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PubMed1998

[The heart and the eosinophil].

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.

Anti-Inflammatory Agents↗

PubMed1980

Primary cardiomyopathies: classification, pathophysiology, clinical recognition and management.

In recent years, the definition of cardiomyopathy has been restricted to the idiopathic forms of myocardial disease and has been grouped into three general categories: (1) congestive or dilated cardiomyopathy, (2) hypertrophic cardiomyopathy, and (3) restrictive cardiomyopathy. The history and physical examination and echocardiography appear to be the most helpful in the clinical recognition of these disorders. In general, the prognosis of patients with congestive cardiomyopathy is guarded. Their survival primarily depends on the natural history and progression of the disease as well as the response to treatment with anticongestive drugs. The recent advent of vasodilator therapy has provided additional help to the patient with refractory congestive heart failure. Hypertrophic cardiomyopathy appears to be much more frequently recognized since the advent of echocardiography. The young patient has a much higher incidence of serious complications (combined right and left ventricular outflow obstruction, more generalized hypertrophic cardiomyopathy, and sudden death), and the patient presenting in later life appears to have fewer associated complications. There is a familial association with hypertrophic cardiomyopathy, although the true incidence and full expression of the association is not well understood at present. The majority of adult patients acieve prolonged survival with medical and/or surgical treatment. The restrictive cardiomyopathies are probably the least well understood. All three subgroups (Löffler's endocarditis, primary restrictive cardiomyopathy, and endomyocardial fibrosis) have a guarded prognosis. The acute form (Löffler's endocarditis) is characterized by a debilitating illness with death usually within a couple of months; however, a small percentage of these patients can have long survival and may actually evolve into a more chronic form, i.e., primary restrictive cardiomyopathy or endomyocardial fibrosis. The latter two restrictive myopathies usually have a slow indolent course, and their prognosis is primarily determined by the amount of myocardial damage and endocardial fibrosis.

Adolescent↗

PubMed1993

[Restrictive cardiomyopathies].

The restrictive cardiomyopathies are the least common of the 3 major categories of cardiomyopathic disorders seen in Western countries. According to the report of the WHO/ISFC Task Force the term restrictive cardiomyopathy applies to only 2 conditions: endomyocardial fibrosis and Loeffler endocarditis while many specific myocardial diseases can develop a restrictive pathophysiologic profile along their natural history. During the last decade this topic has received 2 main contributions: the identification of a common pathophysiologic ground linking Loeffler endocarditis and endomyocardial fibrosis and the identification of the so-called idiopathic restrictive cardiomyopathy. This condition, defined as a myocardial disease with restrictive physiology, unknown etiology and without histological evidence of infiltrative or storage diseases, appears to be the single most frequent type of restrictive cardiomyopathy in Western countries. A revision of the current classification of cardiomyopathies and particularly of restrictive myocardial disease is necessary.

Cardiomyopathy, Restrictive↗

PubMed1989

[Obstructive-restrictive cardiomyopathy. On the clinical aspects and pathology of Löffler endocarditis].

Löffler'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 Löffler'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 Löffler's endocarditis.

Cardiomyopathy, Hypertrophic↗

PubMed1991

Patterns of myocardial fibrosis in idiopathic cardiomyopathies and chronic Chagasic cardiopathy.

OBJECTIVE: To study the fibrillar nature and structural features of the collagenous interstitium of the myocardium in normal and cardiomyopathic human hearts, employing the picrosirius red technique and polarization microscopy. DESIGN: A survey, case series study. SETTING: Referral autopsy service at a university medical centre (Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto). CASES AND METHODS: A total of 46 adult hearts obtained at autopsy were used: five control hearts without evidence of cardiac disease, nine hearts with dilated cardiomyopathy, five with hypertrophic cardiomyopathy, four with endomyocardial fibrosis affecting the left ventricle, and 23 with chronic Chagasic cardiopathy. Fragments of myocardial tissue were obtained from the equator of the left ventricular free wall, fixed in formalin, dehydrated, and embedded in paraffin. Sections were stained with a modification of the picrosirius red technique and examined using direct light and polarization microscopy. RESULTS: The findings in the control myocardium did not differ from those reported in the literature. The myocardium in both dilated and hypertrophic cardiomyopathies showed diffuse fibrosis varying in degree from one case to another, but present in all cases. The basic pattern was characterized by a diffuse increase in both endomysial and perimysial collagen thick fibres, particularly surrounding individual myocytes (endomysial sheath). The microscopic study of the cases of endomyocardial fibrosis showed a thickened fibrotic endocardium consisting predominantly of thick collagen fibres extending as a septum, corresponding to broad perimysial sheaths, into the myocardium. In the superficial muscle fibre bundles usually composed of atrophic fibres, there was an increase in thickness of collagen fibres in both the perimysial and endomysial connective tissue matrix. To a variable degree (but present in all cases) interstitial and diffuse fibrosis could be observed in the chronic myocarditis of Chagas's disease. This was manifested by a diffuse increase in the amount of thick collagen fibres surrounding muscle fibre bundles (perimysial matrix), varying in intensity from one area to another, and around intramural coronary vessels, combined with a less pronounced increase in the endomysial collagen matrix. CONCLUSIONS: These findings extend knowledge of the various expressions of interstitial myocardial fibrosis in the idiopathic cardiomyopathies and chronic Chagasic cardiopathy and perhaps provide insight into pathogenesis. Further research into the patterns and pathogenesis of myocardial fibrosis are needed in order to offer prevention and corrective forms of therapy of the fibrotic process.

