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PubMed1995

Intimate association of eosinophils to collagen bundles in eosinophilic myocarditis and ranitidine-induced hypersensitivity myocarditis.

BACKGROUND: Eosinophilic myocarditis is an inflammatory condition of the heart in which the infiltrate is composed predominately of eosinophils. DESIGN: We identified three cases of eosinophilic myocarditis in which the infiltrating eosinophils showed a remarkable intimate association with bundles of collagen. Two of the hearts examined were explants from heart transplant recipients with hypersensitivity myocarditis at the time of transplant and the third was from an autopsied patient with Churg-Strauss syndrome. These hearts were examined using light and electron microscopy. The cellular infiltrate in all three cases was characterized using immunoperoxidase stains with a panel including antibodies against myeloperoxidase, common leukocyte antigen (CD45), B lymphocytes (CD20), T lymphocytes (CD3), active-memory T lymphocytes (CD45RO), inactive T lymphocytes (CD45RA), and macrophages (CD68). RESULTS: Ultrastructural examination in all three cases confirmed the apposition of eosinophils to both large bundles of collagen and smaller aggregates of collagen fibrils. The eosinophils and the bundles of collagen stained strongly for myeloperoxidase, suggesting at least partial degranulation of the eosinophils. A KP-1 stain (CD68) revealed macrophages admixed with the eosinophils adjacent to the collagen bundles, and stains for CD45RA (naive lymphocytes) and CD45RO (memory T cells) showed an interstitial infiltrate of predominantly CD45RO-positive cells. Clinically, the cardiac decompensation of one of the transplant patients was most likely due to ranitidine-induced hypersensitivity myocarditis. CONCLUSIONS: These results suggest that some cases of eosinophilic myocarditis may be caused by the expression of novel antigens bound to collagen bundles. In one of the patients awaiting cardiac transplant, cardiac decompensation was temporally associated with ranitidine therapy, an agent not previously implicated as a cause of hypersensitivity myocarditis.

Adult↗
PubMed2000

Significance of pericardial cytokines in giant cell myocarditis in rats--pathological comparison to viral myocarditis in mice.

To investigate the precise disease progression in myocarditis, Lewis rats were injected with porcine cardiac myosin, and C3H/He mice were inoculated with coxsackievirus B3. Both were killed serially, and the hearts were stained with hematoxylin-eosin to compare their pathological characteristics. In viral myocarditis, viral replication in the myocardium resulted in myocardial necrosis with inflammation, and the lesions were distributed transmurally, as previously reported. On the other hand, in giant cell myocarditis, inflammatory lesions appeared at first around the capillaries in the epicardium, and thereafter spread transmurally. Pericardial effusion was noticed in all the rats with myocarditis in the fulminant stage. Levels of interleukin (IL) -1beta and IL-6 in the pericardial effusion were elevated compared with the serum cytokines at the peak of inflammation. However, interferon-gamma in both the pericardial effusion and serum was not elevated. The cause of the myocardial lesions that developed in rats with giant cell myocarditis may be some active inflammatory process via the pericardial effusion.

Animals↗
PubMed1996

Nitric oxide and murine coxsackievirus B3 myocarditis: aggravation of myocarditis by inhibition of nitric oxide synthase.

OBJECTIVES: This study sought to investigate the effects of nitric oxide inhibition in a murine model of coxsackievirus B3 myocarditis. BACKGROUND: Little is known about the contribution of nitric oxide to the pathophysiology of myocarditis. METHODS: Antiviral activity was tested in vitro using nitric oxide inhibition by treatment with activated macrophages of NG-nitro-L-arginine methyl ester. In the in vivo experiments, NG-nitro-L-arginine methyl ester and NG-nitro-D-arginine methyl ester (both at 100 micrograms/ml) were administered to C3H/He mice early (days 0 to 14) and late (days 14 to 35) after infection with coxsackievirus B3. RESULTS: In the in vitro experiments with interferon-gamma- and lipopolysaccharide-induced activated murine macrophages, treatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester, but not its inactive enantiomer NG-nitro-D-arginine methyl ester, restored coxsackievirus B3 titers. In the in vivo experiments in the early treatment group, myocardial virus titers were higher in NG-nitro-L-arginine methyl ester-treated than infected untreated animals, and both inflammatory cell infiltration and necrosis were more severe. In the late treatment group, more severe necrosis and more dense myocardial and perivascular fibrosis were observed in NG-nitro-L-arginine methyl ester-treated than in infected untreated animals. NG-Nitro-D-arginine methyl ester administration was ineffective. CONCLUSIONS: Nitric oxide inhibition increases myocardial virus titers, resulting in the aggravation of cardiac pathology in the early stage of coxsackievirus B3 myocarditis. In the late stage, it induces more severe cardiomyopathic lesions. Nitric oxide plays a defensive role in the pathogenesis of coxsackievirus B3 myocarditis.

