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At least 19 recordsLinked to original sources
PubMed1985

Immunologic behavior of lymphocytes in experimental viral myocarditis: significance of T lymphocytes in the severity of myocarditis and silent myocarditis in BALB/c-nu/nu mice.

To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I). B cells were demonstrated by staining with fluorescein isothiocyanate (FITC)-labeled rabbit antimouse immunoglobulin (Ig). T cells were demonstrated with rat anti-Thy1.2 monoclonal antibody plus FITC-labeled antimouse Ig. There was a marked decrease in T cells in peripheral blood and a moderate decrease in the cells in the spleen on day 14. There were no significant changes in B cells in peripheral blood or spleen throughout the entire period and T cells accounted for approximately 80% of the cells in the myocardium on days 7 and 14. To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALB/c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis.

BACKGROUND: Lymphocytic myocarditis causes left ventricular dysfunction that may be persistent or reversible. There are no clinical criteria that predict which patients will recover ventricular function and which cases will progress to dilated cardiomyopathy. We hypothesized that patients with fulminant myocarditis may have a better long-term prognosis than those with acute (nonfulminant) myocarditis. METHODS: We identified 147 patients considered to have myocarditis according to the findings on endomyocardial biopsy and the Dallas histopathological criteria. Fulminant myocarditis was diagnosed on the basis of clinical features at presentation, including the presence of severe hemodynamic compromise, rapid onset of symptoms, and fever. Patients with acute myocarditis did not have these features. The incidence of the end point of this study, death or heart transplantation, was ascertained by contact with the patient or the patient's family or by a search of the National Death Index. The average period of follow-up was 5.6 years. RESULTS: A total of 15 patients met the criteria for fulminant myocarditis, and 132 met the criteria for acute myocarditis. Among the patients with fulminant myocarditis, 93 percent were alive without having received a heart transplant 11 years after biopsy (95 percent confidence interval, 59 to 99 percent), as compared with only 45 percent of those with acute myocarditis (95 percent confidence interval, 30 to 58 percent; P=0.05 by the log-rank test). Fulminant myocarditis was an independent predictor of survival after adjustments were made for age, histopathological findings, and hemodynamic variables. The rate of transplantation-free survival did not differ significantly between the patients considered to have borderline myocarditis and those considered to have active myocarditis according to the Dallas histopathological criteria. CONCLUSIONS: Fulminant myocarditis is a distinct clinical entity with an excellent long-term prognosis. Aggressive hemodynamic support is warranted for patients with this condition.

Acute Disease↗
PubMed1992

Incidental myocarditis with intravenous drug abuse: the pathology, immunopathology, and potential implications for human immunodeficiency virus-associated myocarditis.

Human immunodeficiency virus (HIV)-associated myocarditis is well reported. Many of these patients are also intravenous (IV) drug abusers. This study examined sudden death victims from the Office of the Chief Medical Examiner, State of Maryland, for active myocarditis. A group of HIV-negative drug abusers is compared with a group of HIV-negative victims without any known risk factors for the acquired immunodeficiency syndrome. Using modified Dallas criteria combined with an avidin-biotin-labeled immunoperoxidase procedure, the cases were classified as active, borderline, or absent myocarditis. Serologic analysis for circulating antimyocardial antibody was performed along with phenotypic analysis of the infiltrate. Of the 15 IV drug abuse cases examined, none were positive for HIV (enzyme-linked immunosorbent assay and Western blot). With IV drug abuse as the primary risk factor, five cases demonstrated active myocarditis, while five others had borderline myocarditis. Only one of 10 low-risk patients had a lymphocytic infiltrate consistent with borderline myocarditis. Drug abuse-related myocarditis was associated with cardiac pathology resulting in sudden death in only one case. Antimyocardial antibodies were positive in four of the 15 IV drug abuse cases, including patients with active, borderline, and absent myocarditis. The phenotypic expression of the lymphocytic infiltrates was similar to the findings reported for idiopathic and HIV-related myocarditis (Am J Pathol 137:1365-1371, 1990). Toxicology studies did not implicate any particular drug of abuse, but the increased frequency of myocarditis observed may reflect complications of cocaine or the combined effects of opiates and cocaine. Intravenous drug abuse is an independent risk factor for myocarditis and must be taken into consideration in studies of HIV-associated myocarditis.

Adult↗
PubMed1997

Circulating cardiac-specific autoantibodies as markers of autoimmunity in clinical and biopsy-proven myocarditis. The Myocarditis Treatment Trial Investigators.

