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

Thirty-one patients with systemic candidiasis at postmortem examination were found to have Candida involvement of the myocardium without valvulitis. Retrospective examination of their clinical course demonstrated that a new conduction disturbance was seen in 10, supraventricular arrhythmias in 5,QRS changes mimicking myocardial infarction in 3, and pronounced T wave changes in 13. Hypotension or shock was seen in 13 patients and could not be explained by coexistent bacteremia or blood loss in 8. One patient died suddenly. Of 19 patients with systemic candidiasis without myocardial invasion, 4 had minor T wave changes and one had a supraventricular arrhythmia. Candida invasion of the heart significantly complicates the clinical course in systemic candidiasis and should be suspected when a young person without preexistent heart disease has cultures positive for a Candida organism, a significant arrhythmia, conduction distrubance or other dramatic QRS change. The effect of therapy on Candida invasion of the heart is unknown.
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PMID:Candida myocarditis without valvulitis. 99 27

Five cases of aortic incompetence and nodular seropositive rheumatoid arthritis are presented. Four cases underwent aortic valve replacement. Two of these had granulomatous involvement of the aortic cusps similar to subcutaneous rheumatoid nodules, and another showed a nonspecific fibrosis. One case had definite coincidental rheumatic aortic and mitral heart disease. Two patients had undergone pericardectomy previously for constrictive pericarditis. Good results were obtained in all four operated cases and cardiac surgery enabled continuation of rehabilitation for the rheumatoid arthritis, including major orthopaedic procedures. A review of 22 cases from the literature with rheumatoid granulomata within the aortic valve shows that they are associated with mitral valve granulomata in 63-6%. Congestive cardiac failure was found in 75%. Macroscopical evidence of aortic incompetence was seen in 36-8% and of aortic stenosis in 15-8%. Associated pericarditis occurred in 59-1%, which was severe or complicated in 13.6%. The associated arthritis was severe in 77-8% with subcutaneous nodules (71-5%), rheumatoid factor (83-6%), and episcleritis (66-6%). From these cases and a review of the literature the following points are emphasized. (1) Both the granulomatous and nonspecific aortic valvulitis of rheumatoid arthritis may result in significant haemodynamic abnormality. (2) The valve lesions found are often clinically and macroscopically indistinguishable from rheumatic valve lesions. (3) Granulomata, when present, are usually found in the valve cusp or ring and only occasionally in the aortic wall. (4) Associated joint disease, although usually severe, may be mild. (5) The valve lesion may be accompanied by a severe pericardial involvement--either tamponade or constriction. (6) Aortic valve replacement for aortic incompetence in rheumatoid arthritis is both feasible and worthwile, despite severe joint disease.
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PMID:Aortic valve incompetence and replacement in rheumatoid arthritis. 119 Aug 51

The authors describe the results obtained during retrospective examinations of 45 subjects who suffered from acute rheumatic fever 10-14 years before. Of these, 19 subjects were treated with prednisolone in the acute disease period, 16 with indomethacin, and 8 subjects with voltaren. The examinations were mostly randomized (30 subjects); no differences in the anti-inflammatory effect were discovered. Heart disease was found in 9 persons (20%). Of these, 6 were treated with prednisolone, 2 with indomethacin, and 1 with voltaren. The disease relapses were recorded in 4 of them, the signs of valvulitis in the past were shown only by 2 persons (echocardiographically). 12 persons (27%) had mitral valve prolapse which had not been diagnosed on the first admission to the hospital, with any clinical signs of hypermotility lacking. In 18 persons (40%) having no valve lesions (disease, prolapse), an x-ray examination revealed a slight increase of the heart size, estimated as a manifestation of postmyocardial cardiosclerosis. Thus, it has been shown that modern anti-inflammatory therapy does not prevent the development of heart disease. Apparently, its onset is related to specific proneness in some of the patients.
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PMID:[The results of a retrospective examination of patients with acute rheumatic fever]. 145 87

Rheumatic fever is still the leading cause of acquired heart disease in children and young adults in developing countries. Recent reports have documented a rising incidence of rheumatic fever in both the USA and Europe. The disease is characterized by specific lesions in the heart muscle and valves called Aschoff nodules. The Aschoff nodule has been neglected in the last few decades as most of the studies were conducted in the 1960s on autopsy tissues. This study examines Aschoff nodules using heart valve material obtained at valve surgery with updated commercially available immunohistochemical antibodies to determine the phenotypic characteristics of the cells involved in the formation of these lesions. Fifteen cases of rheumatic valvulitis, as indicated by the presence of Aschoff nodules, were examined. The Anitschkow and Aschoff cells stained prominently with macrophage markers. Three stages of nodules with Aschoff and Anitschkow cells were identified: stage 1, central fibrinoid necrosis without lymphocytes, stage 2 with occasional T lymphocytes (< 10) and stage 3 with lymphoid aggregates containing both T- and B-lymphocytes (with occasional admixed macrophages). We propose that the stage 1 lesion is the earliest granulomatous stage with the lymphoid aggregates being a later stage in the development of Aschoff nodules. The Aschoff and Anitschkow cells demonstrated mitotic activity and stained with antibodies to the proliferation cell nuclear antigen (PCNA) suggesting that the multinucleated giant cells may be formed, at least partially, by nuclear division rather than fusion.
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PMID:Rheumatic Aschoff nodules revisited: an immunohistological reappraisal of the cellular component. 857 37