Animals↗
PubMed1995

A clinical trial of immunosuppressive therapy for myocarditis. The Myocarditis Treatment Trial Investigators.

BACKGROUND: Myocarditis is a serious disorder, and treatment options are limited. This trial was designed to determine whether immunosuppressive therapy improves left ventricular function in patients with myocarditis and to examine measures of the immune response as predictors of the severity and outcome of disease. METHODS: We randomly assigned 111 patients with a histopathological diagnosis of myocarditis and a left ventricular ejection fraction of less than 0.45 to receive conventional therapy alone or combined with a 24-week regimen of immunosuppressive therapy. Immunosuppressive therapy consisted of prednisone with either cyclosporine or azathioprine. The primary outcome measure was a change in the left ventricular ejection fraction at 28 weeks. RESULTS: In the group as a whole, the mean (+/- SE) left ventricular ejection fraction improved from 0.25 +/- 0.01 at base line to 0.34 +/- 0.02 at 28 weeks (P < 0.001). The mean change in the left ventricular ejection fraction at 28 weeks did not differ significantly between the group of patients who received immunosuppressive therapy (a gain of 0.10; 95 percent confidence interval, 0.07 to 0.12) and the control group (a gain of 0.07; 95 percent confidence interval, 0.03 to 0.12). A higher left ventricular ejection fraction at base line, less intensive conventional drug therapy at base line, and a shorter duration of disease, but not the treatment assignment, were positive independent predictors of the left ventricular ejection fraction at week 28. There was no significant difference in survival between the two groups (P = 0.96). The mortality rate for the entire group was 20 percent at 1 year and 56 percent at 4.3 years. Features suggesting an effective inflammatory response were associated with less severe initial disease. CONCLUSIONS: Our results do not support routine treatment of myocarditis with immunosuppressive drugs. Ventricular function improved regardless of whether patients received immunosuppressive therapy, but long-term mortality was high. Patients with a vigorous inflammatory response had less severe disease.

Adult↗
PubMed2006

Cardiac magnetic resonance appearance of myocarditis caused by high dose IL-2: similarities to community-acquired myocarditis.

The purpose of this study was to describe and compare the cardiac magnetic resonance (CMR) characteristics of myocarditis caused by high dose interleukin-2 (7 patients) with community-acquired myocarditis (14 patients). A total of 21 patients with suspected myocarditis and elevated cardiac enzymes underwent cine CMR followed by delayed enhancement. The mean ejection fraction was mildly decreased in both groups. The location, pattern, and extent of DE were similar in both groups of patients. The CMR similarities between these two populations suggest that cytokine-mediated cytotoxicity may play an important role in community-acquired myocarditis.

Aged↗
PubMed1994

Cytokine and murine coxsackievirus B3 myocarditis. Interleukin-2 suppressed myocarditis in the acute stage but enhanced the condition in the subsequent stage.