AIM: Myocarditis and dilated cardiomyopathy may be phases of an organ-specific autoimmune disease of the myocardium. To provide evidence for autoimmune involvement in myocarditis, cardiac autoantibodies were detected in patient sera from the Myocarditis Treatment Trial. METHODS AND RESULTS: Cardiac antibody status was assessed by indirect immunofluorescence and by anti-alpha-myosin enzyme-linked immunosorbent assay in 53 patients from the Myocarditis Treatment Trial (35 males, aged 42 +/- 15 years); all had clinical myocarditis, but only 24 were classified as having histological myocarditis (Dallas criteria). By immunofluorescence, cardiac antibodies were more common in myocarditis (13/53) than in ischaemic (11/186, P = 0.0001) or in normal controls (24/270, P = 0.001). Abnormally raised anti-alpha-myosin antibodies were also more frequent in myocarditis (9/53) than in ischaemic (4/92, P = 0.01) or normal controls (4/203, P = 0.001); 34% of myocarditis patients were positive with one or both tests. Similar proportions of patients with and without histological myocarditis had antibodies by immunofluorescence (8/24 vs 5/29, P = ns) and by enzyme-linked immunosorbent assay (4/24 vs 5/29, P = ns). CONCLUSION: The detection of disease-specific cardiac autoantibodies supports autoimmune involvement in a subset of patients with clinical myocarditis. The lack of correlation of antibody with biopsy features suggests that diagnosis of myocarditis should not be made on histology alone. Autoimmune markers may provide adjunct diagnostic tools and identify patients in whom immunosuppression is of potential benefit.

Adult↗
PubMed1998

Antimyosin scintigraphy and immunohistologic analysis of endomyocardial biopsy in patients with clinically suspected myocarditis--evidence of myocardial cell damage and inflammation in the absence of histologic signs of myocarditis.

OBJECTIVES: This study compares the results of antimyosin scintigraphy in patients with clinically suspected myocarditis with histologic and immunohistologic findings in the endomyocardial biopsy. BACKGROUND: In patients with clinically suspected myocarditis, antimyosin scintigraphy often demonstrates myocardial cell damage but histologic evaluation of the endomyocardial biopsy often fails to show evidence of myocarditis. Recently developed immunohistologic techniques appear to be more sensitive for the detection of myocardial inflammation than histologic analysis alone. Studies comparing antimyosin scintigraphy and immunohistologic analysis of the endomyocardial biopsy in patients with clinically suspected myocarditis are not yet available. METHODS: Sixty-five patients with clinically suspected myocarditis underwent antimyosin scintigraphy. Antimyosin antibody uptake was correlated with histologic and immunohistologic findings in the endomyocardial biopsy. RESULTS: Antimyosin scintigraphy showed evidence of myocardial cell damage in 36 (55%) of the 65 patients and was negative in 29 (45%) patients. Histologic analysis of the endomyocardial biopsy revealed myocarditis in nine patients: six had a positive and three had a negative antimyosin scan, respectively. Thirty (83%) of 36 patients with evidence of myocardial cell damage on antimyosin scintigraphy were histologically negative for myocarditis. Immunohistologic analysis showed evidence of myocarditis in 31 (86%) of 36 patients with a positive antimyosin scan and also in 17 (59%) of 29 patients with a normal scan (p < 0.047). CONCLUSIONS: Antimyosin scintigraphy often shows myocyte injury in patients with clinically suspected myocarditis. Histologic analysis of the endomyocardial biopsy alone is often negative, but additional immunohistologic analysis of the endomyocardial biopsy frequently provides evidence of myocardial inflammation in these patients. With immunohistologic analysis as the reference method, antimyosin scintigraphy has a high specificity but a lower sensitivity for the detection of myocarditis.

Adult↗
PubMed1995

The epidemiology of infectious myocarditis, lymphocytic myocarditis and dilated cardiomyopathy.