Adult↗

PubMed1983

[Open-heart surgery in tropical Africa. Results and peculiar problems of the 1st 300 cases of extracorporeal circulation performed in Abidjan].

The authors report on their experience of 300 open-heart operations performed in Abidjan for cardiac valve disease (149 cases), congenital cardiopathy (100 cases), endomyocardial fibrosis (40 cases) and other lesions. The operational method involved haemodilution, hypothermia, aortic clamping and cardioplegia. The death rate was 13.3%, mostly due to the severity of the condition prior to surgery. A number of specific points are discussed, including haemodilution without blood perfusions, surgery in patients with sickle-cell anaemia, cardiac valve surgery in children and surgery of endomyocardial fibrosis.

Adolescent↗

PubMed1995

Cerium stimulates protein biosynthesis in rat heart in vivo.

The aim of the study was to ascertain whether Ce, a lanthanide that has been implicated in the pathogenesis of tropical endomyocardial fibrosis, interferes with the biosynthetic repertoire of the cardiac muscle in vivo. Female Sprague-Dawley rats received Ce chloride iv at 1.3 mg/kg body wt.; controls received an equal volume of physiological saline. Rates of protein synthesis and transcription in cardiac muscle, measured in terms of incorporation of (3H)-phenylalanine and (3H)-uridine, respectively, into trichloroacetic acid-insoluble material were found to be significantly higher in Ce-treated animals. As low levels of Ce were earlier shown to stimulate collagen as well as noncollagen protein synthesis in cardiac fibroblasts in vitro, the stimulatory effect of the element in vivo reported here supports the speculation that it may influence the expression of proteins like collagen in the heart and contribute to their accumulation as in endomyocardial fibrosis.

Animals↗

PubMed2004

[Idiopathic hypereosinophilia with cardiac involvement].

HISTORY AND CLINICAL FINDINGS: A 34-year-old previously healthy woman was admitted to another hospital because of abdominal pain, cough and dyspnea. Peripheral eosinophilia was present. Two months later she was admitted to the cardiology department with signs of mitral regurgitation. Dyspnea, fatigue, skin rashes with pruritus and a systolic murmur were noted. INVESTIGATIONS: Laboratory tests showed 11.4/nl leukocytes (normal range 4.8-10.8/nl) with an eosinophilia of 19% (normal range < 4%) corresponding to 2.2/nl. Cardiac magnetic resonance imaging revealed endomyocardial fibrosis involving the posterior mitral leaflet with resulting valvular regurgitation. Doppler ultrasound showed restrictive heart failure. DIAGNOSIS, THERAPY AND FURTHER COURSE: The diagnosis of idiopathic hypereosinophilia most likely as part of hypereosinophilic syndrome with cardiac involvement was made. The patient was treated with digitalis, diuretics and peptidyl dipeptidase (PDP) inhibitor. The treatment with glucocorticoids and cytotoxic agent to achieve a reduction of eosinophil count was ended by the patient a few weeks later. CONCLUSION: The hypereosinophilic syndrome with endomyocardial fibrosis is rare, and its prognosis is grave. The pathophysiological mechanisms are not entirely clear, nearly 70 years after Löffler first described fibrous endocarditis with eosinophilia. Patients receive symptomatic medical therapies. Additional surgical treatment has been reported,. Antihypereosinophilic therapy is used to control the disease.

Adult↗

PubMedDate not supplied

Digoxin and membrane sodium potassium ATPase inhibition in cardiovascular disease.

