Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kawasaki syndrome is a leading cause of pediatric acquired heart disease in the United States. Coronary artery aneurysms or ectasia develop in approximately 15 to 25 per cent of affected children; treatment with intravenous gamma globulin in the acute phase reduces this risk three- to five-fold. Angiographic resolution occurs in approximately one half of aneurysmal arterial segments, but these show persistent histologic and functional abnormalities. The remainder may continue to be aneurysmal, often with development of progressive stenosis or occlusion. Myocarditis is a universal feature of acute Kawasaki syndrome, but the occurrence of late abnormalities of myocardial function among children without coronary artery disease is controversial. Aortic and mitral regurgitation may occur in the acute illness, and late-onset valvar regurgitation has been reported as a rare complication. Continued long-term surveillance in patients with and without detected coronary abnormalities is necessary to determine the nature history of Kawasaki syndrome with respect to coronary artery status, myocardial function, and valvar regurgitation.
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PMID:Kawasaki syndrome. 265 85

The diagnosis, pathogenesis and etiology of myocarditis are often difficult to establish with certainty. Consequently, we investigated cellular regulator and effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps) as well as other inflammatory heart diseases which could not be classified etiologically. In acute myocarditis there was an elevation of B- and activated T-lymphocytes (OKIa 1-positive) but, in contrast, no significant changes in the activity of peripheral suppressor T-cells (OKT 8-positive). The activity of cell-specific lymphocytic effector mechanisms against vital cardiocytes was unchanged or slightly elevated in myocarditis, while the activity of the less target cell specific natural killer cells, which were measured in vitro against K562 tumor cells, was diminished. These findings are indicative of increased activity of target specific cytotoxic effector mechanisms and a reduction in the activity of nonspecific cellular effector mechanisms in peripheral blood.
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PMID:Immunological cellular regulator and effector mechanisms in myocarditis. 285 43

In acute perimyocarditis we found that OKIAI-positive cells were increased, and in dilated cardiomyopathy OKMI-positive cells were increased. No significant alteration in suppressor T cell activity was observed in our patients with either disease. The characteristic immunofluorescent pattern in carditis and postmyocarditic heart disease is the presence of antimyolemmal antibodies with intact rat and human cardiocytes in titers of 1:40-1:320 as antigens. The antimyolemmal fluorescence can be absorbed with the respective causative virus in Coxsackie B, influenza, mumps and EBV-myocarditis, indicating that the antibodies are a cross-reactive. AMLA-positive sera induce cytolysis of vital rat cardiocytes in vitro, suggesting that the antibodies are of pathogenetic relevance. Cytolytic serum activity could be absorbed out with the respective virus. Immunohistologic specimens obtained from patients with carditis demonstrate the fixation of IgG and IgM antibodies; IgG antibodies also occur in dilated cardiomyopathy and coronary artery disease. In dilated postmyocarditic heart disease both antimyolemmal fluorescence and cytolytic activity are preserved at a lower level when compared to carditis. These antibodies can also fix complement. In the acute phase of carditis circulating immune complexes can be demonstrated. Cellular effector mechanisms against vital cardiocytes were maintained or even slightly enhanced in carditis, postmyocarditic and primary dilated cardiomyopathy. In vitro NK cell activity against K 562, however, was decreased. This is compatible with a sustained target-specific cytotoxicity whereas reduced NK cell activity may indicate impairment of this effector organ.
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PMID:Immunologic regulator and effector functions in perimyocarditis, postmyocarditic heart muscle disease and dilated cardiomyopathy. 294 66

We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, asymmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.
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PMID:Idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. 295 39

The diagnosis and etiology of myocarditis and perimyocarditis are often difficult to ascertain. We therefore investigated regulator and humoral and cellular effector mechanisms in patients with viral heart disease (Coxsackie B3, influenza, EBV, mumps). In acute carditis, OKIA1-positive cells were increased and no significant alteration in suppressor cell activity was observed in our patients in contrast to others reports. The characteristic immunofluorescent pattern is the presence of antimyolemmal antibodies (AMLA) with rat and human collagenase-pretreated intact cardiocytes (in titers of 1:40-1:320) as antigens. The pattern is indistinguishable on cardiocytes from antibodies against cytoskeletal antigens (microtubules, intermediate filaments--tubulin/vemitin) when associated with antibodies directed against the Z-bands. In contrast, only anti-interfibrillary antibodies are present in cytomegalovirus myocarditis. The antimyolemmal fluorescence can be absorbed with the respective causative virus, indicating that the antibodies are cross-reactive. AMLA-positive sera induce cytolysis of vital rat cardiocytes in vitro, indicating that the antibodies are of pathogenetic relevance. Cytolytic serum activity could be absorbed out with the respective virus. Immunohistologic specimens obtained from patients with carditis demonstrate the fixation of IgG-type antibodies to the sarcolemma that also fix complement. In the acute phase of carditis, circulating immune complexes were also measured, thus monitoring immunoreactivity. Cellular effector mechanisms against vital cardiocytes were maintained or even slightly enhanced; in vitro NK-cell activity against K 562, however, was decreased. This is compatible with a more target-specific cytotoxicity in carditis but reduced NK-cell activity in peripheral blood cells.
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PMID:Immunologic regulator and effector mechanisms in myocarditis and perimyocarditis. 295 37