Infectious myocarditis is a common condition which often passes unrecognized, and the true incidence is thus unknown. Lymphocytic myocarditis has been recorded in 1.06% of 12,747 unselected routine autopsies performed over a 10-year period. Dilated cardiomyopathy (DCM) has an estimated frequency of 7.5-10% per 100,000 inhabitants per year. Overall, the enteroviruses, and particularly the Coxsackie-B viruses, predominate among viruses as the cause of myocarditis. As new molecular biological techniques have become available, the cytomegaloviruses (CMV) seem to have emerged as a more common cause of myocarditis than was previously recognized. Among the bacterial myocarditides, diphtheric myocarditis has become a serious threat in Russia and adjacent states during the 1990s. Among newly identified bacteria, Borrelia burgdorferi infection is accompanied by cardiac involvement in 1-8% of cases, where myocarditis with conduction disturbances is the most prominent feature. Chlamydia pneumoniae may be associated with myocarditis and sudden unexpected death. In AIDS, myocarditis with variable aetiology occurs in up to 50% of patients, although asymptomatic in most cases. In lymphocytic myocarditis and DCM, enteroviral-specific nucleotide sequences have been detected in about 30% of patients, and CMV-specific nucleotide sequences in 14%. Borrelia burgdorferi may occasionally be implicated in DCM. In this contribution we focus also on sudden unexpected death (SUD) in young athletes, since, in Sweden, an increased frequency of SUD has recently been observed in young orienteers and myocarditis was a common feature.

Bacterial Infections↗
PubMed1990

Induction of major histocompatibility complex antigens within the myocardium of patients with active myocarditis: a nonhistologic marker of myocarditis.

The histologic diagnosis of active myocarditis is frequently difficult to establish. A nonhistologic marker of immune activation would be clinically useful in identifying cases of immune-mediated myocarditis. A viral etiology with subsequent autoimmunity to cardiac antigens has been implicated in human myocarditis. Because autoimmunity and viral disease are commonly associated with increased expression of major histocompatibility complex (MHC) antigens on targeted tissue, we examined endomyocardial biopsy samples from patients with active myocarditis for abnormal levels of MHC antigen expression. Thirteen patients with active myocarditis and eight control patients with other well-defined cardiac diagnoses (coronary disease, amyloidosis or neoplasm) were studied. A sensitive radioimmunoassay was developed that utilized monoclonal antibodies to human MHC class I and class II antigens in order to quantitate the expression of both of these antigens within each biopsy. Abnormal MHC class I and class II antigen expression was present in 11 of 13 myocarditis specimens and 1 of 8 control samples (specificity 88%, sensitivity 84.6%). Active myocarditis samples had approximately a 10-fold increase in MHC class I and class II expression. Immunoperoxidase staining localized abnormal MHC expression primarily within microvascular endothelium and along myocyte surfaces (11 of 13). This study is the first to demonstrate a marked increase in major histocompatibility complex antigen expression within the myocardium of patients with active myocarditis. The identification of abnormal histocompatibility antigen expression within an endomyocardial biopsy may prove a useful adjunct to the histologic diagnosis of myocarditis.

Adult↗
PubMed1987

Coxsackievirus B3 murine myocarditis: a pathologic spectrum of myocarditis in genetically defined inbred strains.

Group B coxsackieviruses are the most frequent causative agents in human viral myocarditis. Susceptibility to viral infections varies widely among individuals. In the mouse, coxsackievirus B3 also causes myocarditis. The differential susceptibility of different inbred strains of mice to coxsackie B3-induced myocarditis also appears to be under genetic control. This study details the histopathology of coxsackie B3 myocarditis in six different inbred strains of mice for the first 45 days after coxsackie B3 infection. These strains differ either in the haplotypes of their major histocompatibility complex or in their background genome. During the first 7 days after coxsackie B3 infection, there are dramatic differences among strains with respect to prevalence and severity of myocarditis. Focal zones of myocyte necrosis involving polymorphonuclear leukocytes as well as contraction band injury appear to be the early manifestations of direct viral injury. Four of the six strains, though, continue to show myocardial inflammation after day 9. This late phase myocarditis is characterized by the emergence of mononuclear cells within healing foci of myocyte necrosis as well as a distinctive diffuse interstitial pattern of myocarditis. The strains that develop this late ongoing myocardial inflammation frequently produce heart-specific autoantibodies. Thus the pathologic features of murine coxsackie B3 myocarditis change over the course of the illness, and genetic susceptibility to both early and late phase myocarditis differs markedly among various mouse strains.

Animals↗
PubMed1981

Drug related myocarditis. I. Hypersensitivity myocarditis.

The purpose of this study was to characterize in detail the morphologic changes in one form of drug related myocarditis: hypersensitivity myocarditis. We reviewed the clinical histories and microscopic findings in 24 patients with validated drug hypersensitivity and myocarditis. The myocarditis in these patients was characterized by a patchy interstitial inflammatory infiltrate rich in eosinophils, focal myocytolysis, prominent perivascular infiltrates, an absence of myocardial fibrosis, and the uniform features of the myocarditis in each patient. Twenty of the 24 patients died suddenly and unexpectedly. In retrospect, the presence of signs and symptoms of hypersensitivity (skin rash, fever, eosinophilia, and malaise) and nonspecific cardiac findings (electrocardiographic changes, tachycardia, or serum enzyme elevations) were suggestive of hypersensitivity myocarditis in these patients. Since early diagnosis is vital in hypersensitivity myocarditis, the presence of nonspecific cardiac findings in a patient receiving any drug associated with hypersensitivity should alert the clinician to the possibility of drug related myocarditis.