BACKGROUND: It has been shown that the development of coxsackievirus B3 (CB3) myocarditis is regulated by T cells and not by B cells. Interleukin-2 (IL-2) is a T-cell-derived cytokine that stimulates the growth of T cells. This study was carried out to determine the effects of IL-2 on CB3-infected BALB/c mice. METHODS AND RESULTS: In two separate experiments, recombinant human IL-2 (5 x 10(4) U) was administered subcutaneously to 30 mice early (days 0 to 7) and 30 mice late (days 7 to 14) after infection with CB3. Each experiment had a control group of infected animals that did not receive IL-2. On days 7 and 10, splenic natural killer (NK) cell activity determined by 51Cr release assay and the distribution of myocardial lymphocyte subsets were compared in the treated and untreated groups. In the early treatment experiment, survival at 7 days was higher in treated compared with control animals, myocardial virus titers were lower, inflammatory cell infiltration was less (as was the severity of necrosis at the time the mice were killed), and NK cell activity was higher. However, in the late treatment experiment, survival at 14 days was lower in treated compared with control animals, and there was more infiltration, more severe necrosis, and more T-cell infiltration, but the NK cell activity did not differ significantly. In a third experiment similar to the late experiment described above but involving infected athymic nude mice, we confirmed the lack of effect of late in vivo administration of IL-2 on outcome. CONCLUSIONS: IL-2 has the capacity to limit CB3 myocarditis by enhancing NK cell activity in the acute viremic stage, resulting in a reduction of cardiac pathology. However, in the subacute aviremic stage, in contrast, IL-2 exacerbates the course and severity of the disease by increasing the number of T cells infiltrating the myocardium. That is, IL-2 has differential effects on acute CB3 myocarditis. IL-2 is beneficial if treatment is given early but later in murine CB3 myocarditis.

Acute Disease↗
PubMed1987

Immunologic identification of lymphocyte subsets in experimental murine myocarditis with encephalomyocarditis virus. Different kinetics of lymphocyte subsets between the heart and the peripheral blood, and significance of Thy 1.2+ (pan T) and Lyt 1+, 23+ (immature T) subsets in the development of myocarditis.

To clarify the immune mechanism in myocarditis, immunofluorescence techniques with laser flow cytometry were used to examine serial changes in lymphocyte subsets in the heart, spleen, and peripheral blood of DBA/2 and BALB/c mice inoculated with encephalomyocarditis virus (Experiment I). B cells were identified by staining with fluorescein isothiocyanate-labelled rabbit anti-mouse immunoglobulin. T-cell subsets were identified with rat anti-Thy 1.2, and nonpolymorphic Lyt 1 and Lyt 2 monoclonal antibodies plus fluorescein isothiocyanate-labelled anti-mouse immunoglobulin. On days 7 and 14 postinfection, the percentage of Thy 1.2+ (pan T) cells in both strains had decreased in the peripheral blood; B cells showed no significant changes throughout the entire period. On the other hand, Thy 1.2+ (pan T) and Lyt 1+, 23+ (precursor and immature) T cells appeared to occupy the major portion of the myocardium on days 7 and 14 when congestive heart failure developed. To confirm this, serial immunohistologic studies (immunoperoxidase staining) of the hearts of DBA/2 and BALB/c mice with encephalomyocarditis virus-induced myocarditis were performed (Experiment II). In Experiment II, most of the stained cells in the hearts of both strains were Thy 1.2 positive and Lyt 1 and Lyt 2 positive on days 7 and 14. Thus, Experiments I and II demonstrated that lymphocytes at the site of inflammation in acute viral myocarditis carried antigenic markers that differed from those of peripheral lymphocytes and suggested that Thy 1.2+ (pan T) cells, especially the Lyt 1+, 23+ subset (immature T cells and T-cell subset precursors) were involved in the development of myocarditis in these animals.

Animals↗
PubMed1995

[Acute myocarditis with severe cardiac dysfunction in the pediatric population. The evolution and differential characteristics with respect to adult myocarditis].

