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

Graves' disease is an autoimmune disorder that comprises the triad of diffuse toxic goiter, ophthalmopathy, and infiltrative dermopathy, although all three are not necessarily present in a given patient. The manifestations of Graves' disease vary, depending on the patient's age and other factors. Choice of therapy is influenced by the patient's age, history of heart disease, pregnancy status, expectations, and preferences. Most patients are treated with either radioactive iodine (sodium iodide I 131 [Iodotope]) or the antithyroid drugs propylthiouracil or methimazole (Tapazole). Antithyroid drugs may be more effective in producing long-term remission if levothyroxine sodium (Levothroid, Levoxine, Synthroid) is added to the regimen after the patient becomes euthyroid. Hypothyroidism occurs in many patients following 131I therapy but is also seen in a substantial number of patients who have been treated with thyroidectomy and even in some who have taken antithyroid drugs. Long-term follow-up is necessary, regardless of type of initial treatment, and should include an annual physical examination and measurement of serum concentrations of thyrotropin and the free thyroxine index, both of which should be maintained in the normal range.
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PMID:Intervention in Graves' disease. Choosing among imperfect but effective treatment options. 128 Aug 17

Recombinant inbred (RI) strains of mice and the closely related recombinant congenic strains offer considerable promise for identifying and characterizing genes causally associated with many different diseases. Loci associated with diseases such as heart disease, autoimmune disease and leukemia have already been identified through the use of these unique strains.
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PMID:Recombinant inbred mouse strains: models for disease study. 136 97

There has been a resurgence of interest in immunologically-mediated heart disease, culminating in a recent meeting. This interest was sparked off by new experimental models of autoimmune myocarditis that have served two useful functions: first, as good models of human myocarditis and second, as paradigms of infection-induced autoimmune disease.
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PMID:Autoimmune myocarditis: concepts and questions. 168 Mar 35

A 40-year-old woman was admitted because of increasing exertional dyspnea. Right heart failure was suggested by the presence of hepatomegaly, pretibial edema and also echocardiographic findings. Physical examination and echocardiography showed no evidence of valvular disease or congenital heart disease except for right ventricular dilatation and tricuspid regurgitation. The ventricular septum deviated toward the left ventricle throughout the cardiac cycle, but left ventricular function was preserved. Severe pulmonary hypertension averaging 44 mmHg was revealed by cardiac catheterization. Digital subtraction angiography and pulmonary blood flow scintigraphy showed no evidence of pulmonary artery embolism, and no interstitial pulmonary lesions that might have caused pulmonary hypertension were recognized. Hypergammaglobulinemia suggested an autoimmune disorder, and signs of systemic lupus erythematosus (SLE), such as pleural effusion, proteinuria, lymphocytopenia, LE cell phenomenon and antinuclear antibodies were present. Several autoimmune diseases are known to be causative factors of pulmonary hypertension. However, only ten cases of SLE complicated by pulmonary hypertension have been reported the present one. These cases were characterized by a high incidence of Raynaud's phenomenon and positivity for anti-RNP antibody. In our present case, SLE activity was suppressed using prednisolone, but pulmonary hypertension persisted and the patient eventually died due to right cardiac failure. Judging from the clinical course of the ten reported cases of SLE-pulmonary hypertension, there seems to be no hope of improving the pulmonary hypertension once it has become established. Therefore it is important to detect and cure pulmonary hypertension as early as possible.
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PMID:[A case of lupus erythematosus preceded by right heart failure due to pulmonary hypertension]. 174 69

