Search

Background. Automated peritoneal dialysis (APD) has been increasingly used in recent years. Our purpose was to investigate whether the good preservation of residual renal function (RRF) that has been reported in patients on continuous ambulatory peritoneal dialysis (CAPD) is also observed in APD. [ABSTRACT FROM PUBLISHER]

This overview examines the immunological rationale for immunosuppressive and immunomodulating therapy in man and experimental animals. The controversy of whether immunosuppressive treatment is beneficial in myocarditis will continue even after the Myocarditis Treatment Trial has been published. It is known that in viral heart disease immunosuppressive drugs should be avoided, but in autoreactive forms of myocarditis with proven humoral and cellular effector mechanisms they may be used in controlled randomized trials to validate or refute their benefit. Immunomodulating factors, e.g. immuno-stimulatory or antiviral substances such as ribaverin, the interleukins and interferons have demonstrated some effect in experimental animal myocarditis but proof of their benefit in man is still lacking. Hyperimmunoglobulin therapy appears to be of particular interest because it incurs few side effects and has positive results in cytomegalovirus-associated myopericarditis in man and suspected myocarditis in children. [ABSTRACT FROM PUBLISHER]

Pericardioscopy is a new diagnostic tool for macroscopic visualization of alterations in both the epicardium and pericardium. We report on 35 patients with pericardial effusion due to inflammatory perimyocardial disease.After puncture of the pericardial effusion, an 8F sheath was introduced over a guidewire under X-ray control. The pericardial pressures were measured; the fluid was removed by aspiration and exchanged with 100 ml of body-warm saline until the pericardial fluid was clear. To visualize the peri- and epicardium, for video- and photo documentation, two sorts of 8F endoscope were used, either a flexible fibreglass version or a rigid 110° one—both made by Storz. Cytology of the fluid and optically guided and controlled epicardial and pericardial biopsies were performed to classify the form of pericarditis. A specific diagnosis of viral pericarditis could thus be established in seven cases—by in situ hybridization for cytomegalovirus (n = 3) and by microneutralization test for enteroviruses and /or coxsackievirus B4 isolation (n = 4); of lymphocytic perimyocarditis in 16; of bacterial pericarditis in seven and antibody-mediated autoreactive pericarditis in five cases. [ABSTRACT FROM PUBLISHER]

Inflammation of the heart muscle is caused either by infection (i.e. coxsackie virus) resulting in myocarditis or by rejection following heart transplantation. These processes induce activation of the immune system. We examined endomyocardial biopsies from patients with myocarditis, perimyocarditis and rejection following heart transplantation and compared these to biopsies from patients with coronary artery disease. The biopsies were examined immunohistologically with specific monoclonal antibodies against class I and class II molecules of the major histocompatibility complex (MHC). MHC class I antigens on the normally negative myocytes were evident in myocarditis (38%) and in rejection after heart transplantation (68%). In the interstitium there was an increase of both MHC class I and class II antigens. MHC class II antigens, however, were never seen on myocytes. MHC class I antigens are required for the action of CD 8 positive cytotoxic T cells. Therefore myocytes which express MHC class I antigens are susceptible to cytotoxic effects of the immune system. MHC class II antigens are essential to T helper cells. By cytokine release, activated T helper cells play a central role in the initiation, regulation and mediation of an immune response in myocarditis and rejection following heart transplantation. [ABSTRACT FROM PUBLISHER]

In this study from two specialized centres 85 patients with histologically proven myocarditis(n = 10) and clinically ascertained perimyocarditis (pericardial effusion and cardiomegaly or segmental wall motion abnormality; n = 75) were followed up for 4·5+1·9 years. Immunosuppressive treatment was not applied.After a mean follow-up period of 4·5 years 55% of patients had improved clinically and 35 % of patients were completely free of symptoms. Relapses had occurred up to three times. Chronic forms were found in 20% of patients, mostly in those with pericarditis and effusions. Eighteen percent of the patients deteriorated gradually. In 20% of the chronic or deteriorating patients congestive heart failure developed (postmyocarditic heart muscle disease). Fifteen percent of the patients died, mainly from bacterial perimyocarditis and to a lesser extent from inflammatory heart disease from enteroviruses. Patients who succumbed after more than 6 months died either suddenly or from progressive heart failure. A favourable outcome was often accompanied by a decrease in titre, but this decrease was less impressive in those who had antimyolemmal and antisarcolemmal antibodies. The persistence of these antibodies in high titres predominated in patients with poor prognosis and postmyocarditic dilated heart muscle disease, as did cytolytic serum activity. [ABSTRACT FROM PUBLISHER]

In myocarditis and dilated cardiomyopathy a secondary immunopathogenesis is likely, since alterations to the humoral and cellular immune system have been repeatedly demonstrated. In rejection after heart transplantation activation of the immune system has been clearly seen. This may be comparable to myocarditis and thus could be a model for inflammatory heart disease. This study was set up to investigate whether an increased expression of antigens of the major histocombatibility complex and of the 112 receptor in endomyocardial biopsies of patients after cardiac transplantation, myocarditis and dilated cardiomyopathy takes place. Cryostat sections were investigated immunohistologically by the immunoperoxidase test. There was an expression of class II antigens (HLA-DR, HLA-DP, HLA-DQ) in acute rejection and in myocarditis and in some patients with dilated cardiomyopathy on endothelial cells, interstitial cells but not on the myocytes. The results for class I (HLA-A, B, C) are similar, but in addition an expression on myocytes was observed in myocarditis and rejection. A second immunopathogenesis is most likely in some patients with dilated cardiomyopathy. The expression of the I12 receptor on interstitial cells as a specific marker of cell activation was only seen in acute rejection and in some cases of myocarditis. [ABSTRACT FROM PUBLISHER]

