Loeffler endomyocarditis, Loeffler fibroblastic endocarditis, Loeffler fibroplastic endomyocarditis, Loeffler syndrome, endomyocardial fibrosis, Loeffler disease, restrictive cardiomyopathy, eosinophilia, eosinophilic myocarditis, hypereosinophilic syndrome, eosinophilic leukemia, eosinophilic endocardial disease, eosinophilic arteritis, eosinophilic endomyocardial disease, idiopathic eosinophilic endomyocarditis.
Echocardiography. 2006 Sep;23(8):689-91.
Evaluation of cardiac involvement in hypereosinophilic syndrome: complementary roles of transthoracic, transesophageal, and contrast echocardiography.
Shah R, Ananthasubramaniam K.
Henry Ford Heart and Vascular Institute, Detroit, Michigan 48202, USA.
Hypereosinophilic syndrome is a rare but important systemic disease with multiple clinical presentations. Approximately 40% of these cases have cardiac involvement. Echocardiography is the most easily available and versatile imaging modality in assessing cardiac involvement in this disease process. As described and reviewed in this case, it may be the first imaging modality to raise suspicion of this disease entity. Hence, clinicians interpreting echocardiograms and caring for patients need to be aware of the manifestations and complementary roles of various echo techniques in delineating cardiac involvement. Furthermore, the importance of a thorough history and laboratory review prior to echocardiography may provide valuable clues which may otherwise be missed.
J Cardiol. 2006 Apr;47(4):207-13.
Surgical treatment for Loffler's endocarditis with left ventricular thrombus and severe mitral regurgitation: a case report.
Tanaka H, Kawai H, Tatsumi K, Kataoka T, Onishi T, Nose T, Mizoguchi T, Yokoyama M, Okita Y.
Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe.
A 65-year-old female was admitted to our hospital because of dyspnea. Laboratory examinations revealed hypereosinophilia at a local hospital. Transthoracic and transesophageal echocardiography showed normal left ventricular dimension and function. The left ventricular apex was obliterated and the posterior and lateral walls were thickened by an abnormal mass. The posterior mitral leaflet was encapsulated by this abnormal mass. The limited motion of the posterior mitral leaflet caused mitral malcoaptation, resulting in severe mitral regurgitation. Hypereosinophilia was considered to be idiopathic, as no other disorders known to cause secondary eosinophilia were found. No other organ dysfunction was associated with the condition. Thus, the diagnosis was Loffler's endocarditis associated with hypereosinophilic syndrome. The patient was given conservative medical treatment immediately on admission. However, heart failure caused by mitral regurgitation would be difficult to treat with conservative medical treatment, so we chose a surgical strategy. The symptoms obviously improved after valve replacement and removal of the abnormal mass, and the patient was discharged. However, she died of cerebral infarction at a local hospital 3 months later.
Eur J Heart Fail. 2005 Oct;7(6):1023-6. Epub 2005 Sep 26.
Ventricular remodeling in Loeffler endocarditis: implications for therapeutic decision making.
Lofiego C, Ferlito M, Rocchi G, Biagini E, Perugini E, Branzi A, Rapezzi C.
Institute of Cardiology, University of Bologna, Policlinico S. Orsola-Malpighi, Via Massarenti 9, 40138 Bologna, Italy.
BACKGROUND: Little is known about the morphological and functional evolution of ventricular abnormalities in Loeffler endocarditis. METHODS AND RESULTS: We describe 5 patients, including 3 with long-term echocardiographic follow-up, in whom apical obliteration due to fibro-thrombotic thickening of the endocardium showed favorable patterns of evolution. In one patient there was almost complete resolution of the obliterative process with consequently increased effective ventricular volume. In two patients formation of a flow-passage in the fibrocalcific apical 'floor' between the main medioventricular cavity and the apical chamber, leading to a 'double-chambered' left ventricle was observed. CONCLUSIONS: Medical therapy and appropriate anticoagulation, can induce favorable long-term ventricular remodeling in Loeffler endocarditis.
South Med J. 2005 Sep;98(9):943-5.
Left ventricular endocardial calcification in a patient with myeloproliferative disease.
Khouzam RN, Shaikh K, D'Cruz IA.
