Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical outcome of 18 patients, who presented with a Coxsackie virus myopericarditis in 1965, was evaluated 23 years later. Five patients had died, two of them had had heart failure. Thirteen patients and 23 healthy control subjects underwent exercise testing with gas exchange analysis. Left ventricular (LV) peak filling rate (PFR) was estimated by digitized M-mode echocardiography. Left ventricular ejection fraction was measured at rest and during exercise by radionuclide angiography. All patients were free of cardiac symptoms. Their clinical examination and the chest X-ray were normal. Peak oxygen consumption was not decreased in the patient group compared with the control group. PFR was significantly lower in the patient group than in the control group, 10.2 +/- 0.4 vs 13.2 +/- 0.4 cm s-1, P less than 0.001 (mean +/- SEM). LV ejection fraction was normal at rest in all patients (58 +/- 1%). An abnormal LV ejection fraction response to exercise was observed in two patients. Our data indicate that long-term prognosis after acute Coxsackie virus myopericarditis is good in a majority of patients.
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PMID:Clinical outcome and left ventricular function 23 years after acute coxsackie virus myopericarditis. 231 17

Recent evidence suggests that the most common form of idiopathic cardiomyopathy in our altitudes, the dilated cardiomyopathy (DCM), is a post-infectious autoimmune disease which is triggered by virus infections. In animal experiments, the development of the coxsackie virus B3 myocarditis to a congestive cardiac insufficiency resembling the clinical picture of DCM was demonstrated. In mice, species-dependent varying disease courses could be observed, which point to a genetically different behaviour of the animals' immunological reactions, either humoral or T-cell mediated immune reactions being responsible. In comparison with non-DCM patients, patients with DCM and chronic myocarditis exhibit significantly higher coxsackie virus antibody titres. Obviously, also a differently long viral persistency in the cardiac muscle plays a role, as enterovirus-specific RNA was detected in myocardial biopsies from patients with DCM. Along with myocardial fibroses, endomyocardial biopsies in DCM frequently reveal mononuclear cellular infiltrates, which, however, only in 20-25% of the cases may be regarded as chronic persisting myocarditis. The clinical and paraclinical findings in DCM and in the so-called latent cardiomyopathy are presented. In congestive heart failure, the best therapeutic results are achieved by the ACE inhibitors, along with vasodilator agents, digitalis glycosides and diuretics. Ultima ratio is the orthotopic heart transplantation, as it is only this intervention that will be able to improve the primarily bad prognosis decisively. Whether the treatment with immunosuppressive drugs exerts an influence upon the prognosis, has thus far remained an open question.
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PMID:[Dilated cardiomyopathy--heart muscle disease of unknown origin or an autoimmune disease? New aspects of etiology, pathogenesis and clinical practice]. 268 30

An autopsy case of a 10-day-old newborn with generalized infection of Coxsackie virus B3 (CBV3) was reported. CBV3 was isolated from the blood before death. The patient died of cardiac failure. An immunofluorescent study was carried out on autopsy specimens fixed in formalin and embedded in paraffin. CBV3 antigen was detected in the heart, brain, kidney, lungs, spleen, thymus, and pancreas. In the pancreas CBV3 antigen was predominantly seen in the islet cells. No CBV3 antigen was found in the liver and adrenal glands. Electron microscopic examination revealed virion-like particles, 20 nm in diameter, in the endothelial cells of the myocardium.
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PMID:An immunofluorescent study of generalized Coxsackie virus B3 infection in a newborn infant. 299 61

A 3-week-old male neonate with heart failure associated with Coxsackie virus infection was imaged with Tc-99m PYP and TI-201. The abnormal imaging pattern suggested myocardial infarction. Autopsy findings indicated that the cause was myocardial necrosis secondary to an acute inflammatory process. Causes of abnormal myocardial uptake of Tc-99m PYP in pediatrics include infarction, myocarditis, cardiomyopathy, bacterial endocarditis, and trauma. Myocardial imaging cannot provide a specific cause diagnosis. Causes of myocardial infarction in pediatrics are listed in Table 1.
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PMID:Myocardial imaging. Coxsackie myocarditis. 302 78

