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

Studies on the pathogenic potential of the human cardiotropic enterovirus, coxsackievirus B5, show that this agent localizes and replicates in the aorta of mice. Nutritionally-induced hypercholesterolemia leads to an increased replication and persistence of virus in tissues, specifically the aorta. Coxsackievirus B cardiopathy is markedly augmented in the hypercholesterolemic host, resulting in a persistent cardiomyolysis which is not evident in virus-infected animals with normal cholesterol levels. Pathological changes in the aorta become evident only months after the acute infection, and only in hypercholesterolemic animals previously infected with coxsackievirus B5. Our findings of coxsackievirus B-induced angiopathy and cardiopathy in the hypercholesterolemic host extend the known pathogenic range of these human viruses, and further emphasizes their potential as etiological agents of cardiovascular disease.
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PMID:Coxsackievirus B cardiopathy and angiopathy in the hypercholesterolemic host. 21 92

Twenty-two cases of Coxsackie virus heart disease diagnosed from November, 1969, to December, 1971, were re-examined after a period of 42 to 68 months from the acute illness. The patients with hypertension, diabetes, chronic alcohol intake, or aged over 35 were eliminated from the trial. With the purpose of assessing myocardial function, the systolic time intervals were recorded by a noninvasive standard technique. The differences in systolic time intervals between the group of patients with previous viral myocarditis and a group of normal control subjects were not statistically significant. However, the pre-ejection period was clearly prolonged in three patients out of 10, a modification consistent with a depressed myocardial function, as in patients with cardiomyopathy.
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PMID:Coxsackie virus heart disease and cardiomyopathy. 84 36

International and local Scottish data illustrate the epidemiology of enteroviruses in recent years. Polioviruses still predominate as causes of serious paralytic disease, except where controlled by vaccination and require continuing surveillance. Aseptic meningitis is the commonest reported illness due to enterovirus infection, but notable clinical manifestations of certain types (particularly coxsackie group A) involve the skin and mucous membranes and the respiratory tract. Gastrointestinal disturbance has been reported in some echovirus infections, and cardiac disease is particularly associated with group B coxsackie virus infections. Although most enterovirus infections are silent or trivial in severity, the trend towards periodic epidemicity of different enteroviruses involving older age-groups may entail the emergence of new disease problems of which heart disease may be one example.
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PMID:The epidemiology of enteroviruses. 111 Oct 84

The antiviral effects of human interferon-beta (IFN-beta) and human recombinant interferon-gamma (rIFN-gamma) were studied in persistently coxsackievirus B3-infected carrier cultures of human myocardial fibroblasts over a period of 21 days. Synergism was observed with concentrations as low as 30 IU of IFN-beta plus 10 IU of rIFN-gamma/mL, reducing mean viral titers from 6.0 x 10(7) to 1.3 x 10(4) pfu/mL and number of infected cells from 14.4% to 0.1% as determined by quantitative in situ hybridization. Higher concentrations of IFNs (both > or = 30 IU/mL) were associated with transient antagonism followed by antiviral synergism. With 100 IU of IFN-beta plus 30 IU of rIFN-gamma/mL, elimination of infectious virus was consistently achieved and sustained for 6 weeks after cessation of IFN application, whereas at least threefold higher concentrations were required with single drugs. In summary, our data support a concept of low-dose IFN combination schedules that might become useful in the treatment of enteroviral heart disease.
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PMID:Synergistic interaction of interferon-beta and interferon-gamma in coxsackievirus B3-infected carrier cultures of human myocardial fibroblasts. 132 9

Enteroviruses are thought to be etiologic agents in some cases of human myocarditis and dilated cardiomyopathy. Murine models of acute coxsackievirus B3 myocarditis implicate coxsackie B viruses as possible causes of human myocarditis. Indirect evidence implicating enteroviruses as causative agents in human heart disease derives from serologic studies. More recently, direct evidence for enteroviral presence in diseased human heart tissues has been obtained by nucleic acid hybridization analyses. Although the data suggest that enteroviral infections may be associated with 18% to 50% of cases of myocarditis or dilated cardiomyopathy, or both, causality has not been established. Unanswered questions remain regarding the specific identity of the enteroviral genomes detected in the human heart and the potential for enteroviruses to persist in the heart.
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PMID:Molecular approaches to enteroviral diagnosis in idiopathic cardiomyopathy and myocarditis. 216 Oct 26

We have developed an in situ hybridization assay capable of detecting enteroviral RNA in myocardial cells, using molecularly cloned coxsackievirus B3 cDNA as a diagnostic probe. Because of the high degree of nucleic acid sequence homology among the numerous enteroviral serotypes, including the group A and B coxsackieviruses and the echoviruses, detection of these various agents commonly implicated in human viral heart disease is possible in a single hybridization assay. We demonstrate the considerable potential of this method for an unequivocal diagnosis of enteroviral heart disease as well as for pathogenicity studies. Using athymic mice persistently infected with coxsackievirus B3 as a model system, we show that the myocardium is affected in a disseminated, multifocal manner.
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PMID:In situ detection of enteroviral genomes in myocardial cells by nucleic acid hybridization: an approach to the diagnosis of viral heart disease. 281 70