University of Tennessee Health Science Center, Division of Cardiovascular Diseases, Memphis, TN, USA. firstname.lastname@example.org
The case of a 57-year-old male with a history significant for myeloproliferative disease, chronic renal failure, hypertension, and prostate cancer is described. His complete blood count was remarkable for neutrophilia and, notably, eosinophilia. Subsequent to two syncopal episodes, a transthoracic echocardiogram was performed as part of the workup, which showed an unusual calcified mass in the left ventricular apical region but separate from the apical myocardium, with normal left ventricular systolic function. A transesophageal echocardiogram and computed tomography of the chest confirmed the presence of extensive calcification in the left ventricle of unusual location and shape. This patient probably had Loeffler endocarditis related to myeloproliferative disorder, complicated by calcification of the endocardial sclerotic lesions.
Leuk Lymphoma. 2004 Dec;45(12):2503-7.
Rapid reversion of Loeffler's endocarditis by imatinib in early stage clonal hypereosinophilic syndrome.
Rotoli B, Catalano L, Galderisi M, Luciano L, Pollio G, Guerriero A, D'Errico A, Mecucci C, La Starza R, Frigeri F, Di Francia R, Pinto A.
Department of Medicina Clinica e Sperimentale Universita Federico II Napoli Italy. email@example.com
Endomyocardial fibrosis (Loeffler's endocarditis) is the main cause of poor outcome in Hyper Eosinophilic Syndrome (HES) and Eosinophilic Leukemia (EL). Reversion of the cardiac damage has been seldom reported, and thrombi can superimpose on infiltrated walls, originating oembolic complications. The tyrosine kynase inhibitor imatinib has been recently employed in patients affected by HES or EL, with impressive results. We have treated with imatinib a young patient affected by Loeffler's endocarditis during EL. Loeffler's endocarditis was studied by transthoracic Doppler echocardiography with and without the contrast agent SonoVue. Cytogenetics, FISH and molecular analysis showed the presence of the FIP1L1/PDGFRA fusion gene, recently detected in a majority of HES patients. Standard echocardiography revealed a large infiltration of the apical region, with apparently pedunculate corpora floating in the LV chamber; after SonoVue injection, a thick endo-myocardial infiltration involving papillary muscles and tendinous chords appeared, which simulated mobile thrombi at standard echography. Treatment with low dose imatinib caused rapid regression of both eosinophilic proliferation and endomyocardiopathy. The fusion gene FIP1L1-PDGFRA was found significantly decreased after a few months of treatment. Using a contrast echocardiographic approach, we demonstrated the non-thrombotic origin of the "in plus" image in our patient and its rapid resolution following imatinib treatment. Imatinib is an excellent candidate for first line treatment of Loeffler's endocarditis, especially when the FIP1L1/PDGFA fusion gene is detected.
Heart Vessels. 2003 Mar;18(1):43-6.
Loffler's endocarditis associated with unusual ECG change mimicking posterior myocardial infarction.
Maruyoshi H, Nakatani S, Yasumura Y, Hanatani A, Yamaguchi T, Yutani C, Ishibashi-Ueda H, Miyatake K, Yamagishi M.
Department of Cardiology, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan.
A73-year-old man with a history of bronchial asthma and atrial fibrillation was admitted to our hospital because of dyspnea and back pain. Blood analysis revealed a marked increase in total blood cell and eosinophil counts. The creatine kinase and creatine kinase-MB increased slightly. The ECG demonstrated significant ST-segment depression that mimicked acute posterior myocardial infarction. Emergent coronary angiography showed no stenotic lesions. The histological findings in endomyocardial biopsy showed thickened endocardium associated with significant eosinophilic infiltration, which was compatible with Loffler's endocarditis. After the administration of prednisolone, the patient's general condition, eosinophilia, ECG abnormalities, and histological findings were improved dramatically. The endomyocardial biopsy in the acute phase was helpful for diagnosis and therapeutic decision-making.
Pediatrics. 2002 Nov;110(5):1014-8.
Loffler's endocarditis presenting in 2 children as fever with eosinophilia.
Horenstein MS, Humes R, Epstein ML, Draper D.
Division of Cardiology, Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, MI 48201-2196, USA.
