A National Survey on Myocarditis Associated With the 2009 Influenza A (H1N1) Pandemic in Japan

Ukimura, Akira; Izumi, Tohru; Matsumori, Akira; Myoc, Clinical Research Committee on

doi:10.1253/circj.cj-10-0452

Cited by 73 publications

(59 citation statements)

References 25 publications

(18 reference statements)

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“…The cause of death in at least six cases was not respiratory failure, and instead was encephalopathy (cases 5 and 12), cerebral hemorrhage (cases 9 and 18), and myocardial dysfunction (cases 15 and 16). Encephalopathy 2-4 and myocardial disorders 5,6 have been reported to be associated with 2009 H1N1 virus infection and seasonal influenza virus infection, although the pathogenesis of these diseases and their relationship to influenza virus infection have not yet been elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…However, in some patients, it caused severe respiratory diseases, neurological complications, [2][3][4] and myocardial symptoms. 5,6 The 2009 H1N1 virus caused viral pneumonia with acute respiratory distress syndrome, 7 which is not generally caused by seasonal influenza strains. It was also notable that younger people were affected with severe pneumonia, which was fatal in some cases.…”

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confidence: 99%

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Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection

et al. 2012

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, were histopathologically analyzed. Hematoxylin-eosin staining, immunohistochemistry for type A influenza nucleoprotein antigen, and real-time reverse transcription-PCR assay for viral RNA were performed on formalin-fixed and paraffin-embedded specimens. In addition, the D222G amino acid substitution in influenza virus hemagglutinin, which binds to specific cell receptors, was analyzed in formalinfixed and paraffin-embedded trachea and lung sections by direct sequencing of PCR-amplified products. There were several histopathological patterns in the lung according to the most remarkable findings in each case: acute diffuse alveolar damage (DAD) with a hyaline membrane (four cases), organized DAD (one case), acute massive intra-alveolar edema with variable degrees of hemorrhage (three cases), neutrophilic bronchopneumonia (five cases) and tracheobronchitis with limited histopathological changes in alveoli (four cases). In two cases, the main findings were due to preexisting disease. Influenza virus antigen was only detected in the respiratory tract in 10 cases by immunohistochemistry. The antigen was detected in type II pneumocytes (three cases) in the epithelial cells of the trachea, bronchi and glands (six cases), and in the epithelial cells in both of the above (one case). The four cases with acute DAD presented with antigen-positive type II pneumocytes. In one case, the D222G substitution was detected in the lung as a major sequence, although 222D was prominent in the trachea, suggesting that selection of the viral clones occurred in the respiratory tract. In five

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection

et al. 2012

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“…An influenza pandemic occurred in 2009 [6,9,10]. The causative organism, influenza A (H1N1pdm) virus, has been reported to cause fatal myocarditis as well as pneumonia [11][12][13][14]. Based on national surveillance in Japan, we previously reported that 19 fulminant myocarditis patients (adults: 13, children: 6) with influenza A (H1N1pdm) virus were seen in the 2009/2010 season, while only 2 adult patients were seen in the 2010/2011 season [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

“…It was also difficult to show that the neuraminidase inhibitors significantly improved the survival rate of patients with fulminant myocarditis associated with influenza [6,7,[11][12][13][14]. Peramivir is a selective inhibitor of influenza neuraminidase that is effective when administrated intramuscularly and intravenously for the treatment of influenza virus infection in mouse models [17][18][19][20]23].…”

Section: Introductionmentioning

confidence: 99%

The Neuraminidase Inhibitor Peramivir Ameliorates Myocarditis Induced by Influenza A (H1n1pdm) Virus in a Murine Model

Ukimura¹,

Ooi²,

Kanzaki

2015

Clin Microbiol

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Severe influenza sometimes causes myocarditis. To analyze the effects of peramivir on influenza A (H1N1pdm) virus myocarditis, we investigated survival rates, cardiac function, histological findings and cytokine induction in murine influenza A (H1N1pdm) virus-induced myocarditis. Eight-week-old BALB/c male mice were infected intranasally with influenza A (H1N1pdm) virus, and then divided into 2 groups: control group, which was injected with saline; and peramivir-treatment group, which was treated with peramivir. Histological studies, echocardiograms and quantitative analysis of viral RNA and mRNA for inflammatory cytokines and adhesion molecules were performed. Treatment with peramivir led to a significant improvement in survival (p<0.01 vs. control group). Fractional shortening (FS) of peramivir-treatment group (44.7%, p<0.01) was significantly higher than that of control group (27.7%) on day 8. Histological examinations revealed localized myocarditis with lymphocyte infiltration, and myocarditis lesions were found in perivascular areas or associated with pericarditis; treatment with peramivir improved these findings. Quantity of influenza virus genome in heart and lung tissues was suppressed in peramivirtreatment group. The expression of cytokine and adhesion molecule mRNA was suppressed in peramivir-treatment group. Peramivir improved influenza A (H1N1pdm) virus-induced myocarditis.

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“…4 Recently, myocarditis associated with the 2009 influenza A (H1N1) pandemic was reported in Japan. 5 Viruses such as coxsackie B3 virus can also elaborate protease 2A, which specifically cleaves the hinge 3 region of dystrophin and disrupt the integrity of the sarcolemmal membrane. 6 In addition, cardiac overexpression of protease 2A alone is sufficient to induce cardiomyopathy.…”

mentioning

confidence: 99%

Contribution of Acquired Factors to the Pathogenesis of Dilated Cardiomyopathy - The Cause of Dilated Cardiomyopathy: Genetic or Acquired? (Acquired-Side) -

Yoshikawa

2011

Circ J

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A National Survey on Myocarditis Associated With the 2009 Influenza A (H1N1) Pandemic in Japan

Cited by 73 publications

References 25 publications

Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection

Histopathological and immunohistochemical findings of 20 autopsy cases with 2009 H1N1 virus infection

The Neuraminidase Inhibitor Peramivir Ameliorates Myocarditis Induced by Influenza A (H1n1pdm) Virus in a Murine Model

Contribution of Acquired Factors to the Pathogenesis of Dilated Cardiomyopathy - The Cause of Dilated Cardiomyopathy: Genetic or Acquired? (Acquired-Side) -

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