AIMS: The aim of our study was to assess the spontaneous outcome of acute myocarditis associated with severe cardiac dysfunction in children, as well as to compare these features with those occurring in adult patients. METHODS: Fifty patients consecutively diagnosed of acute myocarditis during the last 7 years in our hospital were studied; 15 patients were children younger than 14 years, and 35 were adults. Immunosuppressive therapy was not used in any patient. RESULTS: Mean age was 2 +/- 3 years in children, ranging from 2 months to 12 years. One patient required temporary pacing for a third-degree atrioventricular block, while the remaining 14 children had severe congestive heart failure, with a left ventricular ejection fraction of 30 +/- 12% (16 to 44%). After a mean follow-up of 21 +/- 26 months, only 3 children died, at 1, 4 and 10 months after the initial diagnosis. Death was sudden in all 3 patients. Left ventricular ejection fraction rose to 45 +/- 14% at 1 month after diagnosis, and to 58 +/- 15% at the end of follow-up. Unfavorable evolution (death or evolution to chronic dilated cardiomyopathy, with a left ventricular ejection fraction < 45%) occurred in 6 children (40%) at 1 month after diagnosis and in only 4 (25%) at the end of follow-up. The 9 children with 1-month favorable outcome were alive and had an ejection fraction > 45% at long-term, while only 2 of the 6 children with 1-month unfavorable outcome were alive and had an ejection fraction > 45% at long-term. Only the 3 children who died had an ejection fraction < 30% at 1-month. Favorable outcome was more frequent in children that in adult patients with acute myocarditis (75% versus 46%). CONCLUSIONS: The outcome of acute myocarditis with severe cardiac dysfunction was favorable in a majority of pediatric patients; this favorable evolution was less frequent in adults. Patients in whom left ventricular ejection fraction did not increase at short-term had a higher risk of death, and they should probably be considered for heart transplantation.

Acute Disease↗
PubMed1996

Streptococcal M protein peptide with similarity to myosin induces CD4+ T cell-dependent myocarditis in MRL/++ mice and induces partial tolerance against coxsakieviral myocarditis.

Immunologic similarities have been demonstrated between Coxsackievirus B3 (CVB3), group A streptococcal M protein, and cardiac myosin. Previous studies have also shown that T lymphocytes obtained from CVB3-infected mice expressing the H-2k MHC haplotype gave an immunodominant proliferative response to the NT4 peptide (GLKTENEGLKTENEGLKTE) of the streptococcal M5 protein. We now show that the NT4 peptide can induce inflammatory heart disease in MRL/++ (H-2k) mice and that induction of anergy to this peptide protects against CVB3-induced myocarditis. MRL/++ mice infected with CVB3 for 7 days or immunized twice at 7-day intervals with the streptococcal NT4 peptide in CFA developed myocarditis. Treatment of the immunized mice with either anti-CD4 or anti-IAk mAbs inhibited cardiac inflammation. Injection of MRL/++ mice with NT4 covalently coupled to syngeneic splenocytes tolerized the animals to this peptide as shown by reduction of the proliferative response. NT4-tolerized mice had significantly reduced myocarditis, although virus titers in the heart were elevated. A control peptide, VP1-10 from the CVB3 capsid protein VP1, did not protect the mice from CVB3-induced myocarditis. The results suggest that immunity to NT4 induced during CVB3 infections is important to the development of cardiac inflammation.

Amino Acid Sequence↗
PubMed2002

National survey of fulminant myocarditis in Japan: therapeutic guidelines and long-term prognosis of using percutaneous cardiopulmonary support for fulminant myocarditis (special report from a scientific committee).

Although fulminant myocarditis is known as a fatal disease, patients have been able to recover and return to normal life with the help of mechanical cardiopulmonary support. However, therapeutic guidelines for using percutaneous cardiopulmonary support (PCPS) for fulminant myocarditis have not been established, and the clinical course and long-term prognosis of such patients are still controversial issues. The present national survey considered the current situation of patients as the basis for proposing therapeutic guidelines. Thirty of 52 patients (57.7%) survived and returned to social life. Important factors concerning the prognosis were the severity and grade of cardiac and renal dysfunction, the adjusted support flow rate to enable recovery from circulatory failure, and prevention of circulatory disturbances of the legs and multiple organ failure directly associated with PCPS. With regard to the long-term prognosis of patients treated with PCPS, the readmission rate was 10%, the exacerbation rate was 3.3%, and mortality was 10% during the average follow-up period of 962 days. Optimal management of the mechanical cardiopulmonary support and curative treatment for the myocarditis further improve the outcome of this disease.

Blood Gas Analysis↗
PubMed1980

Myocarditis in mixed connective tissue disease. Association of myocarditis with antibody to nuclear ribonucleoprotein.

