Cases reported "Myocarditis"

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1/13. The use of molecular technologies for the detection of enteroviral ribonucleic acid in myocarditis.

    The introduction of molecular technology to the field of cardiovascular research has revolutionized the diagnosis and determination of the pathogenesis of diseases. This has been the case for viral myocarditis. Although rapid identification and specific treatment for viral disorders such as myocarditis continue to challenge researchers, molecular detection techniques have provided an insight into the role of viral genomes in this disorder. Although in situ hybridization (ISH) continues to be an effective detection method and is utilized in many laboratories, polymerase chain reaction (PCR) techniques are fast becoming the standard for molecular analysis in patients with viral myocarditis. Following a review of viral myocarditis, the roles of ISH and PCR will be discussed. Lastly, clinical relevance and areas of future research will be presented.
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2/13. influenza a virus infection complicated by fatal myocarditis.

    Influenza virus typically causes a febrile respiratory illness, but it can present with a variety of other clinical manifestations. We report a fatal case of myocarditis associated with influenza A infection. A previously healthy 11-year-old girl had malaise and fever for approximately 1 week before a sudden, witnessed fatal collapse at home. autopsy revealed a pericardial effusion, a mixed lymphocytic and neutrophilic myocarditis, a mild lymphocytic interstitial pneumonia, focal bronchial/bronchiolar mucosal necrosis, and histologic changes consistent with asthma. infection with influenza A (H3N2) was confirmed by virus isolation from a postmortem nasopharyngeal swab. Attempts to isolate virus from heart and lung tissue were unsuccessful. Immunohistochemical tests directed against influenza A antigens and in situ hybridization for influenza A genetic material demonstrated positive staining in bronchial epithelial cells, whereas heart sections were negative. Sudden death is a rare complication of influenza and may be caused by myocarditis. Forensic pathologists should be aware that postmortem nasopharyngeal swabs for viral culture and immunohistochemical or in situ hybridization procedures on lung tissue might be necessary to achieve a diagnosis. Because neither culturable virus nor influenza viral antigen could be identified in heart tissue, the pathogenesis of influenza myocarditis in this case is unlikely to be the result of direct infection of myocardium by the virus. The risk factors for developing myocarditis during an influenza infection are unknown.
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3/13. A cluster of fulminant myocarditis cases in children, baltimore, maryland, 1997.

    The true incidence of myocarditis in children is difficult to estimate because many mild cases go undetected. This study describes an unusual cluster of myocarditis cases that occurred in young children living in the greater baltimore area between May and October 1997. A search of multiple comprehensive databases and interviews with area pediatric cardiologists were conducted to identify unreported cases and determine the background rate of myocarditis in the area. Seven cases of myocarditis were found as well as two with a similar clinical picture and myocardial fibrosis on tissue examination. Six case patients with active myocarditis and one child with fibrosis died. The case children were predominantly black (eight of nine) and male (seven of nine), with no identifiable risk factors. The disease was characterized by a fulminant course with malignant arrhythmias. The greatest number of pediatric myocarditis deaths reported in 1 year prior to 1997 was three. Myocardial tissues were examined using immunohistochemistry, in situ hybridization, and polymerase chain reaction but no etiologic agent was identified. This outbreak is unusual because of both the number of cases and the fulminant course of the disease in this group of children.
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4/13. Lympho-monocytic enteroviral myocarditis: traditional, immunohistological and molecularpathological methods for diagnosis in a case of suspected sudden infant death syndrome (SIDS).

    A 7-month-old boy was found lifeless in his bed by his grandfather. Near the mouth there were some blood and chyme on the bedlinen. His mother reported a chill during the last 8 days. autopsy revealed multiple petechia under the capsule of the thymus, subepicardially and subpleurally, the cause of death was tentative supposed to be a sudden infant death. Histologically parts of the myocardium showed a lympho-monocytic myocarditis according to the DALLAS-criteria. Immunohistological investigations demonstrated an enhanced expression of MHC class II antigens, an increased number of leucocytes as well as t-lymphocytes. in situ hybridization and immunohistochemistry revealed myocardial enterovirus infection. Considering that there were regions in the myocardium without the traditional findings of myocardial necrosis and inflammation but with distinct expression of the above mentioned immunohistologic markers, immunohistological investigations turn out to be an appropriate tool to examine infant fatalities with uncertain cause of death for early stages of myocarditis.
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5/13. CD8 t-lymphocytes infiltrate the myocardium in fulminant herpes virus myocarditis.

    We report two cases of fulminant viral myocarditis in previously healthy children. They were caused by herpes simplex virus (HSV)-1 (in a boy aged 3 years) and Epstein-Barr virus (EBV) (in a boy aged 12 months). We obtained the diagnosis of HSV-1 myocarditis by immunohistochemistry and the diagnosis of EBV myocarditis by in situ hybridization. Histologic examination of heart tissue from the two boys revealed mononuclear cell infiltration of the myocardium. Immunohistochemical staining identified these cells as CD8 t-lymphocytes. CD8 t-lymphocytes induced by herpes virus infections may play an important role in the damage to heart muscle fibers seen in fulminant myocarditis in previously healthy children. To our knowledge, this is the first report of HSV-1 or EBV myocarditis (at least in children) in which viral infection has been demonstrated in the myocardium.
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6/13. Focal parvovirus B19 myocarditis in a patient with brugada syndrome.

