speaking and teaching; Received honoraria from Boeringer Ingelheim for speaking and teaching; Received honoraria from St Jude''''''''s Medical for speaking and teaching; Received honoraria from Boston Scientific corporation for speaking and teaching; Received honoraria from Biotronik for speaking and teaching; Received honoraria from Sanofi Aventis for speaking and teaching.

Coauthor(s)

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.

Fatima Ansari University of Michigan

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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 Physiological Society, American Society for Clinical Investigation, American Society for Investigative Pathology, Association of American Physicians, Texas Medical Association, Southern Society for Clinical Investigation, American Federation for Clinical Research, Association of Professors of Medicine, Association of Professors of Cardiology, American Association for the Advancement of Science, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association

Disclosure: Received honoraria from Pfizer for speaking and teaching; Received honoraria from Merck for speaking and teaching; Received consulting fee from Orthoclinica Diagnostica for consulting.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

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

Disclosure: Nothing to disclose.

Acknowledgements

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.

References
  1. Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of cardiomyopathies. Circulation. 1996 Mar 1. 93(5):841-2. [Medline].

  2. Gotlib J. World Health Organization-defined eosinophilic disorders: 2011 update on diagnosis, risk stratification, and management. Am J Hematol. 2011 Aug. 86(8):677-88. [Medline].

  3. Loeffler W. Endocarditis parietalis fibroplastica mit Blut-eosinophilie, ein eigenartiges Krankheitshild. Schweiz Med Wochenschr;. 1936. 66:817-820.

  4. Oakley CM, Olsen GJ. Eosinophilia and heart disease. Br Heart J. 1977 Mar. 39(3):233-7. [Medline].

  5. Herzog CA, Snover DC, Staley NA. Acute necrotising eosinophilic myocarditis. Br Heart J. 1984 Sep. 52(3):343-8. [Medline].

  6. Tonnesen P, Teglbjaerg CS. An "unexpected" fatal case of the hypereosinophilic syndrome. Eur J Respir Dis. 1984 Jul. 65(5):389-93. [Medline].

  7. Kim CH, Vlietstra RE, Edwards WD, et al. Steroid-responsive eosinophilic myocarditis: diagnosis by endomyocardial biopsy. Am J Cardiol. 1984 May 15. 53(10):1472-3. [Medline].

  8. Isaka N, Araki S, Shibata M, et al. Reversal of coronary artery occlusions in allergic granulomatosis and angiitis (Churg-Strauss syndrome). Am Heart J. 1994 Sep. 128(3):609-13. [Medline].

  9. Seshadri S, Narula J, Chopra P. Asymptomatic eosinophilic myocarditis: 2 + 2 = 4 or 5!. Int J Cardiol. 1991 Jun. 31(3):348-9. [Medline].

  10. Solley GO, Maldonado JE, Gleich GJ, et al. Endomyocardiopathy with eosinophilia. Mayo Clin Proc. 1976 Nov. 51(11):697-708. [Medline].

  11. Olsen EG, Spry CJ. Relation between eosinophilia and endomyocardial disease. Prog Cardiovasc Dis. 1985 Jan-Feb. 27(4):241-54. [Medline].

  12. Priglinger U, Drach J, Ullrich R, et al. Idiopathic eosinophilic endomyocarditis in the absence of peripheral eosinophilia. Leuk Lymphoma. 2002 Jan. 43(1):215-8. [Medline].

  13. Tai PC, Ackerman SJ, Spry CJ, et al. Deposits of eosinophil granule proteins in cardiac tissues of patients with eosinophilic endomyocardial disease. Lancet. 1987 Mar 21. 1(8534):643-7. [Medline].

  14. Spry CJ, Tai PC, Davies J. The cardiotoxicity of eosinophils. Postgrad Med J. 1983 Mar. 59(689):147-53. [Medline].

  15. Gleich GJ, Frigas E, Loegering DA, et al. Cytotoxic properties of the eosinophil major basic protein. J Immunol. 1979 Dec. 123(6):2925-7. [Medline].

  16. Slungaard A, Vercellotti GM, Tran T, et al. Eosinophil cationic granule proteins impair thrombomodulin function. A potential mechanism for thromboembolism in hypereosinophilic heart disease. J Clin Invest. 1993 Apr. 91(4):1721-30. [Medline].

  17. Cunningham K, Davies RA, Catching J, Veinot JP. Pathologic quiz case: a young woman with eosinophilia and heart failure. Primary hypereosinophilic syndrome with loeffler endocarditis. Arch Pathol Lab Med. 2005 Jan. 129(1):e29-30. [Medline].

  18. Cools J, DeAngelo DJ, Gotlib J, et al. A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med. 2003 Mar 27. 348(13):1201-14. [Medline].

  19. Vandenberghe P, Wlodarska I, Michaux L, et al. Clinical and molecular features of FIP1L1-PDFGRA (+) chronic eosinophilic leukemias. Leukemia. 2004 Apr. 18(4):734-42. [Medline].

  20. Rotoli B, Catalano L, Galderisi M, et al. Rapid reversion of Loeffler's endocarditis by imatinib in early stage clonal hypereosinophilic syndrome. Leuk Lymphoma. 2004 Dec. 45(12):2503-7. [Medline].

  21. Alderman EL. Non-infective endocardial disease. Cardiovascular Disease. 1999. 1-7.

  22. Bestetti RB, Corbucci HA, Fornitano LD, et al. Angina-like chest pain and syncope as the clinical presentation of left ventricular endomyocardial fibrosis: a case report. Angiology. 2005 May-Jun. 56(3):339-42. [Medline].