A young black woman with clinical and serologic features of mixed connective tissue disease (MCTD) developed myocarditis with congestive heart failure and ventricular ectopic activity. Despite treatment with steroids and cyclophosphamide, progressive myocarditis resulted in death 20 months after cardiomegaly first developed. Necropsy findings in the myocardium included multiple areas of extensive lymphocytic infiltration and patches of fibrosis. Myocarditis has not previously been described in the adult with MCTD but may be an important complication in patients with a high titer of antibody to nuclear ribonucleoprotein.

Adult↗
PubMed2006

Beta2-Adrenergic agonists suppress rat autoimmune myocarditis: potential role of beta2-adrenergic stimulants as new therapeutic agents for myocarditis.

BACKGROUND: The therapeutic potential of beta2-adrenergic receptor (AR) agonists in the treatment of autoimmune diseases has been reported. However, the role of these drugs in the myocardial structure-induced autoimmune process, which is thought to play a crucial role in the progression of myocarditis to subsequent complications, has not been elucidated. METHODS AND RESULTS: Experimental autoimmune myocarditis (EAM) was induced in rats by immunization with cardiac myosin. On daily administration from day 0 after immunization, the beta2-selective AR agonists formoterol or salbutamol ameliorated EAM on day 21 and increased myocardial interleukin-10/interferon-gamma mRNA levels. Propranolol, a nonselective beta-AR antagonist, aggravated EAM on day 21 and decreased mRNA levels, whereas metoprolol, a beta1-selective AR antagonist, showed no effect. These results were reflected in vivo by the proliferation of cardiac myosin-primed lymph node cells from drug-treated rats. In vitro addition of beta2-selective AR agonists inhibited the activation of cardiac myosin fragment-specific myocarditogenic T lymphocytes, and this effect was reversed by ICI118,551, a beta2-selective AR antagonist. Furthermore, treatment with 2 different beta2-selective AR agonists starting on day 14 also ameliorated EAM on day 21. CONCLUSIONS: beta2-AR stimulation suppressed the development of EAM by inhibiting cardiac myosin-specific T-lymphocyte activation in lymphoid organs and by shifting the imbalance in Th1/Th2 cytokine toward Th2 cytokine. Furthermore, it also ameliorated established myocardial inflammation. beta2-AR-stimulating agents may represent important immunomodulators of the cardiac myosin-induced autoimmune process and have potential as a new therapy for myocarditis.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Fatal Epstein-Barr virus myocarditis in a child with repetitive myocarditis.

Fatal Epstein-Barr virus (EBV) myocarditis occurred in a 9-year-old female with a history of two prior discrete episodes of myocarditis, the first associated with chicken pox and the second of undetermined origin. Serologic studies during the fatal episode were characteristic of acute EBV infection, and EBV genome was detected by polymerase chain reaction (PCR) amplification of DNA extracted from autopsy heart and liver. PCRs for enteroviruses and cardiac viral culture were negative. An intense mononuclear cell infiltrate in the myocardium consisted entirely of T cells, without identifiable B cells. Human leukocyte antigen HLA-DR analysis using frozen tissue obtained postmortem revealed antigens DR4 and DR13. DR4 is associated with some autoimmune disorders, as well as idiopathic dilated cardiomyopathy. We postulate that an aberrant immune response, possibly associated with the DR4 locus, was responsible for the repetitive episodes of myocarditis in this patient.

Acute Disease↗
PubMed1992

[Abramov's "primary myocarditis", Fiedler's myocarditis and dilated cardiomyopathy].

After comparing the clinical and post mortem signs of myocarditis and dilated cardiomyopathy on the basis of correlating the reported data and own data on 28 patients with the appropriate descriptions by S. S. Abramov and A. Fiedler, the authors came to the conclusion that they had described two different diseases. S. S. Abramov had described dilated cardiomyopathy, whereas Fiedler acute diffuse myocarditis. The term Abramov-Fiedler myocarditis used in the Soviet literature does not correspond to the up-to-date classification of myocardial diseases. That is why it is required that these two concepts be separated to the benefit of the treatment.

Adult↗
PubMed2005

[Serious clinical course of myocarditis with "apical ballooning": first presentation of pathogenicity of HHV6 subtype A in myocarditis].