Hypereosinophilic syndromes are defined by the presence of peripheral and bone marrow eosinophilia and by the infiltration of multiple organs by mature eosinophilic cells. Loffler's endocarditis is a condition in which mature eosinophils infiltrate and damage the endocardium and myocardium. Male adults who live in the tropics are the population predominantly affected by this condition. Typical clinical features include weight loss, fever, cough, rash, and congestive heart failure. In this article, we report the typical presentation of an unusual illness that occurred in 2 pediatric patients in different geographic locations. In addition, we believe that these are the youngest patients with Loffler's endocarditis reported.
Cutaneous larva migrans associated with Loffler's syndrome.
Schaub NA, Perruchoud AP, Buechner SA.
Department of Dermatology, University Hospital Basel, Switzerland. firstname.lastname@example.org
We describe a patient who was admitted to hospital after returning from a holiday in Thailand with coronary artery disease and ventricular tachycardia. As an incidental finding, the routine chest radiography showed migratory pulmonary infiltrates. A peripheral blood smear showed eosinophilia. Physical examination revealed multiple, slightly raised, erythematous, serpentine tracks on the buttocks. A clinical diagnosis of larva migrans was made, and the patient was treated with oral albendazole 400 mg on 5 consecutive days and a single dose of oral praziquantel 3600 mg. By the end of treatment, most of the cutaneous lesions, the pulmonary infiltrates and the peripheral eosinophilia had resolved. The final diagnosis was larva migrans associated with Loffler's syndrome. Copyright 2002 S. Karger AG, Basel
Arch Mal Coeur Vaiss. 2001 Mar;94(3):226-30.
Loffler's fibroblastic endocarditis. A report of a case complicating toxocarosis
Prunier F, Delepine S, Victor J, de Gentile L, Moreau C, Laporte J, Dupuis JM, Geslin P.
Service de cardiologie, centre hospitalier universitaire, 4, rue Larrey, 49033 Angers.
The authors report a case of Loffler's fibroblastic endocarditis complicating a toxocarosis infection. Parasitic infestation with toxocara canis is usually asymptomatic, but this was a very rare observation of cerebral involvement associated with symptomatic Loffler's endocarditis. This is an unusual form of restrictive cardiac disease constantly accompanied by prolonged hypereosinophilia. In addition to the classical signs of cardiac failure, an acute febrile illness imitating a connective tissue disease may be observed. Echocardiography helps diagnosis by showing endomyocardial fibrosis and adherent thrombosis at one or both ventricular apices. The management of cardiac failure should include, whenever possible, radical treatment of the hypereosinophilia. At an advanced stage, surgical endocardial decortication is the only means of improving symptoms and the prognosis of these patients.
J Am Soc Echocardiogr. 2000 Jul;13(7):690-2.
Loffler's syndrome: pulmonary vein and transmitral doppler flow analysis by transesophageal echocardiography-report of a case.
Garcia-Pascual J, Gonzalez-Gallarza RD, Jimenez MP, Martinez JP, Carnicer JO, Pajuelo CG.
Cardiology Section, Hospital Universitario Doce de Octubre, Madrid, and the Coronary Unit, Residencia Ntra. Sra. de Alarcos, Ciudad Real.
Loffler's syndrome is defined by prolonged and profound eosinophilia and restrictive cardiomyopathy. Doppler echocardiography is useful in both the diagnosis and management of this entity. On the other hand, diastolic dysfunction is assessed better by transesophageal echocardiography than by transthoracic echocardiography, mainly in the analysis of pulmonary vein Doppler flow. We describe a patient with Loffler's syndrome, whose pulmonary vein flow, obtained by transesophageal echocardiography, was helpful for better management of the disease.
Eur Respir J. 1999 Apr;13(4):930-3.
Systemic lupus erythematosus, eosinophilia and Loffler's endocarditis. An unusual association.
Thomeer M, Moerman P, Westhovens R, Van den Eeckhout A, Dequeker J, Demedts M.
Division of Pulmonary Diseases, University Hospital Gasthuisberg, Katholieke Universiteity Leuven, Belgium.
A 24-yr-old male, known since the age of 11 to have a nonerosive arthritis and later diagnosed as having systemic lupus erythematosus (SLE), developed subacute heart failure with diffuse lung infiltrates and died suddenly after having presented a moderate hypereosinophilia for 6 months for which no other causes besides the SLE were found. A post mortem examination revealed Loffler's endocarditis (endocarditis parietalis fibroplastica) with acute pulmonary capillaritis. This represents Loffler's endocarditis in the setting of SLE. To the best of the authors' knowledge, this association has not been reported before.
