Cases reported "Myocarditis"

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1/27. Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

    A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.
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2/27. 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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3/27. Segmental wall motion abnormalities in an individual with idiopathic pulmonary hemosiderosis.

    Idiopathic pulmonary hemosiderosis (IPH) is a rare condition characterized by diffuse pulmonary hemorrhage of unknown etiology. Cardiac involvement in the form of myocarditis and right ventricular hypertrophy have been reported to occur in association with IPH, although findings on echocardiography have not been described. Herein is presented a case of an adult with IPH and echocardiographic abnormalities.
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4/27. Acute eosinophilic myocarditis in a young woman.

    The first stage of eosinophilic myocarditis is called the necrotizing phase. This stage of eosinophilic myocarditis of unknown cause is often fulminant and rapidly fatal, occurring predominantly in males. Here, we report a case of eosinophilic myocarditis in the acute necrotizing phase occurred without known cause in a 23-year-old Japanese female. Severe diffuse hypokinesis of the left ventricular wall motion (ejection fraction 19.3%), significant concentric edematous thickening of the left ventricular wall (20.1 mm in diastole) and a moderate amount of pericardial effusion (10 mm wide echo free space posteriorly) were revealed by echocardiography. eosinophils were observed and degranulated eosinophilic cationic proteins were stained with antibody against eosinophilic cationic proteins (EG2) in the myocardial specimens obtained by myocardial biopsy. In spite of its severity, the disease resolved promptly with steroid therapy.
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5/27. 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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6/27. Completely inverse images in dual-isotope SPECT with Tl-201 and I-123 MIBG in a patient with myocarditis.

    Dual-isotope myocardial SPECT in a female patient with idiopathic myocarditis showed completely inverse images in Tl-201 and I-123 MIBG SPECT. In the dual-isotope SPECT performed 13 days after her admission, Tl-201 SPECT images showed reduced accumulation in the apex and normal accumulation in the other regions, whereas the corresponding I-123 MIBG SPECT images showed normal findings in the apex and reduced uptake in the other regions. These rare discrepancies were due to the difference in photon attenuation of the two isotopes in the apex and denervated-but-viable myocardium in the basal region, which were suggested by the following findings of gated perfusion SPECT and echocardiography. Gated SPECT with Tc-99m tetrofosmin performed 23 days after admission revealed normal myocardial perfusion and normal wall motion. iodine-123 MIBG SPECT findings reflected impaired wall motion in echocardiography performed on admission, which resembles a phenomenon called "memory image" in coronary artery disease. The present case indicated a pitfall in interpreting dual-isotope imaging.
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7/27. Ultrasonic tissue characterization in acute myocarditis: a case report.

    A 25-year-old woman was admitted because of acute myocarditis. Echocardiogram revealed hypokinesis of the left ventricle with increased wall thickness, but on day 7, the wall motion normalized. Cyclic variation of myocardial integrated backscatter on day I was reduced to 1.8 dB (normal range, 2.9-5.3 dB) and normalized to 3.2 dB on day 3. The normalization of the cyclic variation of integrated backscatter in the myocardium preceded the recovery of the left ventricular wall contractility, suggesting the ability of tissue characterization to predict recovery of cardiac function.
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8/27. magnetic resonance imaging in acute myocarditis: a case report and a review of literature.

    We report a case of acute myocarditis in a 20-year-old male, suggested by the clinical picture, elevated cardiac enzymes, electrocardiography and serology. diagnosis was confirmed by gadolinium-enhanced MRI showing part of the myocardium affected by an infiltrate. Impaired LV function and wall motion abnormalities were documented by echocardiography and FFE MRI. The patient recovered well within two weeks, but will be followed intensively since dilated cardiomyopathy may ensue.
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9/27. parvovirus B19 infection mimicking acute myocardial infarction.

    BACKGROUND: Enteroviruses (EVs) and adenoviruses (ADVs) have been considered common causes of myocarditis and dilated cardiomyopathy. In the present study, we report on the association of parvovirus B19 (PVB19) genomes in the clinical setting of acute myocarditis. methods AND RESULTS: This study included 24 consecutive patients admitted to our hospital within 24 hours after onset of chest pain. Acute myocardial infarction had been excluded in all patients by coronary angiography. Endomyocardial biopsies were analyzed by nested polymerase chain reaction/reverse transcriptase-polymerase chain reaction for EV, ADV, PVB19, human cytomegalovirus, Epstein-Barr virus, chlamydia pneumoniae, influenza virus A and B, and borrelia burgdorferi genomes, respectively, followed by direct sequencing of the amplification products. All patients presented with acute onset of angina pectoris and ST-segment elevations or T-wave inversion mimicking acute myocardial infarction. Mean baseline peak creatinine kinase and creatine kinase-isoenzyme fraction were 342 /-241 U/L and 32 /-20 U/L, respectively. Mean troponin t was increased to 7.5 /-15.0 ng/mL and c-reactive protein to 91 /-98 mg/mL. Eighteen patients had global or regional wall motion abnormalities (ejection fraction 62.5 /-15.5%). Histological analysis excluded the presence of active or borderline myocarditis in all but one patient. PVB19, EV, and ADV genomes were detected in the myocardium of 12, 3, and 2 patients, respectively (71%). Follow-up biopsies of virus-positive patients (11 of 17) demonstrated persistence of PVB19 genomes in 6 of 6 patients, EV genomes in 2 of 3 patients, and ADV genomes in 1 of 2 patients, respectively. CONCLUSIONS: Virus genomes can be demonstrated in 71% of patients with normal coronary anatomy, clinically mimicking acute myocardial infarction. In addition to EVs and ADVs, PVB19 was the most frequent pathogen.
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10/27. Cardiac troponin i release in non-ischemic reversible myocardial injury from parvovirus B19 myocarditis.

    Cardiac troponin i is released from myocytes in both reversible and irreversible myocardial injury. The changes in myocyte membrane permeability resulting from the injury could be enough for the release of cardiac troponins from the free cytosolic pool of myocytes without structural damage. We report a case of parvovirus B19 myocarditis in a 26-year-old male who developed regional wall motion abnormalities and severe left ventricular systolic dysfunction with elevated serum levels of cardiac troponin i (peak=11.7 ng/ml). diagnosis of parvovirus myocarditis was confirmed by presence of high titers of parvovirus B19 IgG and identification of parvovirus B19 dna by polymerase chain reaction. Within a few days of supportive treatment, the regional wall motion abnormalities resolved, the cardiac function recovered, and the elevation in serum cardiac troponin i subsided. This case further denotes the possibility of release of cardiac troponin i in non-ischemic, reversible myocardial injury.
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