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At least 55 records · Page 3Linked to original sources

Clinical and histopathological profile of sarcoidosis of the heart and acute idiopathic myocarditis. Concepts through a study employing endomyocardial biopsy. II. Myocarditis.

Through an approach employing endomyocardial biopsy, early diagnosis of acute idiopathic myocarditis is possible. The histopathological findings consisted of fragmentation of muscle bundles, degenerative changes with lysis of myocytes and interstitial mononuclear cell infiltration. The cells were irregular in size and shape and contained slightly basophilic cytoplasm or were mixed with small round cells. Early clinical symptoms consisted of flu-like symptoms, i. e., higher fever, myalgia, malaise and arthralgia. Initial ECG changes consisted of complete A-V block in 9, bifascicular block in 3, and intraventricular conduction disturbance in 4 cases. Serial biopsies were performed at the early (0--2 weeks), middle (2--4 weeks), and late stages (more than 4 weeks) in 6 cases. Two of these biopsies were performed in 6 cases and all 3 were performed in one case. The numerous interstitial cell infiltration had almost disappeared by the early stage. At the late stage, either a slight or moderate degree of interstitial fibrosis was observed. These observations coincided well with the improvement of the ECG findings. Characteristic laboratory findings consisted of high LDH, GOT, and serum amylase levels. Varieties of treatments such as temporary cardiac pacing, peritoneal or hemo-dialysis, vasodilator therapy effectively to relieve the grave clinical condition. It is concluded that acute myocarditis may heal with remarkable improvement when the appropriate treatment is applied at the early stage of the disease.

Acute Disease↗

The current status of immune modulating therapy for myocarditis: a case of acute parvovirus myocarditis treated with intravenous immunoglobulin.

We present a case of a patient who presented with a febrile illness without obvious source initially, who developed profound cardiac decompensation and left ventricular dysfunction. Viral titers obtained during the course of illness confirmed parvovirus infection. Intravenous aggressive immunoglobulins and medical therapy for heart failure resulted in stabilization and, ultimately, a complete recovery. Recent data from clinical trials are discussed regarding the utility of immunoglobulins in the treatment of myocarditis and heart failure.

Acute Disease↗

Immunosuppression with high doses of cyclophosphamide reduces the severity of myocarditis but increases the mortality in murine Coxsackievirus B3 myocarditis.

To test the therapeutic efficacy of immunosuppression with cyclophosphamide (CYP) on coxsackievirus B3 (CB3) myocarditis, 2-week-old DBA/2 mice were inoculated with 3 X 10(2) plaque-forming units of CB3 virus. CYP (100 mg/kg/day s.c.) was administered daily on days 0-8 (experiment 1; group 2), days 8-21 (experiment 2; group 4), and days 21-34 (experiment 3; group 6). Groups 1, 3, and 5 were infected control groups for each experiment. Spleen, thymus, and body weights were measured. In experiment 1, survival rate in group 2 on day 8 was low compared with group 1 (nine of 51 versus eight of 28; p = NS), and myocardial virus titers in group 2 on day 8 were higher (p less than 0.05) compared with group 1; however, cellular infiltration and myocardial necrosis in group 2 were less severe (p less than 0.05), and serum neutralizing antibody titers were decreased (p less than 0.01). In experiment 2, survival rate in group 4 on day 21 was significantly lower (six of 24 versus 12 of 16; p less than 0.01), but cellular infiltration, myocardial necrosis, and calcification in group 4 were significantly less severe, and serum neutralizing antibody titers were decreased (p less than 0.01). In experiment 3, survival rate, cardiac histopathology, and serum neutralizing antibody titers did not differ between groups 5 and 6. In experiments 1, 2, and 3, the treated groups were characterized by lower spleen-to-body-weight and thymus-to-body-weight ratios and by marked cellular depletion in spleen and thymus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Syncopal convulsions with myocarditis in childhood. A case contribution to the transitory pacemaker treatment of myocarditis-induced heart block].

A ten-year-old girl was admitted to hospital with convulsions due to Adams-Stokes syndrome as a complication of complete heart block. A rheumatic myocarditis was causing the conduction defect. As a temporary measure a pacemaker was used to treat the extremely serious condition. In addition, cortisone, antibiotics and antiphlogistics were given for treatment of the underlying disease. The child was discharged from hospital in good condition with a long-term therapy of penicillin.

Adams-Stokes Syndrome↗

Coxsackievirus-B3-induced myocarditis: virus receptor antibodies modulate myocarditis.

Two variants of coxsackievirus group B, type 3 (CVB3) differ in ability to induce myocarditis in Balb/cCUM mice. Infection with the highly pathogenic variant (CVB3M) stimulates autoimmunity to normal cardiocyte antigens, and tissue injury results primarily from an autoreactive cytolytic T lymphocyte (ACTL). Animals infected with the less pathogenic CVB3o variant do not develop ACTL, although CVB3o replicates to high titers in the heart and polyclonal neutralizing antisera fail to distinguish between the two variant virions. The present study uses two IgM mAb derived by fusing spleen cells from CVB3M-infected mice with NS-1 cells. These mAb investigate important differences between the virus variants that may explain why only selected infections trigger autoimmunity. mAb 8A6 is a virus-neutralizing antibody that prevents infection of HeLa cells and cultured cardiocytes by attaching to the virus. mAb 10A1 also interferes with infection but presumably reacts to the virus receptor on the susceptible cells and shows little or no binding to the virions. While 8A6 is equally effective in neutralizing both CVB3o and CVB3M, suggesting that antigenic epitopes on both variants are either identical or highly cross-reactive, 10A1 distinguishes between the variants, suggesting that the pathogenic and less pathogenic viruses use distinct cell surface receptors. Competitive binding studies using radiolabeled CVB3M and either of the unlabeled variants confirm this hypothesis. Both mAb effectively prevent CVB3M-induced cardiac damage in vivo. mAb 10A1 also inhibits autoreactive ACTL lysis of cardiocytes, indicating that the autoimmune effectors may recognize the virus receptor, and that the receptor utilized by a virus may prove important in triggering auto-sensitization.

Animals↗