Loffler's endomyocarditis in the idiopathic hypereosinophilic syndrome.
Corssmit EP, Trip MD, Durrer JD.
Department of Internal Medicine, Academic Medical Center, Amsterdam, The Netherlands. E.P.Corssmit@amc.uva.nl
The idiopathic hypereosinophilic syndrome (HES) is a leukoproliferative disorder characterized by sustained eosinophilia (> 1.5 x 10(9)/l) and (multi-)organ dysfunction caused by infiltration of eosinophils. Especially the heart is frequently affected. In this report, we describe 2 patients with HES and Loffler's endomyocarditis. Prednisone is the drug of choice for treatment. Both our patients responded very well to prednisone and came into remission. If prednisone fails, there are other therapeutic options like myelosuppressive drugs (hydroxyurea and vincristine) or interferon-alpha. We review the literature with regard to clinical presentation, diagnosis and treatment.
Z Kardiol. 1998 Apr;87(4):293-9.
Comment in: Z Kardiol. 1998 Aug;87(8):644.
Loffler fibroblastic endocarditis in the thrombotic stages in isolated right ventricular tissue eosinophilia
Hagendorff A, Hummelgen M, Omran H, Pizzulli L, Zirbes M, Bierhoff E, Sommer T, Pfeifer U, Kirchhoff PG, Nitsch J, Luderitz B.
Medizinische Universitatsklinik und Poliklinik-Innere Medizin, Bonn.
We report on a male, 31 year old, Turkish patient with an intracardiac mass in the right ventricle, reduction of performance and weight, as well as intermittent fever. No eosinophilia was documented in the peripheral blood; cardiac function was primarily normal. Besides the differential diagnosis of Loffer's endocarditis (endomyocardial fibrosis) an inflammatory disease and a malignant cardiac tumor were suggested. The diagnosis of Loffler's endocarditis could not be confirmed morphologically by echocardiography nor histologically by right ventricular biopsy. Operative removal of the mass lesion was necessary because of fast tumor progression, fulminant pulmonary embolism, and infiltration of the tricuspid valve. Only then, histologically Loffler's eosinophilic endocarditis of thrombotic stage was diagnosed. Antiphlogistic therapy with cortisone was initially performed. With a dose reduction after 6 months, a relapse of the thrombotic mass occurred. Therefore, continuous treatment with cortisone and azathioprine was induced followed by further tumor regression and further clinical stabilization since 8 months of treatment.
Jpn J Thorac Cardiovasc Surg. 1998 May;46(5):455-60.
A case of surgical treatment for Loffler's endomyocarditis
Tamura M, Seki M, Tsubota M, Endo M, Tsunezuka Y, Sato H.
Department of Cardiovascular Surgery, Ishikawa Prefectual Central Hospital, Japan.
We performed surgical treatment in a case of loffler's endocarditis. The patient was a 32-year-old male whose first symptom was easy fatigability. Blood count showed eosinophilia (eosinocyte count 6720/mm3). Echocardiography and vetriculography showed thickened bilateral endocardium and extension disturbance. We diagnosed this case as loffler's endocarditis and performed surgical treatment because medical treatment was unsuccessful. Removal of the thrombus the bilateral ventricles, endocardectomy and mitral valve replacement were performed. Endocardectomy required close attention because the border between thickened endocardium and normal myocardium was obscure. The patient survived surgery, but postoperative echocardiography (15 days) revealed slightly thickened endocardium of the right ventricle. He died of left heart failure 1 month after surgery. At that time, eosinocyte count was 110,000/mm3.
Med Trop (Mars). 1998;58(4 Suppl):459-64.
The heart and the eosinophil
Touze JE, Fourcade L, Heno P, Mafart B, Mourot S.
