Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Myocarditis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed2026

Genetically proxied circulating PD-1/PD-L1 levels and broadly defined myocarditis: A bidirectional Mendelian randomization study with exploratory lipidomic analyses.

Myocarditis is an inflammatory myocardial disease with potentially severe outcomes. Programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) regulate immune tolerance, but the association between lifelong genetically proxied circulating PD-1/PD-L1 levels and broadly defined myocarditis remains uncertain. We investigated these associations and explored related plasma lipid species. We conducted bidirectional 2-sample Mendelian randomization using proteomic genome-wide association data from the UK Biobank Pharma Proteomics Project and INTERVAL. FinnGen Release 10 was the primary broadly defined myocarditis outcome, and an independent myocarditis genome-wide association study (GCST90018882) provided outcome-level validation. Complementary estimators, heterogeneity and pleiotropy diagnostics, influence analyses, MR-RAPS, and supportive meta-analyses were performed. Associations with 179 plasma lipid species were examined in exploratory analyses. Higher genetically proxied circulating PD-L1 was inversely associated with broadly defined myocarditis in UKB-PPP (odds ratio [OR] 0.834, 95% confidence interval [CI] 0.698-0.995; P = .0441), and the independent INTERVAL analysis yielded a concordant inverse estimate (OR 0.619, 95% CI: 0.434-0.883; P = .0083); no clear association was observed for PD-1. The MR-RAPS estimate retained the inverse direction; estimates against the independent broadly defined myocarditis dataset were also inverse, and supportive meta-analyses across protein and outcome sources yielded inverse pooled estimates. Reverse MR did not support effects of broadly defined myocarditis liability on circulating PD-1 or PD-L1. Exploratory lipid analyses identified nominal associations requiring confirmation. Higher genetically proxied circulating PD-L1 may be associated with a lower risk of broadly defined myocarditis, supporting further investigation of PD-L1-related immune regulation. These findings do not directly estimate the effects of pharmacologic PD-1/PD-L1 blockade. The lipid findings are hypothesis-generating.

Myocarditis↗
PubMed1999

Effects of in vivo administration of anti-B7-1/B7-2 monoclonal antibodies on the survival of mice with chronic ongoing myocarditis caused by Coxsackievirus B3.

In acute myocarditis and dilated cardiomyopathy, it has previously been reported that antigen-specific T-cells infiltrate the heart and play an important role in the myocardial damage involved. For antigen-specific T-cell activation to occur, it is necessary for the T-cell to receive co-stimulatory signals provided by co-stimulatory molecules expressed on the antigen-presenting cell (APC), as well as the main signal provided by binding of the T-cell receptor (TCR) to the antigen. To investigate the roles for the co-stimulatory molecules B7-1 and B7-2 in the development of chronic ongoing viral myocarditis, firstly the expression of B7-1/B7-2 was analysed in the hearts of A/J mice with myocarditis induced by Coxsackievirus B3 (CVB3). Secondly the induction of B7-1/B7-2 on cultured cardiac myocytes treated with interferon (IFN)-gamma was evaluated. Thirdly the effects of the in vivo administration of anti-B7-1/B7-2 monoclonal antibodies (MAbs) on the survival of mice with viral myocarditis were examined. CVB3-induced myocarditis resulted in enhanced expression of B7-1/B7-2 on cardiac myocytes. The expression of B7-1/B7-2 on cardiac myocytes could be induced by IFN-gamma in vitro. In vivo anti-B7-1 MAb treatment significantly prolonged the survival of mice with myocarditis, whereas anti-B7-2 MAb treatment abrogated the protective effect of anti-B7-1. These findings indicate that distinct roles for B7-1 and B7-2 antigens are involved in the development of viral myocarditis and raise the possibility of immunotherapy with anti-B7-1 MAb to prevent T-cell-mediated cardiac myocyte injury and to improve the prognosis of viral myocarditis.