Kerala has a high incidence of mucoid angiopathy, metabolic syndrome X and endomyocardial fibrosis. Magnesium deficiency has been reported in these disorders even though the Keralite diet has adequate magnesium. A possible cause of magnesium deficiency is the increased digoxin, a potent inhibitor membrane Na(+)-K+ ATPase which can lead to magnesium depletion. Digoxin is known to be synthesised by the hypothalamus and other tissues and can also be obtained from plant sources in the diet. Inhibition of Na(+)-K+ ATPase can cause intracellular magnesium depletion and increase in intracellular calcium. In view of these, a study has been carried out on the activity of membrane Na(+)-K+ ATPase, using RBC membrane, serum digoxin, magnesium and glycosaminoglycan levels in patients of mucoid angiopathy, endomyocardial fibrosis and syndrome X. Significant decrease in the membrane Na(+)-K+ ATPase was observed in patients while serum digoxin levels showed an increase. Serum magnesium was significantly lower while glycosaminoglycan levels were increased. The inhibition of Na(+)-K+ ATPase activity may be due to increase in endogenous and/or exogenous digoxin. This inhibition leads to depletion of intracellular magnesium and an increase in intracellular calcium load. The role of underlying magnesium-related insulin resistance and the consequence of this intracellular magnesium and calcium alteration in the pathogenesis of these disorders is discussed.

Adult↗

PubMed1989

Eosinophilic products lead to myocardial damage.

Eosinophils have been associated with endomyocardial fibrosis. However, their effect on the myocardium and the reactions they elicit have not been emphasized. We describe four patients with extensive myocardial eosinophilic infiltration with and without endomyocardial fibrosis. Patients with a short duration of disease had eosinophilic infiltrates, myocardial eosinophilic abscesses containing granular eosinophilic material, and/or Charcot-Leyden crystals with and without profuse histiocytic and giant cell reaction with granuloma formation. In the early phase, the granular eosinophilic material can be visualized by the Luna stain and/or by electron microscopic examination. In patients with a long duration of symptoms, well-developed granulomas and profuse fibrosis are seen and eosinophilic material may not be visualized. Toxic eosinophil granular protein may be involved in the development of these lesions.

Adult↗

PubMed1989

Clinical decisions in the management of the cardiomyopathies.

The cardiomyopathies are defined and classified into hypertrophic, dilated and restrictive types. In hypertrophic cardiomyopathy the major abnormalities of structure (massive ventricular hypertrophy, myofibrillar disarray, and narrow intramural coronary arteries) and of function (excessive ventricular contraction, systolic pressure gradients, increased ventricular stiffness with impaired relaxation and a tendency for sudden death) are used as the basis for selective and rational treatment with beta-blocking, calcium blocking, or antiarrhythmic agents, or a combination. Treatment is aimed at relieving symptoms, improving prognosis and slowing the progress of disease. Additional methods of treatment involving pacemakers and defibrillators are covered, and the place of septal resection, mitral valve replacement and cardiac transplantation discussed. General management and advice to the patient, and the treatment of complications such as atrial fibrillation, congestive heart failure and infective endocarditis, are also covered. In dilated cardiomyopathy measures to improve ventricular function by vasodilator therapy and the place of antiarrhythmic and anticoagulant drugs are discussed. The controversial treatment with beta-adrenergic blocking agents is reviewed, and the place of immunosuppressive therapy assessed. The possible use of antiviral agents in the future is commented upon, and cardiac transplantation is emphasised as the most effective, although radical, means of improving prognosis in intractable cases. In restrictive cardiomyopathy due to endomyocardial fibrosis, treatment of the initial inflammatory stage with steroids or sulphonylurea, and of the later fibrotic and thrombotic stage with anticoagulants and endocardectomy, is surveyed. The possible place of cardiac transplantation both for endomyocardial fibrosis and amyloid heart disease is mentioned, caution being urged when either of these conditions involves organs other than the heart.

Cardiomyopathies↗

PubMed2000

[Morpho-functional condition of heart in patients with lymphogranulomatosis late after chemoradiotherapy].

AIM: The study of clinical and echocardiographic status of the heart in patients with lymphogranulomatosis (LGM) late after chemoradiotherapy. MATERIAL AND METHODS: 44 patients with IIA-IV stage of LGM exposed to irradiation of lymph nodes and polychemotherapy according to the schemes ACOP, ABVD, COPP, CHOP, CVPP were examined. Echocardiography was carried out on the unit Sigma-44 and Toshiba. RESULTS: Some changes in the heart by type of myocardiodystrophy or endomyocardial fibrosis were found. The latter are characterized by diminution of the left and (or) right ventricles due to apex obliteration, hardening and thickening of the endocardium and subvalvular structures, diastolic dysfunction and pulmonary hypertension. The main and additional signs are distinguished. The reasons of endomyocardial fibrosis are discussed: severity of the disease, frequent exacerbations and, consequently, higher doses of specific chemoradiotherapy. CONCLUSION: It is necessary to employ sparing policy in planning radiotherapy after high loading antracycline antibiotics.