  23. Coelho-Filho OR, Mongeon FP, Mitchell RN, Blankstein R, Jerosch-Herold M, Kwong RY. Images in cardiovascular medicine. Loeffler endocarditis presenting with recurrent polymorphic ventricular tachycardia diagnosed by cardiac magnetic resonance imaging. Circulation. 2010 Jul 6. 122(1):96-9. [Medline].

  24. Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood. 1994 May 15. 83(10):2759-79. [Medline].

  25. Maruyoshi H, Nakatani S, Yasumura Y, et al. Loffler's endocarditis associated with unusual ECG change mimicking posterior myocardial infarction. Heart Vessels. 2003 Mar. 18(1):43-6. [Medline].

  26. Mor A, Segev A, Hershkovits R, et al. Hypereosinophilic syndrome presenting as acute myocardial infarction. Allergy. 2000 Sep. 55(9):899-900. [Medline].

  27. Gudmundsson GS, Ohr J, Leya F, et al. An unusual case of recurrent Loffler endomyocarditis of the aortic valve. Arch Pathol Lab Med. 2003 May. 127(5):606-9. [Medline].

  28. Niemeijer ND, van Daele PL, Caliskan K, Oei FB, Loosveld OJ, van der Meer NJ. Loffler endocarditis: a rare cause of acute cardiac failure. J Cardiothorac Surg. 2012 Oct 10. 7:109. [Medline]. [Full Text].

  29. Klag T, Schnetzke U, Benz R, et al. Leriche's syndrome and Loffler endocarditis in a 30-year-old patient presenting with hypereosinophilic syndrome. Ann Hematol. 2012 Jan. 91(1):139-41. [Medline].

  30. Simonnet B, Jacquier A, Salaun E, Hubert S, Habib G. Cardiac involvement in hypereosinophilic syndrome: role of multimodality imaging. Eur Heart J Cardiovasc Imaging. 2014 Oct 9. [Medline].

  31. Parrillo JE. Heart disease and the eosinophil. N Engl J Med. 1990 Nov 29. 323(22):1560-1. [Medline].

  32. Del Bene MR, Cappelli F, Rega L, Venditti F, Barletta G. Characterization of Loeffler Eosinophilic Myocarditis by Means of Real Time Three-Dimensional Contrast-Enhanced Echocardiography. Echocardiography. 2011 Nov 8. [Medline].

  33. Spyrou N, Foale R. Restrictive cardiomyopathies. Curr Opin Cardiol. 1994 May. 9(3):344-8. [Medline].

  34. Child JS, Perloff JK. The restrictive cardiomyopathies. Cardiol Clin. 1988 May. 6(2):289-316. [Medline].

  35. Watanabe K, Tournilhac O, Camilleri LF. Recurrent thrombosis of prosthetic mitral valve in idiopathic hypereosinophilic syndrome. J Heart Valve Dis. 2002 May. 11(3):447-9. [Medline].

  36. Zakhama L, Slama I, Boussabah E, Harbegue B, Mimouni M, Abdelaali N, et al. Recurrent native and prosthetic mitral valve thrombosis in idiopathic hypereosinophilic syndrome. J Heart Valve Dis. 2014 Mar. 23(2):168-70. [Medline].

  37. Paydar A, Ordovas KG, Reddy GP. Magnetic resonance imaging for endomyocardial fibrosis. Pediatr Cardiol. 2008 Sep. 29(5):1004-5. [Medline].

  38. Langwieser N, von Olshausen G, Rischpler C, Ibrahim T. Confirmation of diagnosis and graduation of inflammatory activity of Loeffler endocarditis by hybrid positron emission tomography/magnetic resonance imaging. Eur Heart J. 2014 Sep 21. 35(36):2496. [Medline].

  39. Arnold M, McGuire L, Lee JC. Loeffler's fibroplastic endocarditis. Pathology. 1988 Jan. 20(1):79-82. [Medline].

  40. Fawzy ME, Ziady G, Halim M, et al. Endomyocardial fibrosis: report of eight cases. J Am Coll Cardiol. 1985 Apr. 5(4):983-8. [Medline].

  41. Felice PV, Sawicki J, Anto J. Endomyocardial disease and eosinophilia. Angiology. 1993 Nov. 44(11):869-74. [Medline].

  42. Uetsuka Y, Kasahara S, Tanaka N, et al. Hemodynamic and scintigraphic improvement after steroid therapy in a case with acute eosinophilic heart disease. Heart Vessels Suppl. 1990. 5:8-12. [Medline].

  43. Butterfield JH, Gleich GJ. Interferon-alpha treatment of six patients with the idiopathic hypereosinophilic syndrome. Ann Intern Med. 1994 Nov 1. 121(9):648-53. [Medline].

  44. Tanaka H, Kawai H, Tatsumi K, Kataoka T, Onishi T, Yokoyama M, et al. Surgical treatment for Loffler's Endocarditis with left ventricular thrombus and severe mitral regurgitation: a case report. J Cardiol. April, 2006. 47 (4):207-13. [Medline].

  45. Jategaonkar S, Butz T, Faber L. [Surgical treatment of the hypereosinophilic syndrome with cardiac involvement (Loffler's endocarditis)]. Dtsch Med Wochenschr. Mar. 2007. 7133(12):50-52. [Medline].

  46. Abonia JP, Putnam PE. Mepolizumab in eosinophilic disorders. Expert Rev Clin Immunol. 2011 Jul. 7(4):411-7. [Medline]. [Full Text].

 
Previous
Next
 
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.