Cases reported "Myocarditis"

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1/116. inflammation of the cardiac conduction system in a case of hyperthyroidism.

    A 37-year-old female showed signs of hyperthyroidism 2 weeks before death after a partial thyroidectomy was carried out 15 years previously. An examination 3 days before death revealed a normal blood cell count, an increased level of thyroidal hormones, sinus tachycardia and a high blood pressure of 170/90 mm Hg. A hyperthyroidism was diagnosed and therapy with carbimazol (2 x 10 mg) was started but 2 days later fever and chill occurred and before death short phases of unconsciousness and dyspnoea. The autopsy findings showed an interstitial inflammation of the AV-node, the His-bundle and its branches which can correlate with typical ECG changes in hyperthyroidism.
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2/116. myocarditis due to salmonella virchow and sudden infant death.

    A strain of salmonella virchow was isolated in the myocardium of a 1 1/2 month child who died suddenly. The source of contamination was the water of a family aquarium containing turtles.
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3/116. association of rickettsia helvetica with chronic perimyocarditis in sudden cardiac death.

    BACKGROUND: rickettsia helvetica is the only non-imported rickettsia found in scandinavia. It was first detected in ixodes ricinus ticks, but has never been linked to human disease. We studied two young Swedish men who died of sudden cardiac failure during exercise, and who showed signs of perimyocarditis similar to those described in rickettsial disease. methods: Samples from the heart and other organs were analysed by PCR and dna sequencing. May-Grunwald-Giemsa, Grocott, and acridine-orange stains were used for histopathological examinations. Staining of R. helvetica grown on shell-vials in vero cells, and the early descriptions of R. rickettsii by H T Ricketts and S B Wohlbach served as controls. immunohistochemistry was done with proteus OX-19 rabbit antisera as the primary antibody. The structure of rickettsia-like organisms was investigated by transmission electron microscopy. Serological analyses were carried out by indirect immunofluorescence with R. helvetica as the antigen. FINDINGS: By use of a semi-nested PCR, with primers specific for the 16S rRNA and 17-kDa outer-membrane-protein genes, and sequence analysis of the amplified products, genetic material from R. helvetica was detected in the pericardium and in a lymph node from the pulmonary hilum in case 1, and in a coronary artery and the heart muscle in case 2. A serological response in case 1 revealed an endpoint titre for R. helvetica of 1/320 (1/256 with R. rickettsii as the antigen). Examination of PCR-positive tissue showed chronic interstitial inflammation and the presence of rickettsia-like organisms predominantly located in the endothelium. These organisms reacted with proteus OX-19 antisera, and their size and form were consistent with rickettsia. Electron microscopy confirmed that the appearance of the organisms was similar to that described for spotted-fever rickettsia. INTERPRETATION: R. helvetica, transmitted by I. ricinus ticks, may be an important pathogen in the aetiology of perimyocarditis, which can result in sudden unexpected cardiac death in young people.
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4/116. Hydrocution in a case of Coxsackie virus infection.

    An apparently healthy 7-year-old boy attempted to demonstrate his ability to dive into a whirlpool but was retrieved from the water in a state of unconsciousness after several minutes. resuscitation was unsuccessful. No characteristic signs of drowning were found at the autopsy but examination of the lymph nodes and the cardiac muscle indicated a pre-existent infection. The histological examination revealed a slight degree of predominantly lymphocytic infiltration of the cardiac muscle. IgM antibodies against Coxsackie virus were detected in the serum sample by means of ELISA. The reverse transcriptase polymerase chain reaction (RT-PCR) performed on an extract of formalin-fixed, paraffin-embedded cardiac muscle tissue revealed a dna sequence specific for Coxsackie B3 virus. Therefore, cardiac failure was due to a myocardial virus infection and the additional strain caused by diving. This case report emphasizes the importance of modern molecular biological methods in cases of sudden death including death by hydrocution.
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5/116. myocarditis and cardiomyopathy associated with clozapine.