Immunofluorescent and electron-microscopic studies were performed to determine the distribution of viral antigens and particles and to clarify the relationship to myocardial lesions in two autopsy cases with generalized infection of Coxsackie virus B3 (CVB3) or cytomegalovirus (CMV). Case 1 was a full-term newborn female infant, without any congenital anomalies, who died of cardiac failure 10 days after birth. CVB3 was isolated from the blood before death. Necrosis of the muscle fibers was observed, frequently accompanying calcification. Numerous histiocytes and a few lymphocytes and neutrophils had infiltrated in and around the necrotic areas. Immunofluorescent study (IF) revealed CVB3 antigen in the muscle fibers and vascular endothelial cells. Case 2 was a female infant, born at 28 weeks of gestation, who died of fatal arrhythmia 50 days after birth. The infant had hemocephalus and a history of idiopathic respiratory distress and underwent an operation for patent ductus arteriosus. Cytomegalic cells were frequently found in the vascular endothelial cells in the myocardium and occasionally in muscle fibers. IF showed the presence of CMV antigen in both endothelial cells and muscle fibers. CVB3 and CMV antigens were detected predominantly in vascular endothelial cells rather than in the muscle fibers. Blood flow disturbance due to endothelial damage is a cause of the myocardial lesion in addition to the direct invasion of the muscle fibers by the virus.
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PMID:Myocardial lesions by Coxsackie virus B3 and cytomegalovirus infection in infants. 303 31

The exact cause of dilated cardiomyopathy (DCM) remains uncertain. However, a possibility of transition from coxsackievirus-infected myocarditis to DCM has been suspected. We investigated the role of enteroviral infection in the pathogenesis of DCM. The nested reverse transcriptase polymerase chain reaction (nRT-PCR) was used to detect enteroviral RNA in 45 endomyocardial biopsy tissues obtained from 35 patients with DCM and 10 patients (controls) with other non-infectious cardiac diseases. Enteroviral RNA was detected in 17 (49%) of the 35 patients with DCM. The progression to cardiac failure was rapid, usually within 12 months, and myocardial fibrosis and myocytic hypertrophy were marked in patients that were enteroviral RNA positive. Enteroviral RNA was not detected in any controls.
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PMID:Enteroviral RNA in dilated cardiomyopathy. 792 15

The human enteroviruses, especially the coxsackie B viruses, have been established as aetiologic agents of human inflammatory heart disease, a condition which may lead to dilated cardiomyopathy and heart failure. It is clear from murine models of coxsackievirus B3-induced inflammatory heart disease that not all strains of the virus are cardiovirulent (able to cause disease). Here, we present preliminary data mapping the site in a coxsackievirus B3 genome which determines a cardiovirulent phenotype.
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PMID:Genetics of coxsackievirus B3 cardiovirulence. 868 85

Myocarditis is defined as an inflammation of the heart muscle and often follows enterovirus infections. Frequently, patients surviving the acute inflammatory stage undergo complete recovery, but myocarditis can result in dilated cardiomyopathy. A murine model of myocarditis has been developed that uses cardiotropic variants of coxsackievirus Group B. Type 3 (CVB3), and either BALB/c (H-2d), MRL+/+ (H-2k), or DBA/2 (H-2d) male mice. Infection of all three mouse strains results in equivalent levels of myocardial inflammation 7 days later. IgG antibodies are detected by immunofluorescent staining in DBA/2 but not BALB/c or MRL+/+ myocardium and correlate with the detection of anti-heart antibodies in the sera of DBA/2 mice by immunofluorescence. CD4+ cell depletion of DBA/2 and MRL+/+ mice prevents myocarditis, but both CD4+ and CD8+ T cells cause cardiac inflammation in BALB/c mice, although CD8+ cells are substantially more pathogenic than CD4+ cells in this strain. No or few CD8+ T cells infiltrate the myocardium of either DBA/2- or MRL+/(+)-infected animals, although this is the predominant T-cell population in BALB/c mice. Apoptosis was measured by terminal deoxynucleotidyl transferase-staining of myocardial sections. No apoptosis was observed in inflamed DBA/2 hearts. Apoptosis was restricted to inflammatory cell infiltrates of infected MRL+/+ hearts, but apoptosis was wide-spread in both the inflammatory cell infiltrates and in myocytes outside inflammatory lesions in BALB/c mice. Atria natriuretic factor (ANF) mRNA expression was only elevated in the left ventricles of BALB/c mice. CD8+ T-cell depletion abrogated the appearance of apoptotic myocytes and ANF mRNA expression. The fact that ventricular ANF production often occurs during cardiac failure suggests that myocardial stress is substantially greater in BALB/c mice than in other strains despite equivalent amounts of cardiac inflammation.
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PMID:Coxsackievirus-induced myocarditis is dependent on distinct immunopathogenic responses in different strains of mice. 916 88

