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

In view of the scarce references concerning the histological data in congenital parvovirus human B19 infection, we intend to provide a description of the pathological features observed in six autopsies. The virus was detected by DNA hybridization (ISH-DBH), PCR and electronmicroscopy (EM) in paraffin-embedded feto-placentary tissues. These cases constitute a subset from 86 Non Immunologic Hydrops Fetalis (NIHF) cases, in which a systemic complex of inflammatory/degenerative lesions of unknown etiology was visualized by optical microscopy. In one case a syphilitic process was detected, typefying a double infection. All fetuses showed a similar pathology--hydrops, hepato-splenomegaly, lung hypoplasia and erythroblastemia, the specific histological feature being the presence of intranuclear inclusions in the erythroid progenitors, in the erythropoietic visceral tissue and in blood marrow. Complex cardiopathy allied to abnormal lung lobulation and polisplenia were observed once; in 2 cases endocardial fibroelastosis was diagnosed. The pulmonary lesions were represented by dysmaturity allied to interstitial mononuclear infiltration. The hepatic consisted of cholestasis, portal fibrosis, canalicular proliferation, hemossiderosis, focal necroses and giant cell transformation. The central nervous system lesions were predominantly anoxic although the autolysis impaired a correct diagnosis.
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PMID:Feto-placentary pathology in human parvovirus B19 infection. 983 Jul 27

Coxsackieviruses and adenoviruses are common agents of viral heart disease. In the majority of exposed individuals they do not cause myocardial disease, however, since they are not primarily cardiotropic. Until recently the molecular basis of their anomalous tropism in patients who develop viral heart disease was unknown. An important step towards clarification of the molecular basis of cardiotropic viral infections was achieved in 1997, when a common receptor for the two structurally unrelated viruses was cloned. This coxsackievirus-adenovirus receptor (CAR) is a key determinant for the cellular uptake of both viruses and for the molecular pathogenesis of coxsackievirus and adenovirus diseases. We have mapped the CAR expression in human hearts and observed highly variable expression patterns. Healthy donor hearts had low CAR expression levels, whereas explanted hearts of patients with dilated cardiomyopathy (DCM) displayed high CAR expression in the myocardium. Remarkably, however, heart failure per se was not associated with CAR induction, since in heart failure of non-DCM origin no induction was found. Additional studies on the molecular mechanisms of CAR induction in cardiomyocytes indicated the existence of a cell-cell contact-dependent molecular mechanism regulating CAR expression, whereas cellular virus uptake and low level replication had no effect. Recombinant expression of human CAR in cardiomyocytes strongly increased their virus uptake rate suggesting that CAR induction enhances cardiac vulnerability to viral disease, whereas healthy myocardium is rather resistant to CAR-dependent viruses. Receptor induction may significantly aggravate the clinical course of viral heart disease, so that the blockade of receptor expression or receptor-virus interactions opens new therapeutic perspectives. Elucidation of the molecular mechanism of CAR induction in DCM, but not in heart failure per se, may reveal a particular pathogenetic process in this disease. A broader analysis of the cardiovascular expression patterns of receptors for other potentially cardiotropic viruses (CMV, EBV, HIV, HHV-6, Parvo-B19, etc.) should lead to a better understanding of individual risk factors for viral heart diseases and of their highly variable clinical courses, and offer new therapeutic options.
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PMID:Highly variable expression of virus receptors in the human cardiovascular system. Implications for cardiotropic viral infections and gene therapy. 1249 Sep 88

