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

The aim of the present study was to determine whether there is an association between Parvovirus B19 infection and hydrops fetalis setting in fetus and neonate. Twenty-nine samples were analyzed by three methods. Each sample was histologically examined for viral nuclear inclusions in fetal organs and placenta, then immunohistochemical study using Parvovirus B19 antibody that recognized the VP2 protein of the Parvovirus B19 capsid was done in tissue embedded in paraffin (lungs, liver, thymus, kidneys, heart and placenta). Nested-PCR analysis was done after DNA extraction from paraffin blocks and using specific primers of the Parvovirus B19 VP1 gene. Apparent causes of hydrops were eliminated such as metabolic diseases, cardiac failure or malformation. The standard histological study objects viral inclusion in one case (lung tissue). However, the immunohistochemical study was negative in all cases. Nested-PCR demonstrates the presence of the viral DNA in five cases. Our study demonstrates that the implication of Parvovirus B19 in hydrops fetalis must be affirmed by the use of more than one method. Nested-PCR is the most sensitive method in our study and can be easily used for the detection of Parvovirus B19 in formalin-fixed paraffin-embedded tissues.
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PMID:Detection of the human Parvovirus B19 in nonimmune hydrops fetalis using immunohistochemistry and nested-PCR in formalin-fixed and paraffin-embedded placenta and fetal tissues. 1824 74

We report a patient with acute heart failure due to human parvovirus B19 infection. The patient was a 36-year-old man with polyarthralgia, fatigue and swelling of his upper eyelids and all four limbs. These symptoms disappeared, but 5 days after the first consultation, the patient presented with severe exertional dyspnoea, chest pain and swelling of his whole body. Erythema was observed on the skin of hands, fingers and abdomen. Pleural and pericardial effusion, ascites and hepatosplenomegaly were detected. Laboratory examination showed positive results for anti-human parvovirus B19 IgM and B19 DNA in the serum. A diagnosis of acute heart failure by pericarditis caused by B19 was made. This case report suggests that B19 should be considered as a cause of acute heart failure through acute pericarditis.
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PMID:Acute heart failure associated with human parvovirus B19 infection. 1835 55

Antiphospholipid syndrome is an autoimmune disease characterized by recurrent thrombosis and the presence of antiphospholipid antibodies. Clinical presentations are dependent on the affected vessels and organs. The most common presentation of antiphospholipid syndrome is arterial or venous thrombosis. An unusual presentation of the disease is characterized by microvascular thrombosis with multiorgan involvement, which is termed catastrophic antiphospholipid syndrome. The diagnosis of catastrophic antiphospholipid syndrome can be difficult because of the heterogeneity of the different clinical forms. Clinical manifestations of catastrophic antiphospholipid syndrome are complex with multiple organ involvement, resulting in renal insufficiency, heart failure, acute respiratory distress syndrome, and liver involvement. Early diagnosis and aggressive therapies are essential in this condition because of the extremely high mortality rate. Herein, the case of a 14-year-old girl with catastrophic antiphospholipid syndrome that was previously misdiagnosed as a vasculitis related to parvovirus B19 infection is presented.
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PMID:A case of catastrophic antiphospholipid syndrome in an adolescent girl with parvovirus B19 infection. 1856 54

A 59-year-old previously healthy man had flulike symptoms of fever and diarrhea for a week, which worsened despite treatment with antibiotics. After admission, his medical condition rapidly deteriorated with renal failure, heart failure, and a marked increase of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. The patient died of a cardiac arrhythmia 3 days after the admission. The autopsy showed diffuse myocarditis with a granulocytic and monocytic infiltrate, necrotizing arteritis of the coronary arteries, and fulminant hepatitis, with microvesicular steatosis and necrosis. Cell-free serum showed high copies of human herpesvirus 6 B variant DNA by polymerase chain reaction. Human herpesvirus 6 B was identified in the heart, liver, lung, and spleen by immunohistochemistry. No parvovirus B19 was evident in the heart by immunohistochemistry. Human herpesvirus 6 is increasingly found in association with myocarditis in immunocompromised patients; however, histopathologic features and the clinical severity of this disease have not yet been clearly defined. Only 4 to 5 cases of human herpesvirus 6 fulminant myocarditis have been reported, all in young children or immunosuppressed patients. To the best of our knowledge, this is the first case in the English literature of human herpesvirus 6 fulminant myocarditis and hepatitis in an immunocompetent adult with a fatal outcome. In addition, several pathologic features of our case have not been previously reported.
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PMID:Human herpesvirus 6-related fulminant myocarditis and hepatitis in an immunocompetent adult with fatal outcome. 1976 69

