Cases reported "Myocarditis"

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1/34. Two cases of right ventricular ischemic injury due to massive pulmonary embolism.

    In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.
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2/34. recurrence of giant cell myocarditis in cardiac allograft.

    BACKGROUND: Giant cell myocarditis causes essentially irreversible fulminant left ventricular dysfunction with associated conduction abnormalities and congestive failure. Response to immunosuppressive therapy is poor and cardiac transplantation is the only viable treatment option. The histologic hallmarks of giant cell myocarditis include a polymorphous inflammatory response with numerous multinucleated giant cells and extensive myocyte necrosis in a geographic pattern. There were 38 patients who received a cardiac transplant for giant cell myocarditis in the Giant Cell myocarditis Registry. Among these patients, there were 9 recurrences of disease in the allograft. Concern has been expressed that recurrence of giant cell myocarditis in the allograft might be a contraindication for cardiac transplantation in the future. methods: In our single-center analysis we describe the clinical and histologic findings of 5 patients transplanted for giant cell myocarditis at the Cleveland Clinic. RESULTS: All but 1 of the patients were new york Heart association (NYHA) class 4 with an average cardiac index (CI) of 1.52 liters/min x m(2). Of the 5 patients transplanted, 1 developed recurrent giant cell myocarditis. Routine right ventricular endomyocardial biopsy at 1 week exhibited severe multifocal myocardial fibrosis in addition to mild acute vascular rejection and mild grade 1A cellular rejection. Follow-up biopsy in this patient indicated grade IIIA moderate acute rejection in addition to multinucleated giant cells. Two distinct inflammatory processes were noted consisting of foci of T-cell inflammation identified by immunohistochemistry to be consistent with rejection, and a second inflammatory process with few mononuclear cells staining for macrophage or T-cell markers with eosinophils and myocyte necrosis consistent with giant cell myocarditis. Follow-up right ventricular endomyocardial biopsies (RVBXs) in this patient have subsequently demonstrated improvement in the degree of inflammatory infiltrate without vascular or significant cellular rejection. Vascular rejection was noted in 1 of the remaining 4 patients and was treated successfully with muramab-CD3 and plasmapheresis. CONCLUSIONS: Giant cell myocarditis should be expected to recur in the allograft and often does so concurrently with rejection. However, the disease in the allograft responds to therapy in a favorable manner, which differs dramatically from that in the native heart. This might be the result of detection of the disease at an earlier stage than in the native heart, or the immunosuppression milieu in the allograft. The favorable response to therapy suggests that the likelihood of recurrence of giant cell myocarditis should not be considered a barrier to transplantation.
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3/34. 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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4/34. The 3-week sulphasalazine syndrome strikes again.

    A 34-year-old lady developed a constellation of dermatitis, fever, lymphadenopathy and hepatitis, beginning on the 17th day of a course of oral sulphasalazine for sero-negative rheumatoid arthritis. Cervical and inguinal lymph node biopsies showed the features of severe necrotising lymphadenitis, associated with erythrophagocytosis and prominent eosinophilic infiltrates, without viral inclusion bodies, suggestive of an adverse drug reaction.A week later, fulminant drug-induced hepatitis, associated with the presence of anti-nuclear autoantibodies (but not with other markers of autoimmunity), and accompanied by multi-organ failure and sepsis, supervened. She subsequently died some 5 weeks after the commencement of her drug therapy.Post-mortem examination showed evidence of massive hepatocellular necrosis, acute hypersensitivity myocarditis, focal acute tubulo-interstitial nephritis and extensive bone marrow necrosis, with no evidence of malignancy. It is thought that the clinico-pathological features and chronology of this case bore the hallmarks of the so-called "3-week sulphasalazine syndrome", a rare, but often fatal, immunoallergic reaction to sulphasalazine.
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5/34. Polyclonal proliferation of lymphocytes containing the epstein-barr virus genome in a patient dying of myocarditis in chronic active Epstein-Barr virus infection.

    An 11-year-old boy had intermittent fever and hepatosplenomegaly. The diagnosis of chronic active Epstein-Barr virus (EBV) infection was established from an abnormal pattern of anti-EBV antibody; EBV was detected in bone marrow cells. Immunochemotherapy alleviated the patient's symptoms. However, when a subsequent oral prednisolone dose was tapered, heart failure ensued and he died. autopsy findings demonstrated that myocarditis resulted from infiltrating T lymphocytes with the EBV genome and a benign histologic appearance. A clonality study of T lymphocytes indicated no such evidence of monoclonality. EBV-infected T cells play an important role in the pathogenesis of myocarditis in chronic active EBV infection.
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6/34. 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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7/34. 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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8/34. sepsis-related microvascular myocardial damage with giant cell inflammation and calcification.

    We report a case of a 27-year-old man who died suddenly 2 days after being discharged from the intensive care unit where he had resided for 25 days due to severe sepsis. On postmortem examination, the findings were restricted to the heart and characterized by microvascular myocardial damage with giant cell inflammation and calcification. The microcirculation seems to be involved in the mechanism of cell injury, very likely due to flow disturbances caused by septic shock. The dystrophic calcification occurred in myocytes showing myocytolysis. Lysozyme produced by macrophages and myocytes in areas of myocytolysis and giant cells appear to function cooperatively and/or synergistically to influence mineralization. In addition, the expression of inducible nitric oxide synthase by myocytes implies that nitric oxide could contribute to myocardial cell damage. Immunolabeling studies of the giant cells confirmed that they are derived from macrophages.
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9/34. An autopsy case of sudden death in a patient with giant cell myocarditis.

    We present a case of a 28-year-old male weight lifter who died suddenly while driving a bicycle. Forensic autopsy and histopathological examinations revealed granulomatous lesions in the myocardium and hilar lymph nodes. The latter had massive caseation necrosis, epithelioid granulomas and Langhans' giant cells suggestive of tuberculosis. However, the myocardium showed predominantly multinucleated foreign body and myogenic giant cells, lymphocytes, plasma cells, macrophages, eosinophils. Staining for acid-fast bacilli was negative. The present case highlights the difficulty in establishing whether the granulomatous lesions in the hilar lymph nodes and the myocardium are incidental findings or whether they are related by the same pathogenetic mechanisms.
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10/34. aspirin intoxication in a child associated with myocardial necrosis: is this a drug-related lesion?

    A 5-year-old girl with a mild upper airways infection was admitted to the hospital because of sudden vomiting and drowsiness that evolved to stupor; she was dehydrated, hypotensive, and tachypneic; laboratory tests revealed noncompensated lactic acidosis. She also had hypoglycemia followed by hyperglycemia, and progressive bradycardia leading to reversible cardiac arrest. Her clinical condition complicated by sinus bradycardia, ventricular tachycardia, third-degree atrioventricular blockage and lethal asystole. At the final stage of her illness, the serum salicylate concentration was 383.8 mcg/mL. Based on this single data, a retrospective toxicological analysis estimated a theoretical peak level of serum salicylate of approximately 1570 mcg/mL (therapeutic range, 20-250 mcg/mL) although the real amount of aspirin that this child ingested is difficult to calculate because aspirin is a drug that shows a so-called zero order kinetics. At autopsy, the most striking finding was multiple foci of coagulative necrosis involving the entire thickness of the myocardium with scant inflammatory infiltrate composed mainly of macrophages and polymorphonuclear leukocytes. The morphologic characteristics of the myocardial lesion in addition to salicylate blood levels suggests the possibility of an adverse drug reaction of the type acute toxic myocarditis.
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