Recent reports demonstrated the expression of inducible-type NO synthase in the heart of viral myocarditis. Since NO has multiple biological actions, a substantial amount of NO produced in the diseased heart may act either as a cytotoxic or as a cytoprotective molecule in the process of myocarditis. In the present study, we examined the effect of inhibition of NO synthesis on the mortality and the extent of myocardial injury in a murine model of coxsackievirus B3-induced myocarditis. We fed the infected mice drinking water containing a relatively low concentration (0.37 mmol/L) of N omega-nitro-L-arginine methyl ester (L-NAME) for 14 days after virus inoculation. This dose of L-NAME did not change virus titers in the heart. However, L-NAME-fed mice showed a significant reduction in mortality compared with those fed normal drinking water (nontreated mice). On the contrary, mice given a higher concentration of L-NAME (3.7 mmol/L) exhibited increased mortality. In addition, mice fed a low concentration of L-NAME showed reductions in the severity of heart failure and in the area of myocardial necrosis. Although systemic blood pressure was reduced in nontreated mice, in mice fed a low concentration of L-NAME, it was maintained at a level similar to that in uninfected control mice, L-NAME-treated mice also exhibited a reduction in the degree of inflammatory cell infiltration associated with decreased production of tissue prostaglandin E2 levels in the heart compared with nontreated mice. Therefore, NO is likely to be involved in the pathogenic mechanisms of myocardial injury and resultant cardiac dysfunction in a murine model of coxsackievirus B3-induced viral myocarditis.
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PMID:Low-dose N omega-nitro-L-arginine methyl ester treatment improves survival rate and decreases myocardial injury in a murine model of viral myocarditis induced by coxsackievirus B3. 931 31

Viral myocarditis is an important cause of heart failure and dilated cardiomyopathy. T lymphocytes are implicated in myocardial damage in murine models of coxsackievirus B3 (CVB3) myocarditis. We used knockout mice lacking CD4 (CD4(-/-)), CD8 (CD8(-/-)), both coreceptors (CD4(-/-)CD8(-/-)), or the T-cell receptor beta chain (TCRbeta(-/-)) to address the contribution of T-cell subpopulations to host susceptibility to CVB3 myocarditis. Severity of disease was magnified in CD8(-/-) mice but attenuated in CD4(-/-) mice, consistent with a pathogenic role for CD4(+) lymphocytes. Elimination of both CD4 and CD8 molecules from T lymphocytes by genetic knockout better protected mice from myocarditis, demonstrating that both CD4(+) and CD8(+) T cells contribute to host susceptibility. The same benefit occurred in TCRbeta(-/-) mice, with prolonged survival and minimal myocardial disease observed after CVB3 infection. Elevated interferon-gamma and decreased tumor necrosis factor-alpha expression are associated with attenuated myocardial damage in CD4(-/-)CD8(-/-) mice. These results show that the presence of TCRalphabeta(+) T cells enhances host susceptibility to myocarditis. The severity of myocardial damage and associated mortality are dependent on the predominant T-cell type available to respond to CVB3 infection. One mechanism by which CD4(+) and CD8(+) T-cell subsets influence the pathogenesis of myocarditis may involve specific cytokine expression patterns.
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PMID:Susceptibility to myocarditis is dependent on the response of alphabeta T lymphocytes to coxsackieviral infection. 1048 59


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