Immunopathogenesis and treatment of myocarditis: The United States myocarditis treatment trial

Mason, Jay W.

doi:10.1016/s1071-9164(96)80074-1

Cited by 14 publications

(8 citation statements)

References 9 publications

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“…115,116 Wojnicz et al 87 used HLA expression on endomyocardial specimens to identify an inflammatory cardiomyopathy cohort. A total of 84 patients who demonstrated increased HLA expression and chronic dilated cardiomyopathy were randomized to receive 3 months of placebo or immunosuppression with prednisone and azathioprine.…”

Section: Treatmentmentioning

confidence: 99%

Myocarditis

2006

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Section: Treatmentmentioning

confidence: 99%

Myocarditis

2006

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“…As cardiomyopathies are progressive diseases, when the heart biopsy is taken may have an influence on this wide disparity. Despite extensive efforts to date, no specific treatment of myocarditis has been demonstrated to be effective in large randomised trials, although the benefit of antiviral, immunomodulating and immunosuppressive treatment with respect to the underlying aetiology have been investigated in randomised placebo controlled treatment trials [79,[85][86][87][88][89]. The reader is directed to other reviews for clinical aspects [90][91][92][93][94].…”

Section: Evidence For Cvb Involvement As Aetiologic Agents In Human Mmentioning

confidence: 99%

The group B coxsackieviruses and myocarditis

Kim¹,

Hufnagel²,

Chapman³

et al. 2001

Reviews in Medical Virology

156

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The six serotypes of the group B coxsackieviruses (CVB) are common human enteroviruses linked etiologically to inflammatory cardiomyopathies. This has been demonstrated by molecular detection of enteroviral RNA in human heart tissue, serologic associations with disease, and virus isolation from cases of fulminant myocarditis. The murine model of CVB-associated myocarditis has demonstrated that CVB can be attenuated through mutations at different genomic sites. Human CVB3 isolates demonstrate varying degrees of cardiovirulence in the murine model; one site of virulence determination has been mapped to domain II of the 5' non-translated region. The interplay of CVB replication and the immune response to that replication in the heart is a complex interaction determining the extent to which the virus replication is limited and the degree to which a pathogenic inflammation of cardiac muscle occurs. Studies of CVB3-induced myocarditis in murine strains lacking subsets of the immune system or genes regulating the immune response have demonstrated a pivotal role of the T cell response to the generation of myocarditis. While CVB are associated with 20-25% of cases of myocarditis or cardiomyopathy, the severity of the disease and the existence of attenuated strains shown to generate protective immunity in animal models indicates that vaccination against the CVBs would be valuable.

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“…Five papers were excluded for the following reasons: duplication (two studies), 9,10) trial did not use biopsy proven diagnosis (one study), 11) and participants with mixed conditions and unable to extract data (two studies). 12,13) Details of the 5 trials included can be found in the Table. Immunosuppressive agents: Five types of immunosuppressive therapy were used in the randomized control studies: prednisone, 8,14) prednisone combined with azathioprine, 7,15,16) prednisone combined with cyclosporine, 7,16) intravenous immune globulin, 13) and immunoadsorption.…”

Section: Resultsmentioning

confidence: 99%

Immunosuppressive Treatment for Inflammatory Cardiomyopathy: Meta-Analysis of Randomized Controlled Trials

2005

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SUMMARYThe use of immunosuppressive therapy for inflammatory cardiomyopathy is controversial.The aim of this review is to summarize the current empirical evidence for immunosuppressive treatment in inflammatory cardiomyopathy.We conducted a meta-analysis of all randomized controlled trials (RCTs) that compared immunosuppressive therapy with either placebo or conventional treatment in patients with inflammatory cardiomyopathy. The pooled outcomes were all-cause death and heart transplantation for inflammatory cardiomyopathy, left ventricular ejection fraction (LVEF), and left ventricular end diastolic dimension (LVEDD).Five trials involving 316 patients were included. Overall, immunosuppressive therapy was not superior to placebo and conventional therapy in the pooled outcome of all-cause death and heart transplantation (odds ratio [OR] 1.03, 95% confidence intervals [CI] 0.58 to 1.80) in the long-term. The pooled data showed that there might be a short-term beneficial effect on LVEF improvement (5.06%, 95% CI -0.07% to 10.18%) in patients receiving immunosuppressive therapy, but no beneficial effect on LVEDD either in the short-term (-0.87 mm; 95% CI, -8.29 to 6.55 in adult patients) or long-term (-0.52 mm, 95% CI -3.64 to 2.60 in adult patients) was observed.There is no evidence to suggest that immunosuppressive therapy has an effect on improving the survival of patients with inflammatory cardiomyopathy. Current therapy in inflammatory cardiomyopathy seems to be limited to supportive measures or transplantation. (Int Heart J 2005; 46: 113-122)

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Immunopathogenesis and treatment of myocarditis: The United States myocarditis treatment trial

Cited by 14 publications

References 9 publications

Myocarditis

Myocarditis

The group B coxsackieviruses and myocarditis

Immunosuppressive Treatment for Inflammatory Cardiomyopathy: Meta-Analysis of Randomized Controlled Trials

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