Endomyocardial biopsy in this study of 1250 biopsied patients (mean of five samples/patient) proved to be a remarkably safe technique with no lethal complications. It may help to detect the underlying cause of heart failure but is handicapped by sampling error in focal disease processes (such as myocarditis and sarcoid heart disease) when conventional light and electron microscopy are used. In this biopsy series 123 patients (9.8%) suffered from severe heart failure; lymphocytic infiltrates were found in only 10 (8%). Immunohistological data suggested a secondary humoral immunopathogenesis in all patients with myocarditis and perimyocarditis, in 75% of patients with postmyocarditic heart muscle disease and in 48% of patients with primary dilated cardiomyopathy. There may thus be a need for a new classification of heart muscle diseases that includes immunological parameters of humoral and cellular autoreactivity. [ABSTRACT FROM PUBLISHER]

Twenty-seven patients with bronchopulmonary or generalised sarcoidosis were classified with a clinical score as certain, probable, possible or no cardiac sarcoidosis. Certain cardiac involvement was assumed only when endomyocardial biopsy or necropsy showed a granuloma of the heart (N = I); it was probable (N = 14) when a resting or an exercise-induced defect in the thallium scan was found and severe arrhythmia (Lown III-V), A–V block (2nd or 3rd degree), cardiomegaly, pericardial effusion or segmental wall motion abnormality was detected in addition; it was considered possible (N = 7) when only one of the above-mentioned criteria (rhythm disturbances, cardiomegaly/pericardial effusion, exercise-induced defect in the thallium scan) was positive.With thallium-201 scintigraphy a defect at rest was found in nine, on exercise in six, at rest and on exercise in six, and no defects were found in six cases. Determination of antimyocardial antibodies with adult human and rat cardiocytes and with cryostat sections, and of circulating immune complexes, showed differences from non-cardiac controls but not from patients with sarcoidosis and a negative score for cardiac manifestations. Antimyolemmal antibodies of the IgG class were found in all patients, and of the IgM class in 30–50% of all patients irrespective of cardiac involvement. Only complement fixation to the myolemma was cardiospecific. Cytolytic serum activity, NK cell activity, antibody-dependent (ADCC) and -independent lymphocytotoxicity against vital heart cells could not be detected in any group of patients. [ABSTRACT FROM PUBLISHER]

Diagnosis of myocarditis has improved with the application of new techniques such as immunohistochemistry, polymerase chain reaction, in situ hybridization and Southern blot in endomyocardial biopsies. Treatment of inflammatory heart disease is still difficult and not yet validated by a study with patient numbers sufficient to allow statistical analysis. The European Study of Epidemiology and Treatment of Cardiac Inflammatory Disease (ESETCID) addresses problems of aetiology, pathogenesis and specific treatment of myocarditis. It is the first multicentre, double-blind placebo-controlled randomized study, apart from the Myocarditis Treatment Trial, to discriminate between different forms of myocarditis. Patients with cytomegalovirus-induced myocarditis are treated by hyperimmunoglobulin compared to placebo. Patients with enterovirus-positive myocarditis will receive interferon alpha vs placebo. Patients with virus-negative myocarditis, which is considered autoimmune, will be treated with immunosuppression compared to placebo. The primary endpoint of this study is an improvement in ejection fraction of more than 5%. This trial may give a better understanding of the course of myocarditis, leading to more specific treatment which may in turn reduce the number of patients with post-myocardial heart muscle disease who require heart transplantation as a final therapeutic remedy [ABSTRACT FROM PUBLISHER]

The human enteroviruses, especially the coxsackie B viruses, have been established as aetiologic agents of human inflammatory heart disease, a condition which may lead to dilated cardiomyopathy and heart failure. It is clear from murine models of coxsackievirus B3-induced inflammatory heart disease that not all strains of the virus are cardiovindent (able to cause disease). Here, we present preliminary data mapping the site in a coxsackievirus B3 genome which determines a cardiovindent phenotype. [ABSTRACT FROM PUBLISHER]

The most extensively studied animal model of coxsackievirus B3 (CVB3) -induced inflammatory heart muscle disease is the murine model. In the acute and chronic phase of the disease, it has been suggested that autoimmune mechanisms play a major role in the pathogenesis of the disease. In this study, C3H mice without functional T- and B-lymphocytes (C3H SCID) were inoculated either with a cardiovindent (CVB3/20) or a non-cardiovirulent (CVB3/0) strain of coxsackievirus B3. Both viruses caused myocarditis in SCID mice. Furthermore, it could be demonstrated, that CVB3/0 had mutated to a cardio-virulent phenotype, able to cause myocarditis in immunocompetent mice. [ABSTRACT FROM PUBLISHER]