    BACKGROUND: clozapine is effective for resistant schizophrenia. After two sudden deaths in physically well young men soon after starting clozapine, we investigated the cardiovascular complications for this drug. methods: From January, 1993, to March, 1999, 8000 patients started clozapine treatment in australia, and were registered with a mandatory monitoring service. We identified cases of myocarditis and cardiomyopathy from voluntary reports to the Australian Adverse Drug Reaction Committee and sought details of the relevant diagnostic studies, necropsies that had been done in suspicious cases, or both. FINDINGS: 23 cases (20 men, three women, mean age 36 years [SD 9]) were identified: 15 of myocarditis and eight of cardiomyopathy associated with clozapine treatment. Six patients died. All cases of myocarditis (five deaths) occurred within 3 weeks of starting clozapine. Cardiomyopathy (one death) was diagnosed up to 36 months after clozapine was started. Necropsy results showed mainly eosinophilic infiltrates with myocytolysis, consistent with an acute drug reaction. INTERPRETATION: clozapine therapy may be associated with potentially fatal myocarditis and cardiomyopathy in physically healthy young adults with schizophrenia.
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6/116. Disseminated fatal human cytomegalovirus disease after severe trauma.

    OBJECTIVE: Disseminated human cytomegalovirus (HCMV) disease is considered to be uncommon in critically ill but otherwise not immunosuppressed patients. We describe the case of a trauma victim who developed fatal HCMV disease that initially presented as pseudomembranous colitis and resulted in sudden cardiac death. DESIGN: Case report of fatal HCMV disease in a previously healthy patient after multiple trauma. SETTING: Surgical intensive care unit (ICU). PATIENT: A 63-yr-old male patient with multiple injuries. INTERVENTIONS AND MEASUREMENTS: Under ICU treatment, symptoms of HCMV reactivation presenting as pseudomembranous colitis appeared 32 days after trauma. Detailed laboratory examinations for HCMV infection were performed, including complement fixation titer, immunoglobulin g and M, polymerase chain reaction, and virus isolation. RESULTS: The intravital detection of HCMV dna in serum, leukocytes, and a colonic biopsy specimen indicated HCMV reactivation. Postmortem examination findings, including positive viral cultures, showed severe disseminated HCMV disease with involvement of the colon and myocardium. CONCLUSIONS: The lack of specific clinical symptoms of HCMV disease and the delay until viral culture results are available make an exact and timely diagnosis of HCMV disease difficult. Its prevalence in critically ill but otherwise not immunosuppressed patients is currently unknown and possibly underestimated. Because severe illness or trauma can cause immunodysfunction and, thus, may contribute to an increased rate of HCMV disease, detailed studies are warranted to evaluate the real risk in the ICU setting.
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7/116. Chronic right-sided myocarditis mimicking arrhythmogenic right ventricular dysplasia.

    arrhythmogenic right ventricular dysplasia (ARVD) is a cause of right ventricular heart failure and has been implicated in some cases of sudden death in young adults. It is well known that a large majority of patients with ARVD have histological evidence suggestive of inflammation. Here we report a unique case of chronic myocarditis limited to the right ventricle and right side of the interventricular septum which presented clinically as ARVD. The fact that right sided myocarditis can clinically mimic the genetic disease of classic arrhythmogenic right ventricular dysplasia has therapeutic implications for the patient and relatives.
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8/116. Prolonged QT interval and sudden infant death--report of two cases.

    In the two cases where infants died suddenly and unexpectedly the electrocardiogram (ECG) of a younger sibling (case 1) and of a living twin (case 2) led to the suspicion that the two infants could have died from long qt syndrome (LQTS). In case 1, a His bundle (HB) dispersion and a pronounced hypoplasia of the right external nucleus arcuatus were detected. In case 2, a severe interstitial pneumonia and an accompanying mild myocarditis were found by histology. Molecular genetic investigations of the coding regions of the genes, HERG, KVLQT1 and SCN5A gave no indication for the mutations, thus, affecting related myocardial ion channels as possible sources of inhomogeneity of repolarisation.Since a molecular genetic deviation could not yet be elaborated the possible role of related disturbance remains unknown.
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9/116. 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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10/116. 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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