Although enteroviruses have long been considered the most common cause of inflammatory heart muscle diseases, parvovirus B19 (PVB19) is emerging as a new and important candidate for myocarditis and dilated cardiomyopathy with inflammation (DCMi) and without inflammation (DCM). We investigated left ventricular endomyocardial biopsy specimens from 110 patients with suspected inflammatory heart disease for the presence of PVB19, Coxsackie virus (CVB), and adenovirus (Ad2) genome by polymerase chain reaction. Diagnosis of myocarditis (36 patients), DCM (18 patients), DCMi (13 patients), and perimyocarditis (12 patients) was made by immunohistochemical and histopathological investigation of endomyocardial biopsy specimens. A control group consisting of patients with arterial hypertension was also investigated. Prevalence of the PVB19 genome in endomyocardial biopsy specimens was highest in patients with DCMi (3 of 13) and patients with myocarditis (7 of 36); in patients with DCM and perimyocarditis, prevalence was 3 of 13 and 2 of 12, respectively. In patients with resolved myocarditis, no PVB19 DNA was detected; in patients with no inflammation and controls, prevalence was only 4% and 7%, respectively. CVB-RNA was detected in endomyocardial biopsy specimens from 3 of 37 patients with myocarditis; Ad2-DNA was found in 1 patient with DCM and 1 patient with perimyocarditis. These findings suggest an association of the PVB19 genome in endomyocardial biopsy specimens of adults with the development of DCM, DCMi, and chronic myocarditis more frequently than previously expected. PVB19 should therefore be recognized as a potential cardiotropic pathogen in patients of all ages.
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PMID:Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens. 1279 25

Inflammatory heart disease is causally linked with progressive left ventricular dysfunction and congestive heart failure. In childhood, infection with parvovirus B19 (PVB19) is usually benign, causing erythema infectiosum. However, severe fetal PVB19 infection may be associated with hydrops fetalis and fetal death caused by myocarditis. Here we report a PVB19-induced myocarditis in a previously healthy 37-year-old patient admitted to the hospital because of chest pain and dyspnea due to left ventricular dysfunction. Four weeks after the onset of symptoms, we found lymphocytic infiltrates and PVB19 genome in left ventricular endomyocardial biopsy specimens. Consistently, acute PVB19 infection was indicated serologically by elevated IgM titers and the presence of PVB19 genome in peripheral blood lymphocytes. In conclusion, PVB19 infection may be complicated by acute myocarditis in immunocompetent adults. Because PVB19 myocarditis may progress to chronic dilated cardiomyopathy, early diagnosis by endomyocardial biopsy is important to initiate anti-inflammatory treatment.
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PMID:Acute parvovirus B19 infection associated with myocarditis in an immunocompetent adult. 1287 72

Several investigations showed that in addition to genetic factors also virological and chronic inflammatory aspects are relevant pathogenic mechanisms for the development of dilated cardiomyopathy (DCM). Based on the etiopathogenic importance of viral persistence and chronic myocardial inflammation for disease progression, novel rational therapeutic strategies have been developed. The diagnosis of chronic myocardial inflammation and viral persistence has been a controversial issue for a long time due to diagnostic pitfalls. Detection of persistence of viral genomes with adequate sensitivity and specificity succeeded only by the establishment of sensitive molecular biological techniques such as in situ hybridization and nested polymerase chain reaction (nPCR). By the use of these molecular biological methods, further viruses have been detected in DCM patients in addition to the classic cardiotropic viruses (entero- and adenoviruses), particularly parvovirus B19, human herpes virus type 6 (HHV-6), and Epstein-Barr virus. Considering these different cardiotropic viruses, viral persistence can be proven in > 50% of the DCM patients, consistent with the diagnosis of viral heart disease. This differentiated diagnosis enables, in addition to symptomatic therapy of heart failure, novel rational therapeutic regimens (e. g., beta-interferon) in the setting of randomized trials such as the BICC Study (Betaferon In Patients with Chronic Viral Cardiomyopathy).
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PMID:[Antiviral therapy in viral heart disease]. 1591 37