Service de Cardiologie, Hopital d'Instruction des Armees Laveran, Marseille, France. email@example.com
The beneficial effects of polynuclear eosinophils (PE) are well known. However, under certain circumstances, PE can be harmful. The heart is a prime target for PE toxicity which is due to release of basic proteins by eosinophils including major basic protein, cationic protein, and peroxidase. The most common manifestation of PE toxicity is chronic parietal endocarditis (CPE) which regroups two entities: Loeffler's fibroplastic endocarditis and Davies' endomyocardial fibrosis. Loeffler's fibroplastic endocarditis occurs mainly in temperate climates. Patients present high, persistent eosinophil levels similar to those observed in essential hypereosinophilic syndrome (EHS) or Chusid syndrome. Davies' endomyocardial fibrosis occurs in tropical countries where eosinophilic helminthiasis are endemic. The incidence of eosinophilic myocarditis (EM) is low but probably underestimated. EM can be observed in any case involving PE and has been described in many cases of drug-induced atopy, in Churg and Strauss syndrome, and in EHS. The most common cause of death is short-term occurrence of cardiogenic shock or dilated hypokinetic cardiomyopathy. Some patients have been successfully treated by early, intensive corticosteroid therapy and/or heart transplantation. The nosological classification of EM and CPE remains controversial. The two disorders may form a continuum with CPE as the second phase. Other authors have suggested that EM and CPE result from the action of PE on two distinct targets, i.e. endothelial cells for EM and myocytes for CPE. In the future, it may be possible to identify subjects with a predisposition to PE-induced heart disease by studying of genes coding for interleukins (IL-5, IL-4, IL-3) and GM-CSF in the 5q31-q33 region of chromosome 5.
Dtsch Med Wochenschr. 1997 Feb 14;122(7):182-7.
Dtsch Med Wochenschr. 1997 Jun 13;122(24):802.
Loffler's parietal fibroplastic endocarditis. Echocardiographic course over 5 years
Metzler B, Gunther E, Perier P, Braun B, Hust MH.
Medizinische Klinik, Kreiskrankenhaus Reutlingen.
HISTORY AND CLINICAL FINDINGS: A 28-year-old man, who had sustained a traumatic displaced fracture of the left lateral clavicle requiring operative realignment, was admitted to hospital because of the incidental finding of pathological electrocardiographic findings (suggestive of past anterior myocardial infarction). He had dyspnoea on effort and episodes of irregular tachycardia without other cardiac symptoms, as well as regular tachycardia (120/min) without pulse deficit. Body temperature was 37.3 degrees C, blood pressure 110/70 mm Hg. INVESTIGATIONS: Transoesophageal echocardiography showed regular myocardial contractility but a 3.27 cm cap-like area of echo-poor and echo-dense layers at the left ventricular apex. There was leucocytosis (25,400/microliter) with 45% eosinophilia (11,430/microliter). IgE was raised to 134.6 kU/l. Bone marrow smear showed marked eosinophilic but little neutrophilic hyperplasia. Parasitic infection was excluded. TREATMENT AND COURSE: The clinical and echocardiographic findings suggested the diagnosis of Loffler's eosinophilic endocarditis (endomyocardial fibrosis), later confirmed histologically. After initial treatment, first only with cortisone then also hydroxyurea, the eosinophilia finally responded to combined cortisone and interferon alpha 2. The dosage schedule was governed by the clinical and echocardiographic findings. In the further course of the disease there occurred progressive heart failure with severe tricuspid and mitral regurgitation, secondary pulmonary hypertension and severe fibrosis of both ventricles, 41 months after diagnosis the patient underwent tricuspid and mitral valve reconstruction with removal of the endocardial fibrotic layers. Follow-up examinations found the cardiac condition to be adequately controlled without further cardiac infiltration since 20 months. CONCLUSIONS: Echocardiography, in conjunction with the clinical findings, provides a firm foundation for successfully treating Loffler's endocarditis. In selected cases cardiac surgery can markedly improve the course.
Cesk Patol. 1994 Aug;30(3):93-6.
Loffler's endocarditis (with manifestations of restrictive cardiomyopathy and hypereosinophilia)
Macak J, Indrak K, Dusek J.
Oddeleni patologie Fakultni nemocnice, Olomouc.
Loeffler's endocarditis in a 47-year-old man was followed 5 years. He died of heart failure. His original diagnosis was eosinophilic leukaemia but cytogenetic investigation failed to show any chromosomal aberration and only mature eosinophilic leukocytes were present in peripheral blood. Relation between heart lesions and eosinophilic leukocyte factors (peroxidase, major basic protein, cationic protein, transforming growth factor beta) were discussed.