Animals↗
PubMed1996

Expression of cytokine genes and presence of enteroviral genomic RNA in endomyocardial biopsy tissues of myocarditis and dilated cardiomyopathy.

Viral infection, especially by enteroviruses, has been considered to be the most common cause of myocarditis, which may progress to dilated cardiomyopathy (DCM). Although the mechanism of progression remains uncertain, a cytokine-associated injury of myocytes has been proposed. Using reverse transcriptase polymerase chain reaction (RT-PCR), we examined the expression of interleukin 1 beta (IL-1 beta), IL-6, IL-8 and tumour necrosis factor alpha (TNF-alpha) and the presence of enteroviral genomic RNA in endomyocardial biopsy tissues obtained from patients with myocarditis and DCM. We examined endomyocardial biopsy tissues obtained from 6 patients with myocarditis, 21 with DCM and 15 with non-infectious cardiac diseases as controls. In patients with myocarditis, endomyocardial biopsy was performed twice at an interval of 1 month to 8 years after the onset of myocarditis. We used RT-PCR to detect IL-1 beta, IL-6, IL-8 and TNF-alpha genes expression and nested RT-PCR (nRT-PCR) to detect enteroviral genomic RNA. IL-1 beta, IL-6, IL-8 and TNF-alpha genes were expressed in 100% (6/6) and enteroviral genomic RNA in 67% (4/6) of myocarditis patients at the first biopsy. At the second biopsy, IL-1 beta, IL-6, IL-8 and TNF-alpha genes were expressed in none, 50% (3/6), 67% (4/6) and 67% (4/6), respectively, and enteroviral genomic RNA in 67% (4/6). Four patients with myocarditis, in whom IL-8 and TNF-alpha genes and enteroviral genomic RNA were detected, progressed to DCM at the second biopsy. IL-1 beta, IL-6, IL-8 and TNF-alpha genes were expressed in none, 24% (5/21), 38% (8/21), 57% (12/21) of DCM patients, respectively. Enteroviral genomic RNA was detected in 43% (9/21) of DCM. Neither cytokine expression nor enteroviral genomic RNA were detected in the controls. the high incidence of cytokines, especially IL-6, IL-8 and TNF-alpha, expression in myocarditis and DCM, which might be induced by enteroviral infection, suggests that cytokines play an important role in myocytic damage leading to DCM.

Adult↗
PubMed1985

Current problems in establishing quantitative histopathologic criteria for the diagnosis of lymphocytic myocarditis by endomyocardial biopsy.

Both the clinical and the biopsy diagnoses of myocarditis are prone to false-positive and false-negative interpretations. False-positive clinical diagnoses probably most commonly result from a failure to recognize other disorders, such as cardiomyopathy and myocardial infarction, that may mimic myocarditis. False-negative clinical diagnoses may occur in patients with myocarditis in whom the signs and symptoms are atypical, absent, or misinterpreted. The two most common errors made by pathologists that produce false-positive tissue diagnoses appear to be a failure to recognize the number of lymphocytes that occupy the normal myocardial interstitium and a misinterpretation of noninflammatory interstitial cells as lymphocytes. Sampling error may be the most usual cause of false-negative tissue diagnoses. Since myocarditis is characterized by leukocytic and reparative responses, the most important features to evaluate in endomyocardial biopsy tissues are the type, distribution, and extent of the inflammatory infiltrate and the presence and extent of interstitial and endocardial fibrosis. Although no single histopathologic criterion is both sensitive and specific for myocarditis, it appears that quantitative evidence of an interstitial leukocytic infiltrate is currently the best available hallmark for myocarditis in biopsy specimens. It is suggested that a mean lymphocyte count greater than 5.0/high-power (X 400) microscopic field be considered indicative of lymphocytic myocarditis and that a mean count less than this be interpreted as myocarditis only if discrete clusters of lymphocytes are identified, since differentiation of low-grade diffuse infiltrates from expected normal lymphocytic populations is problematic at levels less than 5.0.

