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

We present a case of a patient who presented with a febrile illness without obvious source initially, who developed profound cardiac decompensation and left ventricular dysfunction. Viral titers obtained during the course of illness confirmed parvovirus infection. Intravenous aggressive immunoglobulins and medical therapy for heart failure resulted in stabilization and, ultimately, a complete recovery. Recent data from clinical trials are discussed regarding the utility of immunoglobulins in the treatment of myocarditis and heart failure.
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PMID:The current status of immune modulating therapy for myocarditis: a case of acute parvovirus myocarditis treated with intravenous immunoglobulin. 1467 1

Parvovirus infection during pregnancy is an important cause of hydrops fetalis. It is attributed to anemia caused by viral-induced destruction of red blood cells. Infection of other organs has been reported including the heart, liver, and lungs. Few of these reports, however, convincingly demonstrate virions within the functional parenchyma of the tissue. This is of particular concern regarding myocardium in the context of hydrops fetalis which is, in part, due to cardiac failure. The problem in routine pathology practice is that most fetuses with the infection are macerated. This, in part, probably explains the paucity of published information on cardiac involvement. This study examined five cases of fatal hydrops fetalis with variable maceration with serologically proven parvovirus B19 infection. Transmission electron microscopy of cardiac tissue demonstrated intranuclear virions in both erythroid precursor cells and in cardiac myocytes in three of these cases. In each of these, immuno-gold electron microscopy provided confirmatory evidence of parvovirus infection. Virions were not identifiable where maceration had caused disintegration of nuclei in the myocytes. In addition, virions were absent in the three negative control cases where retroplacental hemorrhage was confirmed as the cause of death. This study suggests that parvovirus infection of cardiac myocytes may play a more important role in causing hydrops fetalis than previously realized. It also demonstrates that maceration should not discourage the use of electron microscopy.
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PMID:Parvovirus infects cardiac myocytes in hydrops fetalis. 1470 34

Parvovirus B19 (PB19) has been identified as a possible cause of myocarditis and heart failure in both children and adult patients. This study used real time PCR analysis, to determine the frequency and to quantify PB19 viral genomes in endomyocardial tissue samples from 80 adult patients with clinically suspected myocarditis or idiopathic left ventricular dysfunction and from 36 controls. Histological (Dallas classification) and immunohistological analyses were performed to detect myocardial inflammation in the endomyocardial biopsies.PB19 genomic DNA was found in nine of 80 patients (11.2%), 4 out of 31 (12.9%) patients with inflammatory infiltrates detected via immunohistological methods and 5 out of 49 (10.2%) patients with left ventricular dysfunction without myocardial inflammation. The copy numbers for PB19 DNA ranged between 30 and 3900 per microg of cellular DNA. Four patients with clinically suspected myocarditis had copy numbers for PB19 DNA of 70, 740, 3400 and 3900, respectively, per microg of cellular DNA in the endomyocardial biopsy. Five patients with idiopathic left ventricular dysfunction had copy numbers for PB19 DNA of 30, 38, 52, 58 and 90, respectively, per microg of cellular DNA in the endomyocardial biopsy. The amplicon of one of the nine positive PCR fragment was sequenced and was found to be fully identical in the highly conserved sequence of published Parvovirus B19 VP1/VP2 genes (NCBI gene bank). In all patients, acute myocarditis was excluded according to the Dallas classification. All biopsies of 36 controls with no history of myocarditis or recent viral infection were negative for myocardial inflammation and parvovirus B19 genomes. In summary, Parvovirus B19 DNA is present within the myocardium of patients with suspected myocarditis and idiopathic left ventricular dysfunction and can be detected and quantified in endomyocardial specimens via real time PCR.
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PMID:Frequency and quantity of the parvovirus B19 genome in endomyocardial biopsies from patients with suspected myocarditis or idiopathic left ventricular dysfunction. 1508 75

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

Nonimmune hydrops fetalis (NIHF) or generalized soft tissue edema and cavity effusions may be due to cardiovascular diseases, congenital infections, genitourinary malformations, thoracic masses, placental conditions, chromosomal abnormalities, and idiopathic. We report 32 cases of NIHF from among 429 neonates who underwent autopsies (incidence 7.45%). Sixteen cases (50%) had cardiovascular disease; all were due to low output cardiac failure; 7 had structural congenital heart disease. Three of the children with congenital heart disease also had chromosomal abnormalities: 2 had trisomy 18 and 1 had Noonan syndrome. Among myocardial conditions were five subjects with cardiomyopathies (1 of each of the following types): oncocytic, dilated, endocardial fibroelastosis, cardiac glycogenosis, and carnitine deficiency; 3 had myocarditis, and 1 had cardiac rhabdomyomas. Congenital infections were due to cytomegalovirus in 3 cases, bacteria in 2, and parvovirus in 1. The mechanism of NIHF in these cases might be a combination of decreased myocardial contractility due to myocarditis and fetal anemia. Genitourinary diseases were present in 5 newborns: Two had congenital nephrotic syndrome, 1 had VACTER association, 1 had prune-belly syndrome, and 1 had urogenital sinus malformation. Intrathoracic lesions were found in 2 babies (pulmonary sequestration and diaphragmatic hernia). One twin died of volume overload due to twin transfusion syndrome. Only 2 newborns were classified as idiopathic. Our study shows that cardiovascular diseases that lead to heart failure or impaired venous return are more common in the liveborn (50%), whereas congenital infections are more common in the stillborn with NIHF.
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PMID:Nonimmune hydrops fetalis in the liveborn: series of 32 autopsies. 1601 Apr 81