Herz. 1994 Jun;19(3):138-43.
Loffler endocarditis fibroplastica with simultaneous infectious endocarditis
Menz V, Drude L, Schonian U, Herzum M, Bethge C, Maisch B.
Abteilung Innere Medizin-Kardiologie, Philipps-Universitat Marburg.
The clinical and immunological 8-year follow-up of a 45-year old female with hypereosinophilic syndrome and cardiac involvement of Loffler's fibroplastic endocarditis which was complicated by infective endocarditis during immunosuppressive treatment is presented. All 3 stages of the disease were documented by clinical and histologic data: stage 1 by biopsy proven eosinophilic myocarditis and arteritis, stage 2 with Berlin blue positive parietal thrombosis, and the fibrotic features of stage 3 both by fibrosis in the latest biopsies and by echocardiography. It was remarkable, however, that this classic clinical case of Loffler's endocarditis lacked a few serological markers postulated to be found regularly, e.g., a positive staining for the cationic protein and major ribonucleases. Instead, the patient demonstrated all the immunological features of autoreactive myocarditis with cytolytic, complement fixing antimyolemmal antibodies. After an initial loading dose of 120 mg prednisolone per day for 6 weeks (11/1986), the steroid dosage was reduced to 40 mg (12/1986) and diminished to 15 mg/day in 1988 to 1989. Finally, the patient was on 4 mg prednisolone per day for almost 4 years. In 1987, azathioprine was added in the dose of 150 mg/day for 6 weeks. In 3/1994 the patient developed infective endocarditis with streptococcus sanguis and presented with dyspnoea. By echocardiography a large floating structure was diagnosed on the anterior mitral leaflet and the left atrium was enlarged by severe mitral regurgitation. Infective endocarditis was successfully treated with antibiotics, but mitral regurgitation made valve replacement obligatory.
Chest. 1994 May;105(5):1599-600.
Loffler's syndrome secondary to crack cocaine.
Nadeem S, Nasir N, Israel RH.
Department of Medicine, St. Mary's Hospital, Rochester, NY.
Eosinophilic pulmonary infiltration is an uncommon presentation from cocaine abuse. We present a patient with migratory pulmonary infiltrates and eosinophilia consistent with Loffler's syndrome. Our review uncovered two other similar patients. The importance of early recognition is stressed in our report. Either abstinence from cocaine usage and/or steroids result in resolution of this illness.
Versicherungsmedizin. 1989 Sep 1;41(5):151-4.
Obstructive-restrictive cardiomyopathy. On the clinical aspects and pathology of Loffler endocarditis
Loffler's endocarditis parietalis fibroplastica represents a special entity among the cardiomyopathies which is seldom to be seen. The disease can be diagnosed by clinical findings including a myocardial biopsy. Prognosis is bad because no adequate therapy exists. The mean survival rate is 18 months and congestive heart failure is cause of death. Etiology of endomyocardial fibrosis is unknown. Included is a case report of Loffler's endocarditis in which the patient had an unusually long survival time of more than three years. Characteristic for the disease were an initial right heart failure followed by left heart insufficiency and multiple septic embolies into peripheral organs (spleen, liver, brain). The patient died from a cerebral emboly in the age of 50 years. Autopsy findings showed a severe endomyocardial fibrosis, typical for Loffler's endocarditis.
Taiwan Yi Xue Hui Za Zhi. 1989 Jul;88(7):740-3.
Hypereosinophilic syndrome with Loffler's endomyocarditis: report of an autopsy case
Yu IT, Chiang H, Wang JH.
Hypereosinophilic syndrome (HES) with Loffler's endomyocarditis is a rare disease with poor prognosis. Clinically, it mainly affects young adults, characterized by prolonged idiopathic blood eosinophilia, cardiopulmonary symptoms and hepatosplenomegaly. Pathological features consist of ventricular mural thrombi, marked fibrotic thickening of endocardium with scarring of myocardium, and multiorgan eosinophilic infiltration. We report a 2-year-old girl with idiopathic HES associated with Loffler's endomyocarditis. The girl was noted to have constitutional symptoms, cardiomegaly, and hepatosplenomegaly. Her total eosinophil count reached 150,000/microliters. She had no history of allergic diseases. The microbiological studies were negative. Echocardiography suggested thickened endocardium, mitral stenosis and regurgitation. In spite of intensive medical management, the girl died of refractory congestive heart failure. Autopsy revealed thick fresh mural thrombi involving the biventricular inflow tracts, inflammation and fibrosis of the endomyocardium, systemic thromboembolism and multiorgan eosinophilic infiltration. The pathology and pathogenesis of the disease are discussed and the literature is reviewed.