The inappropriate expression of major histocompatibility complex (MHC) molecules on epithelial and endothelial cells is a recognized marker of autoimmune disease. An autoimmune pathogenesis has been suspected in dilated cardiomyopathy (DCM). In the normal heart, MHC products are usually not detectable on myocytes using immunochemical techniques. MHC molecule expression has not, however, been assessed on cardiac endothelial cells. The aim of this study was to investigate possible autoimmune phenomena and MHC molecule expression in fresh endomyocardial biopsies from 29 patients with DCM. These were compared with those observed in surgical specimens from 63 patients with other acquired cardiac disease and from 22 with congenital heart disease (CHD) as normal controls. Conventional immunofluorescence (IFL) with monoclonal antibodies (MoAbs) to lymphocyte and macrophage markers and to MHC molecules was employed, and double IFL with antiserum to human Factor VIII was used for the identification of endothelial cells. Myocytes did not express MHC molecules in either DCM or controls. In normal hearts, Class II molecules were detected on endothelial and endocardial cells in only a few cases (3/22 and 2/22 respectively). By contrast, endothelial and endocardial cells inappropriately expressed Class II in a high proportion of DCM patients (28/29 and 22/29) but less frequently in other acquired cardiac diseases (19/63, P less than 0.001 and 11/63, P less than 0.001 respectively). In all the DCM biopsies examined there was a hierarchy of Class II subloci product expression (DR greater than DP greater than DQ); lymphocytic infiltration was a rare finding and macrophages/dendritic cells were not prominent. The finding of inappropriate MHC Class II molecule expression on cardiac endothelial and on endocardial cells suggests a possible pathogenic role for these cells in the initiation and/or perpetuation of DCM.
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PMID:Inappropriate major histocompatibility complex expression on cardiac tissue in dilated cardiomyopathy. Relevance for autoimmunity? 218 52

We investigated a large Old Colony (Chortitza) Mennonite kindred with branches across Canada. Six generations of the kindred were traced. There was intermarriage among numerous family members. Insulin-dependent diabetes mellitus (IDDM) was identified in 10 members; all 7 living patients were found to carry the immunogenetic marker HLA-DR4. Nine other close relatives had disorders of carbohydrate metabolism, including gestational diabetes mellitus and non-insulin-dependent diabetes mellitus progressing to insulin use. Ten other relatives had autoimmune diseases, including rheumatoid arthritis, hyperthyroidism, hypothyroidism and multiple sclerosis. Cases of Alport's syndrome, congenital malformations, inborn errors of metabolism and unusual malignant diseases were also found in the kindred. In the small Alberta community in which the kindred was ascertained there were people of Old Colony Mennonite descent with genetic conditions such as Gilles de la Tourette's syndrome and congenital malformations, including congenital heart disease. This kindred represents the largest reported familial aggregation of IDDM. This disease and other disorders of carbohydrate metabolism occur in the context of a strong familial predisposition to autoimmune disease. Study of this family may permit empiric testing of proposed models of inheritance of diseases of complex origin such as IDDM. We report this Old Colony (Chortitza) Mennonite community because it is one of the settlements populated by this religious and genetic isolate, which extends across Canada and Central and South America and affords opportunities for the study of both common and rare inherited diseases.
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PMID:Unusual clustering of diseases in a Canadian Old Colony (Chortitza) Mennonite kindred and community. 337 May 69

Identification of viral myocarditis offers problems; pathologists fail to agree on the definition of the disease and biopsy-proven cases documented in the English literature are still few in number. Though endomyocardial biopsy is becoming a standard procedure at many medical centers, tissue sampling, especially in cases of patchy myocarditis, can result in further diagnostic difficulties. While conventional wisdom holds dilated cardiomyopathy the end-stage of chronic viral myocarditis, a history of preceding viral infection is usually unobtainable. Some research suggests that myocardial necrosis is a cell-mediated immune process and chronic myocarditis an autoimmune disease. Understanding the true relationship between viruses and heart disease will require further research.
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PMID:Viruses and heart disease: a problem in pathogenesis. 353 32

