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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report three patients with a particular form of myocarditis characterized by numerous clusters of lymphocytes. Their common clinical manifestation was progressive and fatal heart failure with a 3- to 6-year duration. Atrioventricular and intraventricular conduction disturbances were observed in two patients. At necropsy, the hearts weighed 480, 530, and 430 gm, respectively, and showed marked dilatation of the bilateral ventricles and atria, with frequent mural thrombi. Histologic examination revealed numerous lymphocytic clusters and scattered foci of acute myocardial cell damage on a background of extensive fibrosis. We propose the term "chronic active myocarditis" to denote clinicopathologic characteristics of the present cases.
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PMID:Lymphocytic active myocarditis characterized by numerous clusters of lymphocytes: a chronic variant of myocarditis? 172 15

A 46-year-old female patient with chronic Chagas' myocarditis without heart failure was submitted to chemotherapy because of Hodgkin's disease. During treatment the frequency of polymorphic ventricular extrasystoles raised and the patient died by a sudden cardiac arrest. Autopsy revealed chronic Chagas myocarditis with an acute exacerbation. Nests of amastygotes with a density of up to 14 pseudocysts/cm2 were found in the myocardium, although restricted to the septum and left ventricular posterolateral wall. Extensive histologic examination did not reveal parasites in other locations. This favors the concept of a localized exacerbation of Chagas' disease due to immunosuppression developing from a persistent parasitic focus in the heart. Although this reactivation during chemotherapy of malignant disease is rarely reported in literature, a careful monitoring of patients with positive Chagas' serology during chemotherapy is recommended.
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PMID:Reactivation of Chagas' myocarditis during therapy of Hodgkin's disease. 175 Jan 19

In 32 patients with dilated cardiomyopathy the percentages of helper (CD4+) and suppressor (CD8+) T lymphocytes, as well as their ratio, have been analyzed. The percentage of CD8+ lymphocytes in the group with dilated cardiomyopathy was 20.62 +/- 8.27% (X +/- SD), vs. 26.38 +/- 6.19% in control group; the difference was not statistically significant. The percentages of CD4+ lymphocytes were similar in both groups, 39.55 +/- 12.86% vs. 40.52 +/- 6.59%. The CD4+/CD8+ ratio was markedly higher in the group with dilated cardiomyopathy, 2.49 +/- 2.10 vs. 1.65 +/- 0.49, but the difference was not statistically significant, probably because of great variability in the group. In the subgroup of 12 patients with possible alcoholic etiology of dilated cardiomyopathy, the values were almost identical to those of the remaining 20 patients. No correlation between echocardiographic fractional shortening of the left ventricle and any of the aforementioned values of T lymphocytes in the group of patients with dilated cardiomyopathy was found. The tendency toward decline in number of suppressor T lymphocytes is in accordance with the hypothesis that the "overreacting" inflammatory response to (viral) myocarditis might be the cause of dilated cardiomyopathy. However, the specificity of the decline of suppressor activity in respect to the other causes of heart failure is questionable and the analysis of its significance is complex. This is due to dynamic character of immune disorders, and a considerable number of other theories considering the etiology and pathogenesis of the disease also exist. The need to perform complex studies is anticipated, including continual observation of clinical, immunologic and bioptic parameters of the disease.
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PMID:[Relation between helper and suppressive/cytotoxic T lymphocytes in the peripheral blood in patients with dilated cardiomyopathy]. 182 36

Previous studies have suggested that some cases of idiopathic dilated cardiomyopathy (IDC) are due to persistent viral infection following an episode of viral myocarditis. Viral RNA sequences have recently been detected in material from patients with IDC using molecular biological techniques. We tested 40 samples from recipients' hearts explanted at cardiac transplantation for the presence of enteroviral RNA sequences, using a Northern blotting technique. Material from 19 cases of IDC and 21 cases of non-cardiomyopathic cardiac failure was examined together with Coxsackie-virus-infected neonatal mouse heart as a positive control and non-infected adult mouse heart as a negative control. A sharp band of viral RNA was detected in the positive control sample. No hybridization signal attributable to viral RNA was obtained for the negative control or for any of the test samples. We conclude that the role of enteroviruses in the pathogenesis of cardiomyopathy is not fully established and that further study is warranted.
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PMID:Enteroviruses and idiopathic dilated cardiomyopathy. 184 88

