Cases reported "Myocarditis"

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1/66. Children may survive severe myocarditis with prolonged use of biventricular assist devices.

    The outcome of acute myocarditis with cardiogenic shock is poor. In some children in whom aggressive medical treatment fails, artificial replacement of heart function may offer lifesaving support until the myocardium has recovered. Four previously healthy children (three boys aged 4, 6, and 1 years; one girl aged 5) developed acute myocarditis with ventricular failure and multiorgan dysfunction caused by low cardiac output. Biventricular assist devices (BVAD) were implanted for prolonged support. In three children cardiac function improved and after up to 21 days mechanical support could be withdrawn. They had full recovery of heart function. In the fourth patient there was no myocardial recovery after a period of 20 days. He underwent orthotopic heart transplantation with an uneventful postoperative course. Prolonged circulatory support with BVAD is an effective method for bridging until cardiac recovery or transplantation in children.
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2/66. A probable primary hiv infection associated with acute non-specific myocarditis causing severe dilated cardiomyopathy.

    A patient with a probable primary hiv infection and a biopsy proven non-specific myocarditis is reported. The patient developed a severe dilated cardiomyopathy and initially presented with global heartfailure and fever. The left ventricular function partially recovered. One week after discharge the patient was readmitted in a septic shock and died. Current hypotheses concerning the etiology of left ventricular dysfunction in hiv infection are discussed.
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3/66. Giant cell myocarditis responding to immunosuppressive therapy.

    An unusual case of giant cell myocarditis presenting with cardiogenic shock that dramatically responded to conventional dose of steroids and azathioprine is reported. Cardiac recovery was rapid, complete (left ventricular ejection fraction rose to 55% from 10%), and was accompanied by the disappearance of the inflammatory infiltrates including giant cells in the control endomyocardial biopsy. maintenance of the recovery at 16 months of follow-up on a low dose of azathioprine suggests that giant cell myocarditis might be a heterogeneous disease having either a negative untreatable trend necessitating cardiac transplantation, or a curable substrate responding to immunosuppressive drugs.
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4/66. atrioventricular block in a toxic child: do not forget diphtheria.

    We describe a 4.5-year-old girl who presented with severe febrile throat infection and who, after a few days, developed ventricular tachycardia followed by atrioventricular block. Although a pacemaker was inserted, she died of cardiogenic shock. Throat cultures were positive for corynebacterium diphtheriae.
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5/66. Mechanical bridge to recovery in fulminant myocarditis.

    A patient with acute fulminant lymphocytic myocarditis and cardiogenic shock was successfully treated by mechanical off loading of the left ventricle. A nonpulsatile left-heart bypass was undertaken with an implantable centrifugal blood pump. Careful weaning resulted in device removal on the seventh day. Left and right ventricular function is sustained at 7 months. Widespread application of this method depends on the availability of an inexpensive user friendly blood pump, appropriate weaning protocols and emerging strategies to promote sustainable myocardial recovery.
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6/66. Left ventricular free wall rupture in acute fulminant myocarditis during long-term cardiopulmonary support.

    A 77-year-old woman with acute myocarditis developed cardiogenic shock soon after admission and was given mechanical cardiopulmonary support. echocardiography revealed severe global left ventricular hypokinesia. After 5 days of mechanical support, left ventricular wall motion gradually began to improve, but the patient died of cardiac tamponade on day 13. At necropsy, a free wall rupture was found where the apical akinetic area bordered the basal portion, an area which had shown better wall motion. Left ventricular free wall rupture in acute myocarditis has not been reported, but this case indicates that it may occur in fulminant myocarditis when a cardiopulmonary support system is used.
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7/66. Clinical manifestations of influenza a myocarditis during the influenza epidemic of winter 1998-1999.