Biopsy↗
PubMed2000

Enteroviral and immune mediated myocarditis in SCID mice.

Severe combined immune deficiency (SCID) mice have been used as an animal model to study both the direct cytopathic effect of enteroviruses on the heart in the absence of an effective immune system and to investigate the role of immune mediated processes in the pathogenesis of human myocarditis. The infection of SCID mice with coxsackievirus B3 resulted in severe myocarditis with very high titers of the virus in the myocardium and severe necrosis of myocytes. This direct cytopathic effect caused an impairment of the myocardial function and resulted in a high mortality rate of the infected animals. For the study of the immune mechanisms in human myocarditis, peripheral blood leukocytes of patients with myocarditis, having an impaired left ventricular function without viral persistence in the myocardium, were transferred into SCID mice. As controls peripheral blood leukocytes of normal donors were used. At 60 days after transfer, human immunoglobulines could be demonstrated in the peripheral blood of the SCID mice, however, human autoantibodies against the adenine nucleotide translocator, a myocardial autoantigen, were only present in the animals receiving peripheral blood leukocytes from patients with myocarditis. Cellular infiltrates of human leukocytes in the myocardium and an impaired left ventricular function were also only observed in animals reconstituted with peripheral blood leukocytes from patients. These effects were T cell dependent as shown by differential transfer. These results are of interest for the treatment of human myocarditis, suggesting the avoidance of an immunosuppressive therapy in acute or chronic myocarditis with viral persistence to prevent a direct cytopathic effect in the absence of an effective immune system. However, in the setting of a chronic, (auto-)immunological myocarditis with the proven absence of entero- or adenoviral sequences an immunomodulatory therapy seems to be effective and safe.

Animals↗
PubMed1991

Clinicopathologic description of myocarditis.

Histologic evidence of myocarditis was demonstrated in 35 of 348 patients submitted to endomyocardial biopsy over 5 years. Analysis of the histologic findings and clinical course of these patients resulted in a new clinicopathologic classification of myocarditis in which four distinct subgroups are identified. Patients with fulminant myocarditis become acutely ill after a distinct viral prodrome, have severe cardiovascular compromise, multiple foci of active myocarditis by histologic study and ventricular dysfunction that either resolves spontaneously or results in death. Patients with acute, chronic active and chronic persistent myocarditis have a less distinct onset of illness. Patients with acute myocarditis present with established ventricular dysfunction and may respond to immunosuppressive therapy or their condition may progress to dilated cardiomyopathy. Those with chronic active myocarditis initially respond to immunosuppressive therapy, but they have clinical and histologic relapses and develop ventricular dysfunction associated with chronic inflammatory changes including giant cells on histologic study. Chronic persistent myocarditis is characterized by a persistent histologic infiltrate, often with foci of myocyte necrosis but without ventricular dysfunction despite other cardiovascular symptoms such as chest pain or palpitation.

Acute Disease↗
PubMed1994

Autoantibodies against human ventricular myosin in sera of patients with acute and chronic myocarditis.

OBJECTIVES: The present study investigated the presence of antimyosin autoantibodies in sera of patients with myocarditis and in three control groups: healthy blood donors, patients with alcoholic cardiomyopathy and patients with other cardiac diseases. BACKGROUND: An increasing body of evidence indicates that in the course of myocarditis, autoimmunologic mechanisms may play a pathogenetic role. Animal studies with Coxsackie B3 virus-induced murine myocarditis could demonstrate the appearance of circulating autoantibodies against cardiac myosin. METHODS: Sera were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western blot with human left ventricular myosin as antigen. RESULTS: Seventeen (42%) of 40 serum samples from patients with myocarditis showed antibody-binding against myosin, whereas only 1 (2.5%) of 39 samples from healthy blood donors and 9 (21%) of 43 samples from patients with other cardiac diseases showed autoantibodies against myosin (p < 0.05 vs. myocarditis). In sera from patients with alcoholic cardiomyopathy (n = 12), no antibodies against human ventricular myosin could be detected. In Western blots, the antimyosin antibodies in patients with myocarditis bound to the myosin heavy chain. Using protein-A sepharose chromatography, it could be shown that the antimyosin autoantibodies are of the immunoglobulin G (IgG) type. In ELISA, the antimyosin autoantibodies bind equally to myosin prepared from either cardiac or skeletal muscle, respectively. CONCLUSIONS: These results demonstrate the presence of autoantibodies against human ventricular myosin in patients with myocarditis. The prevalence of these autoantibodies is significantly higher in patients with myocarditis than in patients with other cardiac diseases. No organ specificity of the autoantibodies could be detected.