Inflammatory processes induced by viral or bacterial infections are believed to be one of the major pathogenetic mechanisms in myocardial diseases. Although the reason for progression to myocardial failure is not fully understood, postulated mechanisms include persistent viral infection alone or in combination with autoimmune processes. A variety of cardiotropic viruses have been identified to elicit myocarditis, with enteroviruses and adenoviruses as the most frequent causative agents in children and adolescents. However, parvovirus B19 (PVB19) has recently emerged as another potential pathogen in adult patients associated with inflammatory heart disease. Many dimensions of inflammatory heart disease coexist while different phases of the disease progress simultaneously: phase 1 is dominated by viral infection, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation without the role of an infectious agent and cardiac inflammation. Taking these mechanisms into account, screening for viral and bacterial genome by polymerase chain reaction (PCR) and detection of inflammatory infiltrates by immunohistochemistry are considered crucial for establishing an aetiological diagnosis, thereby allowing initiation of specific therapeutic strategies. In a large cohort of 3345 consecutive patients with left ventricular dysfunction evaluated over a period of 10 years, prevalence of PVB19, coxsackievirus (CVB), human cytomegalovirus (HCMV), influenza A virus and adenovirus (ADV) genome was assessed by PCR. Inflammatory infiltrates within the myocardium were detected by immunohistochemistry according to the WHF criteria and by histopathology according to the Dallas criteria of myocarditis. For control, endomyocardial samples of patients with arterial hypertension were studied. Parvovirus B19 was the most often detected virus in all patient subgroups, with positivity ranging from 17% to 33%. Except for PVB19, CVB RNA (3%), ADV (2%) and CMV (3.9%) were the most frequently detected viral genomes. Interestingly, detection of PVB19 genome was significantly correlated with inflammatory heart disease and reduced ejection fraction. Importantly, an aetiological diagnosis requires the immunohistochemical and molecular biological investigation of endomyocardial biopsies. Such an approach may change the management of these diseases in the future. One of the aims of the study was to reveal the underlying dominant pathophysiological mechanisms in a for deciding on the most approriate therapy.
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PMID:Pathophysiology and aetiological diagnosis of inflammatory myocardial diseases with a special focus on parvovirus B19. 1631 98

Giant cell myocarditis (GCM) is an uncommon inflammatory heart disease with a rapid progression and a devastating outcome. Its exact cause is unknown, but it has been associated with various inflammatory and autoimmune disorders. The authors report a case where GCM is triggered by a parvovirus B19 (PVB19) infection.
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PMID:Giant cell myocarditis triggered by a parvovirus B19 infection. 1828 May 93

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

While myocardial parvovirus B19 (B19V), aside from enteroviruses (EV) and adenoviruses (ADV), has recently been found often in patients with myocarditis and idiopathic dilated cardiomyopathy (IDC), the pathogenetic significance of B19V genomes in those patients has not yet been sufficiently elucidated. In the present study, left ventricular endomyocardial biopsies from 24 patients with left ventricular ejection fraction (LVEF) below 55% due to IDC, and tissue from the right atrial appendage of 10 control patients undergoing bypass surgery with normal LVEF (>55%) were investigated for B19V, ADV, and EV genomes by specific nested polymerase chain reaction (PCR), by real time PCR or by reverse-transcription PCR, respectively. The myocardial tissue samples from the 10 controls were analyzed each in three different virological laboratories for B19V. In the IDC group, the frequency of the myocardial virus genomes found in 54% (13/24) of the patients was as follows: B19V: 50% (12/24), EV: 8% (2/24), including one patient with B19V and EV, and ADV: 0% (0/24). For comparison, the prevalence of B19V genomes was between 30% and 60% in the control group as detected in three different laboratories, but all these control subjects were EV- and ADV-negative. The number of B19V gene copies, however, was very low and similar both in the IDC and control group. In the majority of patients myocardial B19V persistence was associated with a low virus load irrespective of the underlying heart disease so that it may be of no importance in the pathogenesis of IDC.
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PMID:Low level myocardial parvovirus B19 persistence is a frequent finding in patients with heart disease but unrelated to ongoing myocardial injury. 2057 82

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


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