Fungal endocarditis in children is most commonly a complication of palliative or curative surgery for congenital heart disease, rheumatic valvulitis and prolonged indwelling central venous and umbilical catheters. We describe here the case of a 3-y-old patient with chronic diarrhoea and prolonged total parenteral alimentation who developed severe C. tropicalis endocarditis and was treated successfully using a liposomal preparation of amphotericin-B (AmBisome) without surgical intervention.
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PMID:Successful non-surgical treatment of Candida tropicalis endocarditis with liposomal amphotericin-B (AmBisome). 1071 84

Rheumatic heart disease is an autoimmune sequela of group A streptococcal infection. Previous studies have established that streptococcal M protein is structurally and immunologically similar to cardiac myosin, a well-known mediator of inflammatory heart disease. In this study, we investigated the hypothesis that streptococcal M protein could produce inflammatory valvular heart lesions similar to those seen in rheumatic fever (RF). Fifty percent (3 of 6) of Lewis rats immunized with recombinant type 6 streptococcal M protein (rM6) developed valvulitis as well as focal lesions of myocarditis. Valvular lesions initiated at the valve surface endothelium spread into the valve. Anitschkow cells and verruca-like lesions were present. T cells from rM6-immunized rats proliferated in the presence of purified cardiac myosin, but not skeletal myosin. A T-cell line produced from rM6-treated rats proliferated in the presence of cardiac myosin and rM6 protein. The study demonstrates that the Lewis rat is a model of valvular heart disease and that streptococcal M protein can induce an autoimmune cell-mediated immune attack on the heart valve in an animal model. The data support the hypothesis that a bacterial antigen can break immune tolerance in vivo, an important concept in autoimmunity.
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PMID:Induction of autoimmune valvular heart disease by recombinant streptococcal m protein. 1134 78

Rheumatic fever is a multisystem inflammatory disease that occurs as a delayed sequel to group A streptococcal pharyngitis. It is less common than it was 50 years ago but is still a major cause of heart disease in developing areas of the world. The relationship between the site of infection, the type of causative organism, and susceptibility of the host is essential in the development of the disease. Its major clinical manifestations include carditis, migratory polyarthritis, chorea, erythema marginatum, and subcutaneous nodules. It can manifest as an acute febrile illness consisting of migratory polyarthritis involving the large joints, as carditis and valvulitis, or as Sydenham's chorea with involvement of the central nervous system. The disorder in its milder form resolves itself without sequelae. Carditis is the condition most associated with increased mortality and morbidity and may be fatal in its severe forms. Penicillin is the most appropriate primary and secondary prophylaxis. Anti- inflammatory agents provide symptomatic relief but do not prevent rheumatic heart disease.
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PMID:Rheumatic fever. 1156 77

Inflammatory heart diseases such as myocarditis and rheumatic heart disease result from the infiltration of the myocardium or valve with T cells and macrophages that result in scarring of the myocardium or valve and alteration in cardiac function. Our studies of T cells from these diseases have identified cardiac myosin in both rheumatic carditis and myocarditis as an important autoantigen. In rheumatic heart disease, streptococcal M protein specific T cells migrate to valves. By investigating streptococcal M protein and cardiac myosin in the Lewis rat model of myocarditis and valvulitis, T cell mimicry is supported as a potential mechanism in disease. Structural and immunological mimicry between the streptococcal M protein and cardiac myosin is shown directly in the Lewis rat model. Rat T cell lines demonstrate mimicry between cardiac myosin and M protein, and T cells isolated directly from inflammatory lesions in myocarditis respond to streptococcal M protein peptides. Studies in BALB/c mice also support the immunological crossreactivity of T cells primed against cardiac myosin with streptococcal M protein peptides containing cardiac myosin homologies. T cell lines produced from the Lewis rat specific to the cardiac myosin like sequences of streptococcal M protein migrated to the valves after passive transfer of the M protein specific T cell lines. In coxsackieviral myocarditis in the MRL mouse strain, cardiac myosin mimicking M protein peptide NT4 was found to induce tolerance and prevent coxsackieviral induced myocarditis, suggesting T cell mimicry between coxsackievirus and streptococcal M protein, both of which are associated with inflammatory heart disease. T cell mimicry between cardiac myosin and microbial antigens such as the streptococcal M protein may prime the immune system for inflammatory heart disease.
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PMID:T cell mimicry in inflammatory heart disease. 1503 18