Whereas C-reactive protein (CRP) is acknowledged as a cardiovascular risk marker, there is ongoing discussion about its role as a risk factor. Previous studies focused on the effects of CRP on ischaemic heart failure and atherosclerosis. In this study we investigated distribution of CRP, the Terminal Complement Complex (C5b-9) and macrophages (CD68) in the myocardium of patients suffering from non-ischaemic heart failure and their implication on clinical parameters. Endomyocardial biopsies were taken from 66 patients suffering from dilated cardiomyopathy (DCM). Biopsies were analysed by immunohistochemical and immunofluorescent staining for CRP, C5b-9 and CD68. Viral DNA/RNA for adenovirus, enterovirus, parvovirus B19 and human herpes virus 6 was detected by PCR and Southern blot analysis. Myocardial biopsy findings were correlated with plasma level of hsCRP and NT-proBNP as well as echocardiography, exercise test and NYHA class. In 18 (27%) patients, a positive staining for CRP and in 57 (86%) patients a positive staining for C5b-9 was detected. All patients showed myocardial infiltration with macrophages with an average of 39 cells/mm(2). CRP, C5b-9 and CD68 co-localised within the myocardium. No correlation was observed for inflammatory proteins and plasma level of hsCRP, NT-proBNP and clinical parameters. CRP is frequently present in the myocardium of patients suffering from DCM and co-localises with C5b-9 and macrophages. CRP may contribute to myocardial damage in DCM via activation of the complement system and chemotaxis of macrophages.
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PMID:Myocardial inflammation and non-ischaemic heart failure: is there a role for C-reactive protein? 1934 15

Cardiomyopathies are an important and diverse group of heart muscle diseases in which the heart muscle itself is structurally or functionally abnormal and in which coronary artery disease, hypertension, valvular and congenital heart disease are absent or do not sufficiently explain the observed myocardial abnormality. This often results in severe heart failure accompanied by arrhythmias and/or sudden death. Clinical and morphological diversity of cardiomyopathies can reflect the broad spectrum of distinct underlying molecular causes or genetic heterogeneity. In many cases the disease is inherited and is termed familial dilated cardiomyopathy (FDC), which may account for up to 30% of dilated cardiomyopathies (DCM). FDC is principally caused by genetic mutations in FDC genes that encode for cytoskeletal, nuclear and sarcomeric proteins in the cardiac myocyte. In addition, modifying genes, lifestyle and additional factors were reported to influence onset of disease, disease progression, and prognosis. The individual patient's phenotype may reflect a summation and/or interaction of the underlying mutation(s) with other genetic or environmental factors. During the last years major advances have been made in the understanding of the molecular and genetic basis of this type of disease. Nevertheless, much more progress in the identification of underlying mutations, susceptibility genes and modifier genes is important and indispensable for the development of new etiology-orientated forms of therapy. A pivotal role for autoimmunity in a substantial proportion of patients with DCM is supported by the presence of organ-specific autoantibodies, inflammatory infiltrates and pro-inflammatory cytotoxic cytokines. Furthermore, familial occurrence of DCM goes ahead with the presence of autoantibodies and abnormal cytokine profiles in first-degree relatives with asymptomatic left ventricular enlargement. These relatives suffer from a higher risk for the development of DCM after years. This suggests the involvement of a disrupted humoral and cellular immunity early in the development of the disease. There is reasonable clinical and experimental evidence, that DCM in addition may occur as late stage of cardiac infection and inflammation. The large spectrum of clinical forms depends on several factors such as genetic determinants of the infective agent, the genetics, age and gender of the host, and the host immunocompetence. In general, infectious agents, including viruses such as entero-, cytomegalo-, and adenoviruses, bacteria such as Borrelia burgdorferi or Chlamydia pneumoniae, protozoa and even fungi can cause inflammatory heart disease leading to DCM. The infectious agents most often identified in DCM nowadays are parvovirus B19, human herpesvirus 3, and Epstein-Barr virus. Persistence of these viruses within the myocardium is associated with reduction of ejection fraction after 6 months. For patients with suspected inflammatory heart disease the immunohistochemical detection of inflammatory infiltrates is related to poor outcome. Many faces of inflammatory heart disease coexist where different phases of the disease progress simultaneously: phase 1 is dominated by viral infection itself, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation. Further investigations with regard to the etiology of structural heart diseases should include an intensive clinical investigation of the given patient. A possible family history including a pedigree should be ascertained and with regard to a possible inflammatory or viral heart disease, endomyocardial biopsies should be investigated by polymerase chain reaction and immunohistochemistry.
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PMID:[Familial predisposition and microbial etiology in dilated cardiomyopathy]. 1937 Mar 26

