Loeffler Endocarditis Medication

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

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)

 

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.[40]

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
Proceed to Follow-up
 
 
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.

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. Mar 1 1996;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. Aug 2011;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. Mar 1977;39(3):233-7. [Medline].

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

  6. Tonnesen P, Teglbjaerg CS. An "unexpected" fatal case of the hypereosinophilic syndrome. Eur J Respir Dis. Jul 1984;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. May 15 1984;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. Sep 1994;128(3):609-13. [Medline].

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

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

  11. Olsen EG, Spry CJ. Relation between eosinophilia and endomyocardial disease. Prog Cardiovasc Dis. Jan-Feb 1985;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. Jan 2002;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. Mar 21 1987;1(8534):643-7. [Medline].

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

  15. Gleich GJ, Frigas E, Loegering DA, et al. Cytotoxic properties of the eosinophil major basic protein. J Immunol. Dec 1979;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. Apr 1993;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. Jan 2005;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. Mar 27 2003;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. Apr 2004;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. Dec 2004;45(12):2503-7. [Medline].

  21. Alderman EL. Non-infective endocardial disease. In: 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. May-Jun 2005;56(3):339-42. [Medline].

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

  24. Maruyoshi H, Nakatani S, Yasumura Y, Hanatani A, Yamaguchi T, Yutani C, et al. Löffler's endocarditis associated with unusual ECG change mimicking posterior myocardial infarction. Heart Vessels. Mar 2003;18(1):43-6. [Medline].

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

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

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

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

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

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

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

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

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

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

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

  36. 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].

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

  38. 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].

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

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

  41. Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A Textbook of Cardiovascular Medicine. 2001. 6th ed. WB Saunders Co.

  42. Del Giudice P, Desalvador F, Bernard E, Caumes E, Vandenbos F, Marty P, et al. Loeffler's syndrome and cutaneous larva migrans: a rare association. Br J Dermatol. Aug 2002;147(2):386-8. [Medline].

  43. deMello DE, Liapis H, Jureidini S, et al. Cardiac localization of eosinophil-granule major basic protein in acute necrotizing myocarditis. N Engl J Med. Nov 29 1990;323(22):1542-5. [Medline].

  44. Fauci AS, Harley JB, Roberts WC, et al. NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations. Ann Intern Med. Jul 1982;97(1):78-92. [Medline].

  45. [Best Evidence] Flood-Page P, Swenson C, Faiferman I, Matthews J, Williams M, Brannick L, et al. A study to evaluate safety and efficacy of mepolizumab in patients with moderate persistent asthma. Am J Respir Crit Care Med. Dec 1 2007;176(11):1062-71. [Medline].

  46. Garrett JK, Jameson SC, Thomson B, Collins MH, Wagoner LE, Freese DK, et al. Anti-interleukin-5 (mepolizumab) therapy for hypereosinophilic syndromes. J Allergy Clin Immunol. Jan 2004;113(1):115-9. [Medline].

  47. Genovesi-Ebert A, Lombardi M, Capochiani E, et al. Heart involvement in T cell lymphoma through hypereosinophilic syndrome: a common complication of a rare condition. J Cardiovasc Magn Reson. 2005;7(2):495-9. [Medline].

  48. Gottdiener JS, Maron BJ, Schooley RT, et al. Two-dimensional echocardiographic assessment of the idiopathic hypereosinophilic syndrome. Anatomic basis of mitral regurgitation and peripheral embolization. Circulation. Mar 1983;67(3):572-8. [Medline].

  49. Hayashi S, Furuya S, Imamura H. Fulminant eosinophilic endomyocarditis in an asthmatic patient treated with pranlukast after corticosteroid withdrawal. Heart. Sep 2001;86(3):E7. [Medline].

  50. Mepolizumab: 240563, anti-IL-5 monoclonal antibody - GlaxoSmithKline, anti-interleukin-5 monoclonal antibody - GlaxoSmithKline, SB 240563. Drugs R D. 2008;9(2):125-30. [Medline].

  51. Ohnishi T, Kita H, Weiler D, et al. IL-5 is the predominant eosinophil-active cytokine in the antigen- induced pulmonary late-phase reaction. Am Rev Respir Dis. Apr 1993;147(4):901-7. [Medline].

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 © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.