The frequency of actual infections by selected types of coxsackie virus (B1-B6, A7, A9) has been followed up in adult patients hospitalized for reason of heart disease. Criteria of actual coxsackie virus infection have been defined, including a significant rise of titer of virus neutralizing antibodies and/or presence of virus-specific IgM antibodies. An actual coxsackie virus infection has been found in 71 (46.3%) out of 153 patients. Most frequently coxsackie B1 virus infection (24 times) and B4 (17 times) could be proved. In sera of patients with actual coxsackie virus infection, a higher proportion of infection with some types of coxsackie viruses, along with the presence of antibodies against a larger number of coxsackie virus types has been found, as compared to sera from patients without actual coxsackie virus infection, and/or, in sera of healthy blood donors (control group). The role of repeated infections with different types of coxsackie virus in the etiology of heart disease has been discussed.
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PMID:Coxsackie virus infection in association with heart affection in man. 282 2

From 1969 to 1973, 68 patients were admitted to the 4th Division of Medicine of the Brescia Civil Hospital with the diagnosis of viral myocarditis. The patients were divided into two groups according to the results of the Coxsackie virus complement fixing antibodies test: Group 1 (42 patients) with a fourfold or greater rising antibody titre; Group 2 (26 patients) with a negative serum test. Both groups were examined after a follow-up period of 15 years. Ten patients from Group 1 died. The diagnoses were chronic myocarditis (three cases); chronic cardiomyopathy-pulmonary embolism (one case); chronic cardiomyopathy-liver cirrhosis (one case); dilated cardiomyopathy-sudden death (two cases); congestive cardiomyopathy (three cases). No Group 2 patients died. The 15-year mortality rate of Group 1 was significantly higher than that of Group 2 (Fisher Test: p less than 0.005). In conclusion, the natural history of Coxsackie virus heart disease is characterized by two possibilities: a complete recovery from a clinical point of view, in some cases with only minor T wave abnormalities, or evolution into a chronic disease (dilated cardiomyopathy) having a high mortality rate within 10 years of the onset of the acute disease.
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PMID:Coxsackie virus heart disease: 15 years after. 322 24

After infection with coxsackie virus B3 (CB3), H-2 congenic mice on an A- background develop immunologically mediated myocarditis associated with an increased titer of myosin autoantibody, part of which is specific for the cardiac myosin isoform. The present study demonstrates that cardiac myosin itself induces severe myocarditis and high titers of myosin autoantibodies in A/J, A.SW/SnJ, and A.CA/SnJ mice. As in CB3-induced myocarditis, one population of these autoantibodies was specific for cardiac myosin. A.BY/SnJ and B10.A/SgSnJ mice also developed the disease after immunization, but the prevalence and the myosin autoantibody titers were lower. In contrast, C57BL/6J and C57BL/10J mice were resistant to myocarditis induced by cardiac myosin and did not develop increased myosin autoantibodies or cardiac myosin-specific autoantibodies. Immunization with skeletal muscle myosin had no effect compared with controls injected with complete Freund's adjuvant, thereby suggesting that the immunogenic epitopes are unique to the cardiac myosin isoform. Furthermore, we found that susceptibility to myocarditis induced by cardiac myosin is influenced by the major histocompatibility complex and by genes not closely linked to the major histocompatibility complex. Because there are parallels between myocarditis induced by cardiac myosin and that induced by CB3, this new animal model can be used to analyze the pathologic mechanisms in autoimmune heart disease.
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PMID:Cardiac myosin induces myocarditis in genetically predisposed mice. 368 Sep 46

Male Balb/c mice inoculated with a heart-adapted variant of coxsackievirus, group B, type 3 (CVB3M) develop severe myocarditis characterized by extensive focal lesions of inflammatory cells and necrosis of the myocardium. Females generally develop minimal myocarditis except when infected during the first and third trimesters of pregnancy. Enhanced myocarditis is usually accompanied by elevations in virus concentrations in the heart, virus-specific antibody titers, and lymphocyte mediated cytolytic activity to both uninfected and CVB3M-infected myocytes in vitro. As previously shown in males, T-lymphocyte-depleted pregnant female mice inoculated with the virus do not develop significant myocarditis indicating that immune rather than virus-mediated myocyte damage is important in myocarditis. Progesterone increases during gestation reaching maximum concentrations during the third week when heart disease is most severe. Administration of progesterone to castrated male and female mice prior to virus inoculation resulted in increased virus concentrations, cellular and humoral CVB3M-specific immunity, and myocarditis. Two hypotheses for exacerbation of the disease with elevated progesterone concentrations have been postulated: the hormone either indirectly increases cellular immune responses by enhancing virus replication, or independently enhances both T-cell responses and virus replication.
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PMID:Aggravation of coxsackievirus, group B, type 3-induced myocarditis and increase in cellular immunity to myocyte antigens in pregnant Balb/c mice and animals treated with progesterone. 608 88


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