    OBJECTIVES: The clinical features of myocarditis that developed during the influenza epidemic of winter 1998-1999 were investigated to emphasize the need for medical attention to this disease. methods: Nine patients were treated under diagnoses of acute myocarditis during the winter of 1998-1999. Five (two males and three females, mean age 52 /- 18 years) were examined with myocarditis associated with influenza A. The diagnosis of influenza A myocarditis was based on electrocardiographic and echocardiographic abnormalities, increased creatine kinase levels and at least a four-fold increase in influenza a virus titers using paired sera. RESULTS: All patients had preceding flu-like symptoms and fever. Cardiac involvement developed between 4 and 7 days after the onset of influenza symptoms. dyspnea progressively worsened in three patients, one went into shock and one had persistent fever, cough and mild dyspnea without apparent cardiac symptoms. Three patients had ST elevation associated with Q waves and one had complete left bundle branch block. The creatine kinase levels were abnormally increased and global wall motion of the left ventricle on echocardiography was decreased in all patients. Two patients had diagnoses of fulminant myocarditis. One patient died of pneumonia following cerebral infarction, but the left ventricular dysfunction normalized in the remaining four patients. CONCLUSIONS: Cardiac involvement occurred between 4 and 7 days after the onset of influenza symptoms, and worsening dyspnea was the most common symptom. electrocardiography, echocardiography and creatine kinase levels should be checked to determine the potential for cardiac involvement when patients present with suspected influenza associated with worsening dyspnea or prolonged weakness. Increasing the awareness of influenza myocarditis may help in the earlier identification and treatment of this disease during influenza epidemics.
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8/66. Fulminant eosinophilic endomyocarditis in an asthmatic patient treated with pranlukast after corticosteroid withdrawal.

    Several cases of eosinophilic conditions including churg-strauss syndrome have been reported in association with the use of cysteinyl leukotriene receptor antagonists, including zafirlukast, montelukast, and pranlukast, in asthmatic patients. The case of a 26 year old woman with a three year history of asthma, rhinitis, and nasal polyps is reported in whom eosinophilia, pulmonary infiltrates, and fulminant eosinophilic endomyocarditis accompanied by cardiogenic shock developed during pranlukast treatment after corticosteroid withdrawal. Acute necrotising eosinophilic endomyocarditis was confirmed by endomyocardial biopsy. The patient recovered after intensive treatment, including mechanical assistance involving intra-aortic balloon pumping and steroid pulse therapy, along with the discontinuation of pranlukast. It is recommended that careful attention must be paid to signs of a systemic eosinophilic condition or even fulminant eosinophilic myocarditis in asthmatic patients who have begun treatment with antileukotriene drugs following withdrawal of steroids.
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9/66. meningoencephalitis, myocarditis and disseminated intravascular coagulation in a patient with scrub typhus.

    A 21-year-old male soldier was admitted due to a sore throat, headache, generalized lymphadenopathy and persistent fever for 12 days. Despite empirical antibiotic treatment for four days at a clinic prior to admission, he continued to have persistent abdominal pain over his right upper quadrant region and progressive jaundice was followed by shock. After admission, he developed an episode of clonic seizures and became delirious and agitated. An electrocardiogram showed first degree atrioventricular (AV) block and non-specific ST-T wave changes. Hematological studies revealed thrombocytopenia, hypofibrinogenemia, abnormal partial thromboplastin time (PTT) and a positive test for D-dimer. The cerebrospinal fluid analysis showed pleocytosis with white cells of 84/mm3 with a lymphocyte predominance, protein of 97 mg/dL and glucose of 79 mg/dL. Indirect immunofluorescence assay showed a fourfold rise in antibodies to orientia tsutsugamushi in paired serum with IgM antibody titer of 1:640. The patient had a favorable response after parenteral chloramphenicol in addition to oral tetracycline. Early ricognition of scrub typhus and early prescription of anti-rickettsial agents prevent complications of central nervous system involvement and further deterioration of cardiac and hematological function.
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10/66. Fulminant myocarditis in polymyositis.

    Cardiac involvement in patients with polymyositis is usually asymptomatic and associated with a mild clinical course. A female patient with muscle weakness and cardiogenic shock, who was diagnosed with polymyositis and fulminant myocarditis, is described. A large amount of methylprednisolone, in addition to intra-aortic balloon pumping and percutaneous cardiopulmonary support, led to the recovery of her cardiac function. However, a massive cerebral embolism occurred and she died. Postmortem histopathological examination showed necroses of muscles and diffuse invasion of mononuclear cells in both the myocardium and the biceps muscle of her arm. Although the mechanism of cardiac dysfunction is not clear, immunosuppressive therapy was effective for fulminant myocarditis in the present case.
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