Acute Disease↗
PubMed1997

Review and hypothesis: the eosinophil and peripartum heart disease (myocarditis and coronary artery dissection)--coincidence or pathogenetic significance?

OBJECTIVES: To examine a possible relationship between peripartum heart disease (myocarditis and spontaneous coronary dissection) and the presence of eosinophils. BACKGROUND: Eosinophils have been shown to have potential collagenolytic and cytotoxic activity. Eosinophils may play a role in postpartum uterine involution. The presence of eosinophils in spontaneous coronary dissection and myocarditis in the postpartum period raises the possibility of a role for eosinophils in these diseases. METHODS: We reviewed the files of one of us (S.M.F.) for cases of peripartum myocarditis and spontaneous coronary dissection and assessed the frequency of eosinophilic inflammation. Seventeen postpartum myocarditis and/or cardiomyopathy cases were found and two spontaneous coronary dissections. Fifteen sex- and age-matched controls on non-postpartum myocarditis and borderline myocarditis were evaluated and eosinophil counts per unit area compared. Also, a Medline search of all previously published cases of spontaneous coronary dissection was performed back to 1966. RESULTS: Of the 16 heart biopsies and one autopsy in the peripartum period, 10 were shown to contain easily identified eosinophils (6 myocarditis, 1 borderline, 3 cardiomyopathy). When presence of eosinophils was compared with the control group, a statistically significant difference was obtained (P = 0.036). The two new spontaneous coronary dissection cases had eosinophils along the dissection plane; the literature search produced 13 of 24 autopsied peripartum spontaneous coronary dissections with eosinophils for a total of 15 of 26 with our cases. CONCLUSIONS: An association exists between eosinophils and peripartum cardiac disease (myocarditis and spontaneous coronary dissection). The role of eosinophils in labor, uterine involution and collagenolysis and the possible relation to cardiac disease are discussed.

Aortic Dissection↗
PubMed1997

Late persistent expressions of ICAM-1 and VCAM-1 on myocardial tissue in children with lymphocytic myocarditis.

BACKGROUND: Both intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been implicated in cardiac allograft rejection. However, there is little information about the relationship between the expression of these adhesion molecules and myocarditis in children. METHODS AND RESULTS: Immunoreactivities of ICAM-1 and VCAM-1 were examined by enzyme immunoassay in 31 biopsy specimens obtained from 11 pediatric patients with biopsy-proven myocarditis or cardiomyopathy. Five of the 11 patients had clear evidence of acute myocarditis. The other 6 had ECG abnormalities identified by mass screening for heart disease, and subsequently had been histologically diagnosed as having non-specific cardiomyopathy. The period between onset of myocarditis or identification of ECG abnormality and immunohistochemical studies was 23 to 60 days and 8 months to 3 years, respectively. Expression of ICAM-1 and VCAM-1 was assessed by counting ICAM-1 and VCAM-1 positive vessels and dividing by the total number of vessels. ICAM-1 was significantly present on 81% (P < 0.01) of myocardial tissue samples in the 5 patients with healing-stage acute myocarditis, and on 45% (P < 0.05) in the remaining 6 patients with non-specific cardiomyopathy, compared with 24% in control specimens obtained from right ventricular muscle resected at surgery for tetralogy of Fallot. VCAM-1 was also present on 50% (P < 0.05) of the samples from the 5 patients with acute myocarditis, but was not present in those with non-specific cardiomyopathy. CONCLUSION: This persistent expression of ICAM-1 suggests that myocardial cell damage may persist immunologically for a long period in myocarditis. In addition, immunostaining for these adhesion molecules may be diagnostic value in clinically silent lymphocytic myocarditis and chronic cardiomyopathy.