Cardiac involvement is being identified more often clinically and at autopsy in patients with AIDS. Recent estimates suggest that in the United States as many as 5000 patients per year may have cardiac complications resulting from HIV infection. Patients with AIDS may have pericardial, myocardial, and/or endocardial disease. Pericardial tamponade and/or constriction may be related to neoplasms, infections, or nonspecific effusions. Myocardial dysfunction may result from specific neoplastic infiltration or myocarditis. Particularly intriguing is the role of HIV-1 in the nonspecific myocarditis and dilated cardiomyopathy that occurs in patients with AIDS. As in other debilitating conditions patients with AIDS can have nonbacterial thrombotic endocarditis. Infective endocarditis may be a complication, especially in AIDS associated with intravenous drug abuse. Most patients with AIDS have no overt clinical evidence of cardiac disease. When cardiac dysfunction does develop, the signs and symptoms are often misinterpreted to be the result of noncardiac causes (pulmonary failure or infection) which can mimic heart failure. This review is intended to alert the reader to the cardiac manifestations of AIDS, which present a number of diagnostic and therapeutic challenges.
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PMID:Cardiac manifestations of acquired immune deficiency syndrome: a 1991 update. 185 38

Thirteen clinical charts belonging to children with Kawasaki disease admitted to different hospitals were analyzed. The average age among the children was three years (from nine months to nine years), with a predominance of this disease in males with a ratio of 3.3:1. Echocardiograms were obtained from 10 of the patients; seven showed coronary aneurysms (70%). Other complications seen were myocarditis in six children, and one case in each of the following: arthritis, pericarditis, cardiac failure, coronary thrombosis, hydropic gall bladder and aseptic meningitis. All of the patients recovered successfully; only four of the patients with aneurysms were followed-up with an echocardiogram. The echocardiogram showed the aneurysms to have disappeared in three of the children one to five months later, and the other showed a persistent aneurysm plus dilated myocardiopathy 2.5 years later in the remaining patient. It is worth noting the high incidence of aneurysms (70%) compared to other series (20-65%) which may be due to the suspicion of this diagnosis in only typical cases.
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PMID:[Kawasaki disease in Mexico: an analysis of 13 cases]. 191 May 55

Over the last 10 years, our knowledge of immunologically mediated processes involving the myocardium appears to have made quantum leaps. New and important disease entities such as AIDS have appeared and the cardiologist now becomes an important member of the "AIDS team." Our understanding of "older diseases" such as sarcoidosis, Lyme disease, systemic lupus and other connective tissue syndromes has significantly increased. The concept of high-dose steroid therapy for these processes may, in fact, turn out to be futile and more selective, as less dangerous immunosuppression is being introduced. This concept has significantly advanced in the field of cardiac transplantation where immunosuppression has now been usurped by specific immunotherapy aimed at selective aspects of the immune sequence. New and exciting concepts will emerge from the molecular biology laboratory that will have direct bearing on the management of patients with cardiovascular disorders. This information explosion will force the cardiovascular physician to become more in tune with the world of immunology and molecular biology. Many obvious, significant problems remain, such as accelerated atherosclerosis in the transplant patient and the role of myocarditis in the patient with heart failure. However, it will truly be an exciting decade in which to work and watch the unraveling of these mysteries and hopefully, the study of today's problems will give way to solutions and a clearer understanding of the heart as a target of immune injury.
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PMID:The heart as a target organ of immune injury. 191 12

To identify a cardiac protein that could cause a serious autoimmune myocarditis, membranous proteins and myosin as antigens were investigated. In mice immunized with membranous proteins, the lesions induced were limited on the histological level. On the other hand, in Lewis rats immunized with cardiac myosin, serious myocarditis was induced. Every rat showed evidence of heart failure which was fatal in a few. Histology disclosed extensive cell infiltrates and myocardial necrosis. Among those lesions, giant cells were present. This myocarditis could be also transferred adoptively by lectin-activated spleen cells, T-lymphocytes, but not by IgG fraction. Thus, cardiac myosin can induce autoimmune giant cell myocarditis in Lewis rats.
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PMID:Experimental giant cell myocarditis induced by cardiac myosin immunization. 191 48

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


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