New aspects in the research of myocarditis and dilated cardiomyopathy in West Germany have evolved from molecular biology, immunobiology of the mitochondrion, immunoserology, and immunohistology. Coxsackie B3 virus inoculated into fetal human myocytes induced myocytolysis in the absence of immunologic effector mechanisms. By pretreatment with beta-interferon, the virus yield from the myocytes was reduced significantly. In myocarditis and dilated cardiomyopathy, antibodies against an organ-specific autoantigen of cardiac mitochondria, the adenine nucleotide translocator, were demonstrated. Antibody titers roughly correlated with the ejection fraction using the Elisa technique. It could also be shown that in 13% of cases in myocarditis and 31% in dilated cardiomyopathy heart-associated antimitochondrial antibodies are found, called anti-M7. Most of the patients had an interfibrillary staining pattern in the immunofluorescence test. No correlation with the severity of heart disease could be established. In dilated cardiomyopathy and myocarditis, there has recently been controversy over low suppressor T-cell activity. Whereas other groups have demonstrated a low concanavaldin-A-induced suppressor T-cell activity in both diseases, we have not been able to confirm reduced Con-A-induced or spontaneous T-suppressor cell activity in the different indicator systems used in analysis.
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PMID:Cardiomyopathy and myocarditis--a review of new aspects in research in West Germany. 295 41

In a series of 256 patients with acromegaly, 10 had evidence of heart disease for which no explanation apart from the acromegaly could be found. Heart disease presented with effort dyspnoea, cardiac failure, palpitation, ECG changes or cardiomegaly. Initial chest radiographs showed cardiac enlargement in seven patients. Electrocardiograms were abnormal in nine patients with repolarisation disorders or intraventricular conduction defects. Rhythm disturbances were found in six. Echocardiograms were performed on six patients; all were abnormal showing left ventricular hypertrophy or impaired function. In five patients radionuclide ventriculography was also performed. Cardiac catheterisation was undertaken on seven patients; all showed either hypertrophy or dilatation of the left ventricle. Coronary arteries were widely dilated in two patients and in another there was dilation of the proximal segment only. In six of the 10 patients, acromegaly was cured by transsphenoidal surgery. This resulted in limited improvement of cardiac function in two patients only. Of the four patients who were not cured, three died and one was lost to the study. Four patients in total died and autopsies were obtained in two: one showed changes suggesting myocarditis and the other diffuse fibrosis. It is concluded that acromegaly may infrequently lead to heart disease, and that if recognised at an early stage progression may, in a proportion of patients, be arrested by successful treatment.
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PMID:Acromegalic heart disease: influence of treatment of the acromegaly on the heart. 296 20

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.
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PMID:The use of endomyocardial biopsy in heart failure. 297 42

Postinfection sera from A.CA/SnJ A.SW/SnJ, B10.S/SgSf, and B10.PL/SgSf mouse strains which varied in their susceptibility to Coxsackievirus B3-induced immunopathology were suspected to contain autoantibodies against cardiac tissue. These sera were used to identify the target myocardial autoantigen(s). Sera pools were made during the peak of the early, virus-induced myocarditis at 5 and 7 days and during the peak of the late, immunopathic phase of myocarditis at Days 15 and 21 after infection. Only the A.CA/SnJ and A.SW/SnJ strains which develop the immunopathic heart disease had heart-specific autoantibodies as determined by indirect immunofluorescence. This panel of sera pools was then tested against solubilized extracts from whole heart and skeletal muscles. Results from Western immunoblotting analyses demonstrated that antibodies to myosin were a prominent feature in the sera of strains which developed immunopathic myocarditis. The immunopathic sera pools were subsequently assayed against low-salt, high-salt, and a number of detergent extracts of heart and skeletal muscle. Anti-myosin was still the most notable reactivity, even though other autoantigens were detected. Absorption with cardiac myosin removed the vast majority of heart reactivity from the pooled sera derived from the A.CA/SnJ and A.SW/SnJ strains as determined within the limitations of the immunofluorescent and immunochemical assays. Both sarcolemmal and A-band staining patterns were abolished by the cardiac myosin absorption. These studies suggest that myosin is one of the major autoantigens in Coxsackievirus B3-induced autoimmune myocarditis.
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PMID:Heart-specific autoantibodies induced by Coxsackievirus B3: identification of heart autoantigens. 303 May 91

Several mouse strains are susceptible to immunopathic myocarditis after infection with Coxsackievirus B3 (CB3). This disease is associated with autoantibodies that are directed against myosin. In this study we characterized sera from CB3-infected mice for their reactivity with three different myosin isoforms (heart, skeletal muscle, and brain myosins) and for autoantibody isotype by using an ELISA. Competitive inhibition assays and absorption studies with various myosins demonstrated the presence of two autoantibody populations in sera of susceptible A.CA and A.SW mice. The first was specific for cardiac myosin and was mainly IgG. The second antibody population cross-reacted with heart, skeletal muscle, and brain myosin and was mainly IgM. B10.PL/SgSf and B10.A/SgSf mice, which do not develop immunopathic myocarditis, produced only the IgM autoantibody population cross-reactive with all three myosin isoforms. Because the heart-specific myosin autoantibodies were found exclusively in the mouse strains that developed immunopathic myocarditis, they can be considered a serologic marker for autoimmune heart disease.
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PMID:Autoantibodies specific for the cardiac myosin isoform are found in mice susceptible to Coxsackievirus B3-induced myocarditis. 303 Nov 59


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