We report on a 61-year-old man who presented with new negative T-waves in V3 to V5. Coronary heart disease with a nonsignificant stenosis of the anterior interventricular artery was known for three years without any symptoms of heart failure. Harvested endomyocardial biopsies of the left ventricle during catheterization showed a chronic parvovirus B19-associated myocarditis. A magnetic resonance imaging was carried out and showed a 6 x 3 x 3-cm mass in the right ventricle extending from the apex. The tumor could be completely resected using cardiopulmonary bypass. Histopathological diagnosis was consistent with a benign fibroma.
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PMID:Right ventricular fibroma in a 61-year-old man. 1967 Jan 21

Between 10 and 20% of patients with histologically proven inflammatory disease of the heart muscle develop a chronic disorder after acute myocarditis which results in dilated cardiomyopathy with increasing cardiac insufficiency. Viral infections are a frequent cause of inflammatory heart muscle diseases and thus also responsible for myocardial damage in the initial phase. In the past, evidence for enterovirus, adenovirus, and cytomegalovirus was in the focus of attention. In the meantime, "new" cardiotropic pathogens such as parvovirus B19, Epstein-Barr virus, and human herpesvirus 6 have been detected in patients with dilated cardiomyopathy with and without inflammation. Their persistence in the myocardium correlates with a decline in pumping capability within 6 months. While the virus is still being eliminated, the second phase of the disease begins, which is characterized by autoimmune phenomena and often a cardiac inflammatory response which likewise correlates with a worsening prognosis. The transition to the third and final phase with development of dilated cardiomyopathy occurs gradually and can take years. The goal of every diagnostic and therapeutic intervention must be to eradicate the virus and eliminate the inflammatory response to prevent the disease from progressing to terminal cardiac insufficiency.
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PMID:[The heart in viral infections]. 2053 60

Fulminant myocarditis is a rare inflammatory heart disease affecting relatively young adults. We describe a case of a 27-year-old male with acute onset severe heart failure. A rapid and accurate diagnostic approach suggested parvovirus B19 as the most probable cause for this fulminant viral myocarditis. Initial haemodynamic support, intensive immunosuppressive and antiviral therapy resulted in a complete recovery within 2 weeks. This case demonstrates the importance of a detailed diagnosis, allowing better classification of the underlying pathology and subsequent targeted treatment.
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PMID:Parvovirus-B19-associated fulminant myocarditis successfully treated with immunosuppressive and antiviral therapy. 2058 61

Human parvovirus B19 infection is widespread. Approximately 30-50% of pregnant women are nonimmune, and vertical transmission is common following maternal infection in pregnancy. Fetal infection may be associated with a normal outcome, but fetal death may also occur without ultrasound evidence of infectious sequelae. B19 infection should be considered in any case of nonimmune hydrops. Diagnosis is mainly through serology and polymerase chain reaction. Surveillance requires sequential ultrasound and Doppler screening for signs of fetal anaemia, heart failure and hydrops. Immunoglobulins, antiviral and vaccination are not yet available, but intrauterine transfusion in selected cases can be life saving.
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PMID:Parvovirus B19 infection in human pregnancy. 2104 Mar 96


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