We report of a 67 year-old female who has suffered a flu-like infection three days ago and presented with symptoms of acute coronary syndrome. Coronary heart disease could be excluded. The ventriculography showed a moderate reduced left ventricular function characterized by "apical ballooning". Endomyocardial biopsies and EDTA blood gave a direct proof of human herpes virus 6 subtype A. Histological and immunohistochemical analysis revealed a myocarditis with areas of interstitial macrophages and fibrosis. This case presents for the first time the cross-link of myocarditis with HHV6A infection and the appearance of "apical ballooning".

Aged↗
PubMed1992

Lymphocytic active myocarditis characterized by numerous clusters of lymphocytes: a chronic variant of myocarditis?

We report three patients with a particular form of myocarditis characterized by numerous clusters of lymphocytes. Their common clinical manifestation was progressive and fatal heart failure with a 3- to 6-year duration. Atrioventricular and intraventricular conduction disturbances were observed in two patients. At necropsy, the hearts weighed 480, 530, and 430 gm, respectively, and showed marked dilatation of the bilateral ventricles and atria, with frequent mural thrombi. Histologic examination revealed numerous lymphocytic clusters and scattered foci of acute myocardial cell damage on a background of extensive fibrosis. We propose the term "chronic active myocarditis" to denote clinicopathologic characteristics of the present cases.

Atrial Fibrillation↗
PubMed1995

Colony-stimulating factors and coxackievirus B3 myocarditis in mice: macrophage colony-stimulating factor suppresses acute myocarditis with increasing interferon-alpha.

The effects of macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF) on murine coxsackievirus B3 myocarditis were investigated. A total of 4 x 10(6) U/kg/day M-CSF and 20 micrograms/kg/day G-CSF were injected subcutaneously every day on day 0 to day 14 starting simultaneously with virus inoculation. Serum interferon-alpha was measured periodically. The survival rate of the M-CSF group was higher than that of the untreated control group (p < 0.05). On days 7 and 14 cardiac disease was significantly lower in the M-CSF group than in the untreated control group. Myocardial virus titers on day 7 in the M-CSF group were lower compared with those of the untreated control group. No significant difference was seen in the survival, cardiac disease, or myocardial virus titers between the G-CSF and the control groups. Monocyte counts on days 7 and 14 in the M-CSF group were increased compared with those in the control group. Serum interferon-alpha titers in the M-CSF and G-CSF groups on day 4 and those in the M-CSF group on day 7 were significantly increased in comparison with those of the untreated control group. We conclude that M-CSF but not G-CSF has the potency to limit myocardial virus titers and to reduce cardiac disease in the acute coxsackievirus B3 myocarditis. This ability is associated with an elevated interferon-alpha. Thus macrophages may play a defensive role in this model.

Acute Disease↗
PubMed2002

Electrical remodeling of the ventricular myocardium in myocarditis: studies of rat experimental autoimmune myocarditis.

The purpose of this study was to evaluate the electrical remodeling of the ventricular myocardium in the experimental autoimmune myocarditis (EAM) model in Lewis rats. EAM was induced by immunization with cardiac myosin. During the active myocarditis phase, the effective refractory period (ERP), the duration of the monophasic action potential (MAPD) was extracted from the left ventricular free wall, and the mRNA levels of Kv1.4, 4.2, 4.3 and L type Ca2+ channel were determined by RNase protection assays. The inducibility of ventricular arrhythmia was higher in EAM rats than in the control rat, and the direct relationship between the coupling intervals of the premature stimulus and the ventricular arrhythmia in EAM rats. The ERP was prolonged in EAM rats compared with the control group. The MAPDs determined as 20% and 90% repolarization time, were both longer in EAM rats than in the controls. The level of expression of Kv4.2 mRNA was reduced in EAM rats in comparison with the controls, whereas those of Kv1.4, 4.3 and the L type Ca2+ channel were unchanged. Ventricular vulnerability was higher in EAM rats than in the control rats, and some of the ventricular arrhythmias observed in the EAM group seemed to be based on triggered activity. The level of expression of Kv4.2 mRNA was significantly reduced, and this change was compatible with prolongation of the action potential duration.

Action Potentials↗