Aged↗
PubMed1994

Immunosuppressive treatment for myocarditis and borderline myocarditis in children with ventricular ectopic rhythm.

OBJECTIVES: To ascertain the responsiveness to immunosuppressive treatment of myocarditis and borderline myocarditis in children with ventricular ectopic rhythm (that is, all ventricular arrhythmia except benign premature ventricular contractions). To determine the impact of the diagnostic information provided by an endomyocardial biopsy specimen in these patients. BACKGROUND: The therapeutic value of performing an endomyocardial biopsy in children with ventricular ectopic rhythm is not established. In turn, the treatment of myocarditis with immunosuppressive drugs is also controversial. METHODS: The case notes and endomyocardial biopsy findings of all children with ventricular ectopic rhythm and a biopsy diagnosis of myocarditis were reviewed. RESULTS: Ten (14%) of 69 patients with ventricular ectopic rhythm and an anatomically normal heart had histological evidence of myocarditis or borderline myocarditis. Eight patients received corticosteroids and efficacy was judged by regular 24 hour Holter monitoring. Total resolution of arrhythmia was seen in four, improvement in two, and no change in two patients. At follow up (8-39 months, mean 22 months), arrhythmia recurrence was seen in the two patients who showed an improvement but not resolution during treatment. Both received azathioprine with further reduction in ectopy rates. Patients who responded to treatment were symptomatic (six of six patients) at presentation compared with those who did not respond to treatment (none of two patients) who were not symptomatic. Five patients had a repeat biopsy specimen taken which confirmed histological improvement. CONCLUSIONS: Steroid treatment seems to benefit a subset of children with ventricular ectopic rhythm and a biopsy diagnosis of myocarditis or borderline myocarditis. Because it can identify a treatable cause for the ventricular arrhythmia, endomyocardial biopsy is a valuable investigation in these patients.

Adolescent↗
PubMed1991

Effects of immunosuppressive therapy in biopsy-proved myocarditis and borderline myocarditis on left ventricular function.

Twenty patients with decreased left ventricular (LV) function and endomyocardial biopsy-proved myocarditis (9 patients) or borderline myocarditis (11 patients) were studied to determine whether these 2 histologic subsets of patients with inflammatory heart disease differed in their response to a 6- to 8-week course of immunosuppressive therapy. All patients received a regimen of prednisone, 1.0 mg/kg/day, and azathioprine, 1.5 mg/kg/day, followed by repeat endomyocardial biopsy and reevaluation of LV function. LV function improved significantly in the group with borderline myocarditis, as assessed by LV stroke work--end-diastolic volume ratio (0.26 +/- 0.17 to 0.54 +/- 0.31 kg.m.ml-1, p less than 0.02), heart rate corrected velocity of circumferential shortening (0.49 +/- 0.30 to 0.80 +/- 0.29 circ.s-1, p less than 0.05), and LV ejection fraction (0.30 +/- 0.15 to 0.47 +/- 0.13, p less than 0.05). LV end-diastolic and end-systolic volume indexes also decreased significantly from 129 +/- 40 to 94 +/- 38 (p less than 0.05) and 90 +/- 37 to 49 +/- 26 ml (p less than 0.02), respectively. No significant change in these indexes of LV function or volume occurred in the myocarditis group. Whereas salutory improvements in cardiac output and filling pressures were found in both groups, objective improvement in LV function assessed by complementary indexes of contractility was greatest in the borderline myocarditis group. It is concluded that short-term immunosuppressive therapy improves LV contractile function and appears to be associated with regression of ventricular dilatation in patients with borderline myocarditis to a greater extent than patients with myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Idiopathic giant-cell myocarditis--natural history and treatment. Multicenter Giant Cell Myocarditis Study Group Investigators.