Adolescent↗

PubMed1983

Clinical features of fifteen patients with the hypereosinophilic syndrome.

Fifteen patients with the hypereosinophilic syndrome were studied during a period of 6.5 years. The mean age at onset was 36 years. Two were female. The commonest presenting symptoms were nocturnal sweating with or without severe coughing attacks, symptoms of cardiovascular disease, anorexia and weight loss, neurological and gastrointestinal symptoms and itching with or without skin lesions. The mean blood eosinophil counts at presentation were 20.1 X 10(9)/l. Eight patients had previous allergic or parasitic disease which could have predisposed them to the development of hypereosinophilia. Eight patients had raised serum immunoglobulin levels: IgM in five, IgE in four and IgG in one. Five of nine patients had raised serum eosinophil cationic protein levels. Episodes of clinical relapse occurred with increased white blood counts and were treated with prednisolone and cytotoxic drugs. Thrombotic and embolic complications developed in 10 patients, despite treatment with anticoagulants and inhibitors of platelet function, and were the cause of death in three. Two patients with severe endomyocardial fibrosis responded well to cardiac surgery, and a third required emergency mitral valve replacement. The 12 surviving patients have lived 0.8-11.5 years (mean 4.4), since the onset of their illness. It is concluded that the hypereosinophilic syndrome has distinctive features with an episodic course. The principal complications affect the cardiovascular system, especially endomyocardial fibrosis and thromboembolic occlusion of large and small blood vessels in many organs. Although treatment is usually effective in overcoming relapses, the underlying disease process appears to be unaffected. Despite this, patients can have prolonged periods of remission and may survive for many years.

Adolescent↗

PubMed1992

Paradoxical effect of cerium on collagen synthesis in cardiac fibroblasts.

The present study examined the effect of cerium on collagen synthesis in cultured cardiac fibroblasts and explants. At 100 nM, a concentration comparable with that found in the cardiac tissue of patients with endomyocardial fibrosis, the element was found to enhance the incorporation of tritiated proline into collagen and non-collagen proteins while at 10 microM, it had an inhibitory effect. Cerium was found to have no effect on rates of DNA synthesis in fibroblasts at 100 nM. However, at this concentration, the element markedly enhanced the incorporation of tritiated uridine into RNA, suggesting that cerium may act at the level of transcription to stimulate collagen and non-collagen protein syntheses. The stimulatory action of very low levels of cerium on collagen synthesis may contribute to the accumulation of collagen seen in endomyocardial fibrosis.

Animals↗

PubMed1988

Lymphomatoid papulosis and its relationship to "idiopathic" hypereosinophilic syndrome.

Persistent hypereosinophilia, endomyocardial fibrosis, and a recurrent self-healing papulonodular eruption with the histologic features of lymphomatoid papulosis are described in three patients. One patient died after developing an acute myeloblastic transformation in the eosinophil series. Immunocytochemical studies of cutaneous lesions in two of the patients suggested a mature T-cell phenotype with a predominant population of CD4-positive cells. Immunostaining of cutaneous tissue with monoclonal antibodies BE1 and BE2 yielded negative findings. Because it is now known from in vitro studies that T lymphocytes secrete the eosinopoietic factor, interleukin 5, it is possible that the cutaneous lesions, hypereosinophilia, and associated endomyocardial fibrosis were induced by transformed helper T lymphocytes in these three patients.

Eosinophilia↗

PubMed1976

Studies on blood eosinophils. II. Patients with Löffler's cardiomyopathy.