    The brugada syndrome is characterized by a distinct ECG pattern consisting of ST segment elevation in the right precordial leads and right bundle branch block, a propensity for life-threatening arrhythmias, and an apparently structurally normal heart. The authors describe the case of a patient with an aborted sudden cardiac death and the typical ECG signs of brugada syndrome. Nevertheless, magnetic resonance imaging displayed signal enhancement in the left ventricular myocardium. Additionally, histologic examination, in-situ hybridization, and PCR revealed evidence of a locally restricted inflammation due to parvovirus B19. brugada syndrome is regarded as a primary electrical disease due to dysfunction of distinctive ion channels, but focal myocarditis may serve as a trigger for ventricular arrhythmias in this patient. Further morphologic studies will be helpful to establish the possible role of structural changes in the pathophysiology of this syndrome.
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7/13. Fatal parvovirus B19-associated myocarditis clinically mimicking ischemic heart disease: an endothelial cell-mediated disease.

    We report the case of a 34-year-old female patient who died 4 days after hospital admission of acute heart failure clinically mimicking ischemic heart disease. Microscopic examination of the heart showed severe myocarditis. Polymerase chain reaction (PCR), including quantitative real-time PCR, disclosed exclusively parvovirus B19 (PVB19), with a high viral load of 4.3x10(5) PVB19 viral genome equivalents per microg myocardial nucleic acid. Radioactive in situ hybridization detected viral genomes in endothelial cells (ECs) predominantly in the venular compartment and (to a lesser degree) in small arteries and arterioles of the heart, but not in cardiac myocytes or other tissue components. Concomitant with EC infection, marked expression of the adhesion molecule e-selectin was noted, accompanied by margination, adherence, penetration, and perivascular infiltration of T lymphocytes. We speculate that, due to the high viral load in cardiac ECs, PVB19 infection of endothelial cells was sufficient to induce impaired coronary microcirculation with secondary cardiac myocyte necrosis.
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8/13. Analysis of the presence of trypanosoma cruzi in the heart tissue of three patients with chronic Chagas' heart disease.

    It is still unclear to what extent myocarditis-associated, chronic Chagas' heart disease is due to persisting trypanosoma cruzi. In the present study, we have analyzed tissue samples from the hearts of three patients with this disease. in situ hybridization provided little evidence for the presence of intact T. cruzi even at sites of strong inflammation. Nevertheless, micromanipulation techniques detected remnants of both T. cruzi kinetoplast dna and nuclear dna. trypanosoma cruzi dna was also detected in single macrophages dissected directly from frozen heart tissue sections. Thus, this analysis demonstrates that T. cruzi kinetoplast dna and nuclear dna are widely dispersed in the heart tissue, although in low amounts. Since we rarely detected intact T. cruzi parasites during the chronic phase of Chagas' heart disease, we can exclude heart tissue as a major parasite reservoir.
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9/13. Epstein-Barr virus myocarditis as a cause of sudden death: two autopsy cases.

    Although the Epstein-Barr virus (EBV) causes acute infection accompanied by a high fever in young people, there appears to be few reports of a fatal outcome involving myocarditis. We report two cases of unexpected sudden death due to acute myocarditis possibly caused by the EBV. They each visited a hospital due to common cold-like symptoms and unexpectedly died several days later. In both cases, autopsy revealed myocardial necrosis with marked lymphocytic infiltration. polymerase chain reaction (PCR) screening was positive for the EBV, whereas immunohistochemistry and in situ hybridization for the EBV were negative. Serological investigations showed a mild elevation in antiviral capsid antigen IgG and anti-EBV nuclear antigen IgG in both cases. Immunohistochemical study of lymphocytic infiltrates showed strong positivity for a T-cell marker (CD45R0) in the myocardium and pharyngeal mucosa. These cases suggest the potential risk of mortality from acute EBV infection in young people, even without severe clinical manifestations, and the importance of microbiological investigations, including PCR procedures, in postmortem diagnosis of infectious diseases.
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10/13. cytomegalovirus endomyocarditis in a transplanted heart. A case report with in situ hybridization.

    A 64-year-old man underwent cardiac transplantation for long-standing severe dilated cardiomyopathy. postoperative complications included primary cytomegalovirus (CMV) infection with several episodes of moderate acute rejection and severe pneumonia. Six months after transplantation, an endomyocardial biopsy specimen revealed focal necrotizing myocarditis with intranuclear inclusions consistent with CMV. The patient subsequently developed fulminant pneumonia and died 7 months after transplantation. Postmortem examination revealed that the cause of death was acute necrotizing bronchopneumonia due to staphylococcus aureus, with underlying CMV pneumonitis. The transplanted heart had left ventricular hypertrophy with multiple organizing myocardial infarcts, moderate coronary atherosclerosis, and organizing thrombi of the left atrium. Characteristic inclusions of CMV were identified, predominantly within endothelial cells, in the left coronary artery, left ventricular endocardium, and myocardium. With in situ hybridization, the presence of CMV was verified in the inclusions, as well as in many fibroblasts without inclusions. in situ hybridization is warranted in myocardial biopsy specimens when suspicious inclusions or infiltrates are present, to confirm CMV infection, so that appropriate therapy can be initiated.
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