In too many cases, the cause of dilated cardiomyopathy (DCM) remains undetermined. Coronary or valvular heart diseases, connective tissue disorders, toxic causes and signs of infection are systematically investigated. With the exceptions of coronary and sometimes valvular heart disease, the treatment of cardiac failure remains symptomatic treating the consequences but not the cause of DCM, which is therefore diagnosed as "idiopathic". This artericle reports the clinical history of 4 patients followed up for apparently "idiopathic" DCM in whom the presence of chronic Parvovirus B-19 infection was demonstrated. Based on these 4 cases, the hypothesis of an infectious cause of DCM and the role of myocardial biopsy, given the progress in molecular biology, are reconsidered. Parvovirus B-19 infection has recently been recognised not only as a cause of myocarditis but also of chronic viral cardiomyopathy, as in adeno and enteroviral infection. The authors conclude that the progress in molecular biology, the recognition of a viral aetiology and the efficacy of immuno-modulator therapy such as beta-interferon, may lead to a new management strategy of patients with DCM in cardiological referral centres.
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PMID:[Viral cardiomyopathy]. 1629 44

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

Parvovirus B19 is a widespread infection that may affects 1-5% of pregnant women, mainly with normal pregnancy outcome. The prevalence of infection is higher during epidemics - between 3 and 20% with sero-conversion rate of 3-34%. Infection during pregnancy can cause a variety of other signs of fetal damage. The risk of adverse fetal outcome is increased if maternal infection occurs during the first two trimesters of pregnancy but may also happen during the third trimester. It is a significant cause of fetal loss throughout pregnancy, but has a higher impact in the second half of pregnancy when spontaneous fetal loss from other causes is relatively rare. Parvovirus infection can cause severe fetal anemia as a result of fetal erythroid progenitor cells infection with shortened half life of erythrocytes, causing high output cardiac failure and therefore nonimmune hydrops fetalis (NIHF). The P antigen expressed on fetal cardiac myocytes enables the Parvovirus B19 to infect myocardial cells and produce myocarditis that aggravates the cardiac failure. Although there are several reports of major congenital anomalies among offspring of mothers infected by Parvovirus, the virus does not seem to be a significant teratogen. Since Parvovirus B19 infection can cause severe morbidity and mortality, it should be part of the routine work up of complicated pregnancies. Risk assessment for maternal infection during pregnancy is especially important during epidemics when sero-conversion rates are high.
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PMID:Parvovirus B19 in pregnancy. 1658 Sep 42

Parvovirus B19 infection during pregnancy is at risk of adverse fetal outcome. The risk is increased if maternal infection occurs during the first two trimesters, but may also happen during the third trimester. Adverse first and third trimester fetal outcome were recently highlighted by polymerase chain reaction (PCR) viral DNA detection. Parvovirus does not seem to be a significant teratogen. Infection during pregnancy can cause severe fetal anaemia and nonimmune hydrops fetalis. Cardiac tropism of the virus can cause myocarditis and aggravate the cardiac failure. Follow up of in utero anaemia is based upon the middle cerebral artery peak systolic flow velocity evaluation and treatment is based upon cordocentesis transfusion.
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PMID:[Parvovirus B19 in pregnancy: literature review]. 1800 56

Viral infections often affect the heart. In the majority of cases, the course of the disease is benign and patients recover spontaneously. However, viral infection may persist and lead to acute cardiac failure or progress to dilated cardiomyopathy. Viral infections are considered to be the most common causes of myocarditis. There is evidence that intramyocardial viral persistence is associated with progressive ventricular dysfunction, even when the infiltrate is sparse or missing. The diagnosis of viral myocarditis necessitates the detection of viral genome by molecular biology techniques and the evaluation of myocardial inflammation by the immunohistochemistry on endomyocardial biopsy samples. Autoreactive myocarditis can also only be diagnosed by endomyocardial biopsy. Infiltration of leukocytes and a negative polymerase chain reaction on microbial agents are their hallmarks. Apart from symptomatic or supportive therapy, etiologic treatment strategies have to address the underlying causative virus or the autoimmune process. In symptomatic or deteriorating patients, targeted antiviral therapy is a reasonable algorithm to eradicate the virus, which will contribute to resolving inflammation or apoptosis, thus confining myocardial damage. The Marburg registry favors intravenous immunoglobulin treatment in biopsy-proven adenovirus and parvovirus B19 myocarditis combined with optimal conventional therapy to achieve virus clearance. In fulminant myocarditis, biopsy is mandatory to identify giant cell myocarditis and cardiac sarcoidosis to be treated by immunosuppression. In cardiogenic shock, the use of mechanical circulatory support by means of a ventricular assist device as a bridge to recovery may be a lifesaving approach. In perimyocarditis with dominant pericardial affection, colchicine over a period of 1 to 6 months can dissolve the pericardial effusion effectively in more than 80% of cases.
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PMID:Diagnosis and treatment of myocarditis: the role of endomyocardial biopsy. 1822 99


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