Studies were done on blood eosinophils from four patients with raised blood eosinophil counts and heart failure. In three of the patients cardiological studies demonstrated the distinctive endocardial lesions and restrictive cardiomyopathy of Löffler's endocarditis and endomyocardial fibrosis. The fourth patient died with similar symptoms and signs. In blood films it was found that all four had more than 1 X 10(9) eosinophils per litre which were vacuolated and contained reduced numbers of crystalloid granules which were also shown to have ultrastructural changes. Unlike eosinophils from normal individuals the patients' eosinophils possessed receptors for rabbit IgG-coated erythrocytes and actively phagocytosed erythrocytes coated with rabbit IgG or human C3b. It is concluded that in these patients, a large proportion of the circulating eosinophils had developed characteristics of mature or stimulated eosinophils. This enabled them to respond to soluble substances in the bloodstream by forming endocytic vacuoles which led to degranulation of the crystalloid granules. These studies, taken in conjunction with other recent work in this field, support the concept that the restrictive cardiomyopathy of hypereosinophilic states, including Löffler's endocarditis and endomyocardial fibrosis, is a result of prolonged release of products from degranulated eosinophils while they are in the circulation.

Adult↗

PubMed1994

Cardiac angiotensin converting enzyme and myocardial fibrosis in the rat.

OBJECTIVE: The aim was to test the hypothesis that cardiac angiotensin converting enzyme (ACE) is related to the accumulation of fibrous tissue in the heart. METHODS: A model of tissue repair (pericardiotomy with left coronary artery ligation) was used, together with the following: quantitative in vitro autoradiography (125I-351A) to determine ACE binding density; immunohistochemistry (monoclonal ACE antibody, 9B9) to identify cells expressing ACE; and in situ hybridisation to localise cells expressing type I collagen mRNA. Age and sex matched rats receiving this operative procedure without subsequent infarction (sham operated) served as controls to those with left ventricular myocardial infarction. Serial heart sections obtained from each group at 3 days and at 1, 2, 4, and 8 weeks following operation were examined for morphological evidence of injury and inflammatory cells (haematoxylin/eosin) and fibrillar collagen (picrosirius red). RESULTS: Following myocardial infarction: (a) on day 3, neutrophils and macrophages were present at the site of infarction, while fibrillar collagen and ACE binding were not increased compared with control; (b) at week 1, fibrillar collagen and ACE binding were present at the site of infarction and became progressively more advanced at 2, 4, and 8 weeks; (c) at week 2, there was increased ACE binding in the right ventricle and interventricular septum, when perivascular fibrosis of intramural coronary arteries and microscopic scars appeared, together with endomyocardial fibrosis of the septum; (d) there was marked ACE binding in the fibrosed visceral pericardium two weeks after operation in both myocardial infarction and sham operated groups; (e) there was type I collagen mRNA expression on postoperative week 1, localised within fibroblasts or fibroblast-like cells found at infarct and fibrous tissue sites in the right ventricle, septum, and pericardium; and (f) ACE-labelled cells included fibroblast-like cells, as well as macrophages and endothelial cells. CONCLUSIONS: Thus in this model of tissue repair, marked ACE binding density is associated with fibrillar collagen formation that appears within and remote to the site of myocardial infarction, including the pericardium. Cardiac ACE, originating from type I collagen producing cells, therefore represents an integral component of fibrous tissue formation in this rat model of tissue injury.

Animals↗

PubMed1990

Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension.

An abnormal elevation in collagen concentration or myocardial fibrosis occurs in the hypertrophied left ventricle of the rat with renovascular hypertension (RHT). The structural nature and functional consequences of this fibrosis and the mechanisms involved in its appearance were reviewed for various phases of hypertrophy. Within days after the onset of renal ischemia, type I collagen messenger ribonucleic acid is expressed. An interstitial fibrosis follows, characterized by an increased dimension of existing perimysial fibers and the appearance of fibrillar collagen in spaces previously devoid of collagen, together with a perivascular fibrosis of intramyocardial coronary arteries. These expressions of myocardial fibrosis are associated with an increase in diastolic and systolic myocardial stiffness. Endomyocardial fibrosis serves to further increase diastolic stiffness while myocytes encircled by fibrillar collagen become atrophic. Each of these consequences of myocardial fibrosis reduce myocyte length-dependent force generation. At 32 weeks of RHT there is an obvious diastolic and systolic dysfunction of the ventricle together with heart failure that includes ventricular dilatation, wall thinning and reduced ejection fraction. The mechanisms involved in mediating fibrosis in RHT appear to be multiple. Myocyte necrosis and fibroblast proliferation have been associated with elevated circulating angiotensin II. Necrosis in RHT was not seen with captopril pretreatment or in the hypertension and hypertrophy that accompanied infrarenal aorta banding. An alteration in coronary artery permeability may be responsible for the perivascular fibrosis that is not seen with captopril pretreatment. Thus in RHT, the hemodynamic status of the ventricle determines myocyte hypertrophy while the elevation in circulating angiotensin II is responsible for the remodeling of nonmyocyte compartments, including the appearance of myocardial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