BACKGROUND: Idiopathic giant-cell myocarditis is a rare and frequently fatal disorder. We used a multicenter data base to define the natural history of giant-cell myocarditis and the effect of treatment. METHODS: We identified 63 patients with idiopathic giant-cell myocarditis through journal announcements and direct mailings to cardiovascular centers worldwide. RESULTS: The patients consisted of 33 men and 30 women with an average age of 42.6 years; 88 percent were white, 5 percent were black, 5 percent were Southeast Asian or Indian, and 2 percent were Middle Eastern. Most presented with congestive heart failure (47 patients, or 75 percent), ventricular arrhythmia (9 patients, or 14 percent), or heart block (3 patients, or 5 percent), although in some cases the initial symptoms resembled those of acute myocardial infarction (4 patients). Nineteen percent had associated autoimmune disorders. The rate of survival was worse than among 111 patients with lymphocytic myocarditis in the Myocarditis Treatment Trial (P<0.001); among our patients, the rate of death or cardiac transplantation was 89 percent, and median survival was only 5.5 months from the onset of symptoms. The 22 patients treated with corticosteroids and cyclosporine, azathioprine, or both therapies survived for an average of 12.3 months, as compared with an average of 3.0 months for the 30 patients who received no immunosuppressive therapy (P=0.001). Of the 34 patients who underwent heart transplantation, 9 (26 percent) had a giant-cell infiltrate in the transplanted heart and 1 died of recurrent giant-cell myocarditis. CONCLUSIONS: Giant-cell myocarditis is a disease of relatively young, predominantly healthy adults. Patients usually die of heart failure and ventricular arrhythmia unless cardiac transplantation is performed. Despite the possibility of fatal disease recurrence, transplantation is the treatment of choice for most patients.

Adolescent↗
PubMed1999

Ventricular remodeling in active myocarditis. Myocarditis Treatment Trial.

BACKGROUND: Remodeling of the left ventricle with the development of a spherical cavity occurs in dilated cardiomyopathy and is associated with a poor long-term prognosis. The early effects of myocarditis on left ventricular geometry have not been previously described or correlated with clinical outcome. METHODS: The baseline echocardiograms of 35 patients with biopsy-confirmed myocarditis were compared with 20 normal controls. Left ventricular end-diastolic volume, long axis length, and mid-cavity diameter were measured. The degree of sphericity was expressed as the ratio of the mid-cavity diameter to the long axis length. Left ventricular ejection fraction was assessed by radionuclide angiography. RESULTS: In patients with myocarditis, mean left ventricular volume of 81 +/- 29 mL/m(2) was significantly greater than 50 +/- 8 mL/m(2) in controls (P =.001). Chamber dilatation occurred primarily along the mid-cavity diameter, which measured 5.3 +/- 0.8 cm in patients with myocarditis versus 4.2 +/- 0.4 cm in controls (P =.001). The degree of left ventricular sphericity in patients with myocarditis, 0.64 +/- 0.08, was significantly greater than that of controls, 0.54 +/- 0.04 (P =.001). When patients were stratified according to left ventricular volume, patients with increased left ventricular volume (>75 mL/m(2)) were associated with a more spherical chamber and lower left ventricular ejection fraction than patients with a more normal left ventricular volume (</=75 mL/m(2)). CONCLUSIONS: Active myocarditis is associated with early left ventricular remodeling and the development of a spherical chamber. These changes correlate with ventricular dilatation and reduced left ventricular ejection fraction.

Adult↗
PubMed1992

Genomic detection of enteroviruses in the myocardium--studies on animal hearts with coxsackievirus B3 myocarditis and endomyocardial biopsies from patients with myocarditis and dilated cardiomyopathy.

We examined myocardial tissues for the presence of enteroviral RNA in animal models with experimental coxsackievirus B3 myocarditis and in endomyocardial biopsy samples obtained from patients clinically diagnosed as having dilated cardiomyopathy or myocarditis using polymerase chain reaction (PCR) gene amplification with enterovirus-generic primers and/or coxsackievirus B3-specific primers. In animal models, coxsackievirus B3 was detected in myocardial tissues up to 28 days, 56 days and 180 days after inoculation, in C3H/He mice, A/J mice and Syrian golden hamsters, respectively. The viral genomes were identified by in situ hybridization in myocardial cells and some interstitial cells in and around the myocarditic lesions in animals. In human endomyocardial biopsy samples, enteroviral RNA sequences were detected in 8 (32%) out of 25 patients with clinical dilated cardiomyopathy and in 3 (33%) out of 9 patients with clinical myocarditis. The patients showing histologic findings of myocarditis and clinical features resembling dilated cardiomyopathy had a high incidence (83%) of positive PCR result for enteroviral RNA sequences. Additionally, 25% of patients with dilated cardiomyopathy showing no histologic findings of myocarditis had positive PCR result. This study supports a link between viral myocarditis and dilated cardiomyopathy.

Adult↗
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↗