Vnitr Lek. 1989 May;35(5):483-8.
Pella J, Lazur J, Stancak B, Matejickova G, Pellova A, Schreter I.
The authors describe Loeffler's endocarditis and the treatment of this clinical entity. Among diagnostic methods which drew attention to a cardiac affection associated with eosinophilia, non-invasive examination methods were of decisive importance. They comprised conventional electrocardiographic examination, X-ray of the chest and two-dimensional echocardiography.
Rev Esp Cardiol. 1989 Feb;42(2):126-30.
Diagnostic usefulness of 2-dimensional echocardiography in eosinophilic endomyocardial disease (Loeffler disease)
Gonzalez Torrecilla E, Rey Perez M, Maravi Petri C, Alvarez Lacruz L, Cordoba Polo M.
We present an uncommon case of idiopathic hypereosinophilic syndrome with cardiac involvement (fibroplastic parietal endocarditis --Loffler's disease--) in a 48-year-old female with congestive heart failure and hypereosinophilia. The 2-D echo findings (biventricular apical obliteration by echogenic endomyocardial proliferations with normal systolic inward motion) were the clue for the diagnosis that was hemodynamically and pathologically confirmed subsequently. We emphasize the diagnostic value of two-dimensional echocardiography in this condition and review the literature on it.
Dtsch Med Wochenschr. 1985 Oct 11;110(41):1573-6.
Therapeutic possibilities in hypereosinophilia syndrome with Loffler's fibroplastic endomyocarditis.Efficacy of cytarabine and 6-thioguanine
Haas R, Mundinger A, Bohn T, Schaz K, Hunstein W.
In two of four patients with hypereosinophilia and Loffler's myocarditis (confirmed by biopsy) the activity of the disease was contained with prednisone, in one instance combined with hydroxycarbamide. In two patients, in whom the disease was taking a fulminant course and other treatment had failed, cytarabine and 6-thioguanine proved effective, providing a 16-month symptom-free period in one of them. But the second patient died from septicaemia associated with treatment-induced bone-marrow hypoplasia. Prednisone (1 mg/kg daily) and hydroxycarbamide (0.5-1.5 g daily) are the drugs of choice in the hypereosinophilia syndrome. If they fail, cytarabine (100 mg/m2 on days 1-5, repeated on day 28) and 6-thioguanine (100 mg/m2 daily) should be given.
Am J Cardiol. 1977 Sep;40(3):438-44.
Loeffler's endocarditis presenting as mitral and tricuspid stenosis.
Weyman AE, Rankin R, King H.
Loeffler's endocarditis characteristically produces cardiac dysfunction by the combined effects of endocardial fibrosis with restriction to diastolic inflow and intracavitary thrombosis with partial cavity obiliteration. Although valve dysfunction may complicate this condition, it is rarely of primary hemodynamic significance. This report describes an unusual case in which mitral and tricuspid stenosis were the primary cardiac lesions. Because of the critical nature of the valve stenosis, surgical intervention was attempted despite evidence of left ventricular involvement. This case suggests than when significant valve dysfunction complicates Loeffler's endocarditis, surgical revision may be undertaken with at least temporary amelioration of the valve disorder and without apparent adverse effect on the underlying disease process.
Postgrad Med J. 1977 Sep;53(623):538-40.
Endomyocardial firbrosis and Loffler's endocarditis parietalis fibroplastica.
The morphological features of endomyocardial fibrosis and Loffler's endocarditis are described. Sixteen cases of the chronic stage of Loffler's endocarditis were compared with pathological material of thirty-two patients with endomyocardial fibrosis. No morphological differences were noted. It is suggested that endomyocardial fibrosis and LOffler's endocarditis are part of the same disease spectrum, the origin of which can be traced back to the presence of eosinophils in the myocardium.
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