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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty patients with decreased left ventricular (LV) function and endomyocardial biopsy-proved myocarditis (9 patients) or borderline myocarditis (11 patients) were studied to determine whether these 2 histologic subsets of patients with inflammatory heart disease differed in their response to a 6- to 8-week course of immunosuppressive therapy. All patients received a regimen of prednisone, 1.0 mg/kg/day, and azathioprine, 1.5 mg/kg/day, followed by repeat endomyocardial biopsy and reevaluation of LV function. LV function improved significantly in the group with borderline myocarditis, as assessed by LV stroke work--end-diastolic volume ratio (0.26 +/- 0.17 to 0.54 +/- 0.31 kg.m.ml-1, p less than 0.02), heart rate corrected velocity of circumferential shortening (0.49 +/- 0.30 to 0.80 +/- 0.29 circ.s-1, p less than 0.05), and LV ejection fraction (0.30 +/- 0.15 to 0.47 +/- 0.13, p less than 0.05). LV end-diastolic and end-systolic volume indexes also decreased significantly from 129 +/- 40 to 94 +/- 38 (p less than 0.05) and 90 +/- 37 to 49 +/- 26 ml (p less than 0.02), respectively. No significant change in these indexes of LV function or volume occurred in the myocarditis group. Whereas salutory improvements in cardiac output and filling pressures were found in both groups, objective improvement in LV function assessed by complementary indexes of contractility was greatest in the borderline myocarditis group. It is concluded that short-term immunosuppressive therapy improves LV contractile function and appears to be associated with regression of ventricular dilatation in patients with borderline myocarditis to a greater extent than patients with myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of immunosuppressive therapy in biopsy-proved myocarditis and borderline myocarditis on left ventricular function. 185 78

Clinical appearance and misdiagnosis in 27 patients having associated preexcitation syndrome and mitral prolapse have been analyzed. Misdiagnosis of myocardial infarction, rheumatic and congenital heart disease, infectious-allergic myocarditis were most typical errors in this condition identification: in 9, 3 and 2 patients, respectively.
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PMID:[Causes of diagnostic errors in ventricular pre-excitation syndrome associated with mitral valve prolapse]. 187 57

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 histocompatibility complex and of the Il2 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 Il2 receptor on interstitial cells as a specific marker of cell activation was only seen in acute rejection and in some cases of myocarditis.
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PMID:Expression of MHC class I and II antigens and the Il-2 receptor in rejection, myocarditis and dilated cardiomyopathy. 191 44

The role of endothelial cells in inflammatory heart disease and rejection after heart transplantation is only partly understood. To determine whether an immune reaction against endothelial cells occurs we examined endomyocardial biopsies from patients with myocarditis (n = 13), dilated cardiomyopathy (n = 23), no clinical rejection (n = 10) and moderate to severe rejection after heart transplantation (n = 10). These were compared to 'normal' donor hearts with monoclonal endothelial-specific antibodies EN4, Pal-E and F VIII-related antigen. Nearly all endothelial cells were stained positively with EN4. There were no significant changes in the binding of the antibodies except in rejection when Pal-E and F VIII-related antigen were significantly increased. It is concluded that apart from their possible role as antigen-presenting cells, endothelial cells are important targets in rejection after heart transplantation. Damage or cytolysis of endothelial cells may cause both altered transendothelial permeability and functional decrease in antigen presentation.
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PMID:Immune response to the endothelium in myocarditis, dilated cardiomyopathy and rejection after heart transplantation. 191 45

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 + 1.9 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.
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PMID:Prognostic determinants in conventionally treated myocarditis and perimyocarditis--focus on antimyolemmal antibodies. 191 61

Endomyocardial biopsy (EMB) is a valuable diagnostic procedure for rejection surveillance in heart allograft recipients and is widely used for evaluation of native heart disease. However, the spectrum and incidence of diagnoses encountered on a heart failure/cardiac transplant service deserve clarification. Of 2300 consecutive EMBs performed during a 2.5-yr period, 79.9% had been performed for rejection surveillance in heart allograft recipients. Of these, 1281 (69.7%) were negative for rejection; 536 (29.1%) were positive (18.9% mild, 9.7% moderate, 0.5% severe); 21 (1.1%) were not interpretable due to insufficient samples. Endocardial lymphocytic infiltrates ("Quilty" effect) were present in 86 (4.7%), ischemia in 12 (0.7%), myocardial calcification in five (0.3%), foreign body giant cells in two (0.1%), valvular tissue in two (0.1%), and liver tissue in one (0.05%). Of the 20.1% of EMBs performed in patients with native heart disease, 298 (64.5%) were abnormal. A total of 239 (51.7%) had myocyte hypertrophy and/or fibrosis, while 37 (8.0%) had active or ongoing myocarditis, two of which were of the giant cell type. Other diagnoses included anthracycline cardiotoxicity in 11 (2.4%), amyloidosis in five (1.1%), hemochromatosis in two (0.4%), healed infarct in two (0.4%), scleroderma in one (0.2%), and foreign body granuloma in one (0.2%). A total of 159 (34.4%) samples had no diagnostic abnormalities; five (1.1%) were insufficient samples. As the number of EMBs performed grows, pathologists must develop expertise in the detection of morphological features pertaining to various cardiac conditions which may have similar clinical presentations.
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PMID:Pathological findings in 2300 consecutive endomyocardial biopsies. 192 75