One of the rare examples of the transfer of autoimmune disease from mother to (unborn) child is the neonatal lupus syndrome. This syndrome comprises the development of fetal heart disease (congenital heart block) or neonatal skin rash and is specifically associated with maternal anti-Ro/SS-A autoantibodies. Previous studies have suggested that especially maternal autoantibody reactivity against the 52 kDa protein of the Ro/SS-A antigen and/or against the La/SS-B antigen is responsible for the development of congenital heart block (CHB). To determine the CHB-associated antibody response in more detail, we analysed the presence of autoantibodies in sera from mothers of children with isolated heart block. All 14 mothers of children with congenital heart block were positive for anti-Ro/SS-A antibodies. Remarkably, their antibody profile, including recognition of different Ro/SS-A proteins and autoantibody levels against these proteins, did not differ from anti-Ro/SS-A positive mothers of healthy children. In contrast, all 8 anti-Ro/SS-A negative mothers had children with acquired heart block. We conclude from our data that maternal anti-Ro/SS-A antibodies are essential for CHB but that fine analysis of this autoantibody response does not predict the occurrence of CHB.
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PMID:Maternal autoantibodies and congenital heart block: no evidence for the existence of a unique heart block-associated anti-Ro/SS-A autoantibody profile. 750 95

An inflammatory cardiomyopathy may develop in humans and experimental animals with chronic Trypanosoma cruzi infection (Chagas' disease). Among the possible mechanisms involved in the pathogenesis of Chagas' cardiomyopathy, induction of heart-specific autoimmune responses has recently received substantial experimental support. The goal of the current study was to determine whether cardiac Ag-specific antibodies are produced in T. cruzi-infected mice with heart disease and, if so, to determine their Ag specificities. Upon infection with the Brazil strain of T. cruzi, C57BL/6 mice develop a cardiomyopathy that is histologically similar to that observed in chronically infected humans. Antisera from these mice were found to react with three cardiac Ag, having relative molecular masses of 200, 150, and 53 kDa. p200 and p150 are specifically found in heart muscle, although p53 is found in skeletal muscle as well. C57BL/6 mice infected with the Guayas strain of T. cruzi, which do not develop cardiomyopathy, did not produce antibodies to p200, p150, or p53, indicating that these antibodies may be specific markers of cardiomyopathy. Finally, p200 and p53 were identified as the contractile protein myosin and the intermediate filament protein desmin, respectively. This last finding is of special interest, because antibodies specific for myosin or desmin have been detected in humans and experimental animals with other natural and experimental cardiomyopathies. This suggests that infection with particular strains of T. cruzi may lead to the development of a cardiac Ag-specific autoimmune disease, possibly involving one or more of the Ag identified in this study.
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PMID:Cardiac antigen-specific autoantibody production is associated with cardiomyopathy in Trypanosoma cruzi-infected mice. 830 Nov 48

A number of interventions for delaying or reversing declines in body functions due to ageing are critically reviewed here, including their relation to neuroendocrine function. Diets severely deficient in calories retard the ageing of body tissues, inhibit the development of disease and tumours, and significantly prolong the lifespan of rats and mice. Such diets also decrease hormone secretion, reduce the metabolism of the whole body, and lower gene expression. Administration of hormones, thymic peptides and other immune factors, and appropriate drugs can improve declining immune function in old rats and mice, thereby increasing resistance to infection, autoimmune disease and tumours. In old rats, correction of faults that develop in the neuroendocrine system with age--particularly in the hypothalamus--can restore oestrous cycles, increase the secretion of growth hormone, increase protein synthesis, inhibit development of disease and tumours, and prolong life. Antioxidants administered to rats and mice in an attempt to reduce damage to cells caused by free radicals, do not significantly retard ageing or prolong the lifespan of these animals. Regular, moderate exercise in elderly humans decreases incidence of heart disease, improves lung function, reduces bone loss, and produces other beneficial effects. Suitable drugs that will improve memory function in elderly humans remain to be developed, although a few have produced small improvements albeit with undesirable side effects. Overall, the neuroendocrine and immune approaches offer the best prospects for delaying and reversing declines in body functions due to ageing.
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PMID:Anti-ageing interventions and their neuroendocrine aspects in mammals. 831 12


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