Cases reported "Myocarditis"

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11/47. 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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12/47. Fatal parvovirus myocarditis in a 5-year-old girl.

    infection with parvovirus B19 is common in children and typically causes mild illness. We report here the case of a 5-year-old girl who died suddenly, 2 weeks after the clinical diagnosis of a parvoviral infection (erythema infectiosum). Microscopic examination of the heart showed severe myocarditis with extensive T-cell and macrophage infiltration. Cultures, serology, and molecular analyses of serum for enteroviridae, adenovirus, influenza, varicella zoster, cytomegalovirus, and herpes simplex viruses were negative. Quantitative polymerase chain reaction (PCR) analysis for parvovirus B19 in peripheral blood, however, showed active infection (91,000 genomes/mL serum; 2.4 genomes/mononuclear cell). Despite the presence of myocarditis, immunostaining for parvoviral surface antigens was negative in the heart. Quantitative PCR analysis of paraffin sections showed that myocardial parvoviral content was significantly less than that of the normal appearing kidney and within the range predicted simply by tissue blood content. Thus, parvovirus B19 infection can be complicated by fatal myocarditis. Because the virus does not appear to have infected the heart, per se, we speculate that myocarditis arose from immunological cross-reaction to epitopes shared between the virus and the myocardium. HUM PATHOL 32:342-345.
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13/47. Fatal atypical mycobacterial infection in a cardiac transplant recipient.

    A 37-year-old female underwent heart transplantation for giant cell myocarditis. The patient died within three-and-a-half months of cardiac transplantation. Postmortem specimens from the heart and lung showed multiple necrotizing granulomas with numerous acid-fast bacilli. Polymerase chain reaction done on both the postmortem samples confirmed the presence of atypical mycobacterial infection. This fatal case of atypical mycobacteriosis in a cardiac transplant patient is reported for its rarity.
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14/47. Fatal acute myocarditis in an infant with human herpesvirus 6 infection.

    A 5 month old girl had typical clinical features of acute myocarditis just after the febrile period of exanthem subitum and died immediately. She had been healthy, with normal development, and there was no family history of particular note. Myocardial postmortem findings were compatible with acute myocarditis. Although the isolation of human herpesvirus 6 (HHV-6) was not attempted, positive IgM antibody to HHV-6 was detected in the patient's serum. Moreover, HHV-6 variant B dna was detected in several tissues, including myocardium, by the polymerase chain reaction (PCR). In contrast, antibody responses to human herpesvirus 7, another causal agent of exanthem subitum, were not found, and enteroviral rna was not detected in myocardial tissues by reverse transcription PCR. Apoptotic changes were seen in infiltrating cells within the myocardial tissues by means of the TUNEL method. HHV-6 antigen was not detected in several tissues (including myocardium) by immunohistochemical analysis. In conclusion, HHV-6 may have been the causative agent of fatal acute myocarditis in this infant.
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15/47. Active, fulminant, lethal myocarditis associated with parvovirus B19 infection in an infant.

    We report a case of fulminant myocarditis in an 11-month-old female infant who had no other clinical signs of parvovirus infection. The patient presented with severe respiratory distress and died in sudden cardiac arrest 3 h after admission. The clinical presentation was similar to that of an asthmatic attack. autopsy revealed signs of acute lymphocytic myocarditis. parvovirus dna was demonstrated by polymerase chain reaction (PCR) analysis of tissue sections obtained from the heart, lungs, liver, kidneys, and spleen. Transmission electron microscopy of myocardial tissue showed crystalline arrays with the appearance of parvovirus. The results of immunohistochemical analysis for the detection of parvovirus antigens were negative, and no viral inclusions were demonstrable. We suggest that the current diagnostic procedure underestimates the prevalence of parvovirus-associated myocarditis. PCR analysis should be used as a complement in suspected cases, to enhance the rate of detection of the infection and to reach a correct diagnosis.
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16/47. Catecholaminergic polymorphic ventricular tachycardia in a 3-year-old with occult myocarditis.

    Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare clinical entity in children. Occult myocarditis has not been previously implicated as an etiologic agent. A 3-year-old female presents with a presumed breath-holding spell and is found to have ventricular fibrillation requiring DC cardioversion. An invasive electrophysiological study was performed demonstrating the absence of inducible ventricular arrhythmias. Low dose epinephrine confirmed the presence CPVT. Right ventricular endomyocardial biopsies sent for polymerase chain reaction (PCR) analysis demonstrated the presence of adenoviral dna. The authors hypothesize that occult myocarditis may be the inciting agent for CPVT in children.
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17/47. CD83 dendritic cells in inflammatory infiltrates of Churg-Strauss myocarditis.

    churg-strauss syndrome (CSS) is characterized by a granulomatous vasculitis of multiple organs with the cardiovascular system being commonly affected. The initiation of the disease is not well understood, but immunologic phenomena are thought to contribute at least partially to the syndrome. We have studied endomyocardial biopsy specimens from a patient with CSS and eosinophilic myocarditis for characterization of infiltrating immune cells by immunofluorescence staining techniques and found a major population to be composed of CD83 CD14-CD19-CD56-HLA-DR dendritic cells (DCs). Further phenotypic characterization of infiltrating CD83 cells in CSS myocarditis showed a surface profile reminiscent of immature DCs. In the same patient, the cytokine expression pattern of mitogen-stimulated peripheral blood mononuclear cells revealed a TH0 response as evidenced by multiplex polymerase chain reaction, and interleukin-5 levels were elevated in plasma analyzed by enzyme-linked immunosorbent assay. Thus, in this case of CSS myocarditis, we found DC-like cells in myocardial lesions, which may suggest that DCs are involved in the inflammatory process possibly triggered or sustained by an imbalance of DCs and their failure to confer tolerance to self-antigens.
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18/47. Fatal parvovirus B19 myocarditis in an 8-year-old boy.

    A report is given on an 8-year-old boy who suddenly and unexpected died. autopsy findings point to acute heart failure. Microscopic examination of the heart showed increased interstitial and perivasal fibrosis and myocarditis with macrophage infiltration. Polymerase chain reaction (PCR) analysis for parvovirus B19 was positive in heart samples and in the spleen. Immunostaining for parvoviral surface antigens was negative. Although the virus does not appear to have infected the cardiomyocytes, we speculate that myocarditis arose from immunological cross-reaction to epitopes shared between the virus and the myocardium.
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19/47. Successful treatment of enterovirus-induced myocarditis with interferon-alpha.

    No randomized, placebo-controlled studies have investigated interferon-alpha therapy in enterovirus-proven myocarditis. This report describes 2 patients with enterovirus-induced myocarditis (1 with associated churg-strauss syndrome) who at follow-up endomyocardial biopsy showed clinical and hemodynamic improvement and viral clearance (using polymerase chain reaction) after interferon-alpha therapy.
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20/47. 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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