Giant cell myocarditis is a serious and frequently fatal inflammatory heart disease of which the etiology remains unknown. In the present study, we investigated the origin of multinucleated giant cells in myocarditis with the use of an experimental model. We also examined the factors relating to the formation of giant cells in myocarditis. Severe myocarditis characterized by the appearance of multinucleated giant cells was induced in Lewis rats by immunization with cardiac myosin in complete Freund's adjuvant. Two types of giant cells, foreign body giant cell-like and myocytelike, were observed in this myocarditis. Immunohistochemical studies revealed that both types of multinucleated giant cells were stained with OX42 and ED1 (macrophage markers) and were not stained with anti-desmin antibody and HHF35 (markers for muscle fibers). Therefore, it is likely that multinucleated giant cells in this myocarditis are derived from macrophages. During the course of the disease, the appearance of multinucleated giant cells was restricted to a period corresponding with the fulminant phase of inflammation. When the severity of the disease was modulated by immunization with various doses of the antigen, multinucleated giant cells appeared only in severe myocarditis after inoculation of a large dose of the antigen. Administration of immunoadjuvants also affected the formation of giant cells. Most of the rats injected with cardiac myosin in complete Freund's adjuvant developed giant cell myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characteristics of giant cells and factors related to the formation of giant cells in myocarditis. 193 32

Toxocara canis infection of abnormal hosts results in a condition in which infective larvae migrate through the soft tissues of the body, exclusive of the skin. This condition is known as visceral larva migrans (VLM) and causes a syndrome characterized by hepatosplenomegaly, hyperglobulinemia, hypereosinophilia, and transient pulmonary infiltrates. Because of the known association between hypereosinophilia and eosinophilic heart disease, we have been studying the hearts of mice infected with T. canis for evidence of myocardial damage and have previously described a severe eosinophilic myocarditis that leads to a marked myocardial fibrosis. We have measured eosinophil peroxidase (EPO) levels (a marker enzyme for specific granules of eosinophils) in homogenized lungs, homogenized hearts, and eosinophils recovered from the lungs of mice infected with T. canis over a 6-wk period. A marked accumulation of EPO was observed in the lungs of infected mice from day 14 postinfection (PI) to at least 6 wk of infection. Most of the EPO was associated with eosinophils that comprise the bulk of the pulmonary infiltrates associated with the VLM syndrome. However, following bronchoalveolar lavage, cytochemical localization of EPO activity in lungs from infected mice suggested that eosinophil degranulation had resulted in this marker enzyme being deposited within the pulmonary parenchyma. Peak levels of EPO were found in the myocardium by day 14 PI and declined over the 6-wk period. These levels equaled about 1/3 of the levels seen in the lungs of the same mice. These studies suggest that in mice infected with T. canis, the presence of increased numbers of eosinophils may lead to marked peroxidatic cardiopulmonary damage.
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PMID:Eosinophil peroxidase levels in hearts and lungs of mice infected with Toxocara canis. 195 50

Despite all our efforts, the clinical diagnosis viral myocarditis is usually only a tentative one. This diagnosis can be established with a high degree of probability only on the basis of a combination of virological, histological and immunohistological findings in myocardial biopsies. The use of highly specific monoclonal antibodies against lymphocyte subpopulations and histocompatibility antigens makes possible a differentiated consideration of the diagnosis, severity and course of the disease. Although the etiopathogenesis, the natural course and the destructive mechanisms of the viral heart disease have not yet been finally clarified, numerous clinical and experimental findings indicate that underlying the viral myocarditis or the resulting dilatative cardiomyopathy is a viral infection-induced loss of self-tolerance with subsequent autoaggression against myocardial structures.
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PMID:[Acute viral myocarditis. 1: Pathogenesis, clinical manifestations, diagnosis]. 202 75

Myocarditis is an inflammatory form of heart disease which is usually preceded by a viral infection. Giant cell myocarditis is an uncommon and nonspecific form of this disease. Sporadic reports have linked giant cell myocarditis with thymoma and concomitant myositis. The authors report a patient with leprosy who, six months after initiation of treatment, developed sudden onset of congestive heart failure and cardiac arrhythmias unresponsive to aggressive medical therapy. In addition to confirming leprosy, autopsy showed a mixed cell type thymoma, severe giant cell myocarditis and extensive myositis.
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PMID:Giant cell myocarditis and myositis associated with thymoma and leprosy. 204 17


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