Adolescent↗
PubMed2002

Giant cell myocarditis: clinical presentation, bridge to transplantation with mechanical circulatory support, and long-term outcome.

BACKGROUND: The multicenter Giant Cell Myocarditis Registry recorded 64 cases from 36 centers before 1996. The median transplant-free survival of 30 patients without immunosuppression was 3 months. Of 34 patients who received heart transplantations, 9 experienced recurrence of giant cell myocarditis in their transplanted hearts and 1 patient died. METHODS: We reviewed our experience in 340 heart transplantations since 1984. Unexpected giant cell myocarditis was found in the explanted hearts of 7 patients (6 men and 1 female, aged 18-65 years). RESULTS: The duration from the onset of symptoms to assist-device implant or transplantation ranged from 11 days to 9 years, whereas the time interval from referral or deterioration ranged from 2 days to 4 months. Four patients required mechanical circulatory support before surgery (total artificial hearts in 2 and left ventricular assist devices in 2), and 3 patients required inotropic drugs. Six patients are alive with no sign of recurrent giant cell myocarditis at 12 to 113 months after surgery. One patient died suddenly 75 months after surgery, and autopsy showed severe graft vascular disease with no recurrence of giant cell myocarditis. Surveillance, right ventricular endomyocardial biopsy specimens showed recurrent asymptomatic giant cell myocarditis in 3 patients at 5 to 13 months after surgery, and found recurrence in 1 patient 30 months after surgery. This patient received augmented immunosuppression. CONCLUSIONS: Giant cell myocarditis often is not diagnosed before transplantation. It can present as dilated cardiomyopathy with late deterioration, or it can present with rapid hemodynamic deterioration. In our experience, these patients can be bridged successfully to transplant with mechanical circulatory assist. Giant cell myocarditis may recur after transplantation but may respond to augmented immunosuppression.

Adolescent↗
PubMed2002

Myocarditis and sudden infant death syndrome.

This is a retrospective survey of findings of myocarditis in 437 infants under the age of 1 year who died suddenly and unexpectedly between 1982 and 1999, and were investigated at the Department of Forensic Medicine in Stockholm, Sweden. Myocarditis was diagnosed in 69/410 infants who died naturally (16.8%) and in 2/27 violent deaths (7.4%). In 43/410 natural deaths (10.5%) the myocarditis was an isolated finding and the only explanation for cause of death and in 26 (6.3%) there were additional possible causes of death. The myocarditis was acute in 45/69 and chronic in 24/69 natural deaths, and was found to occur as early as at a few weeks of age. No specific risk factors were found when reviewing critical time of year, age, gender, previous symptoms, sleeping position, aspiration of gastric contents and environmental factors in infant deaths with finding of myocarditis compared to 313 deaths due to sudden infant death syndrome. Myocarditis was found in 13 of 37 deaths where cultures for cytomegalovirus were positive. More than 50% of the foci of the isolated myocarditis were located in the upper part of the interventricular septum and the adjacent part of the right atrium, areas including parts of the conduction system. This localisation is significant for the cause of death when comparing deaths with myocarditis as an isolated finding to deaths with other possible causes.

Acute Disease↗
PubMed2003

Expression of Toll-like receptor 4 is associated with enteroviral replication in human myocarditis.

Previous studies have demonstrated that inflammatory cytokine expression associated with enteroviral (EV) infection may play an important role in human myocarditis. However, the mechanism of the host immune response against viral pathogens has not been fully understood. The aim of the present study was to determine whether Toll-like receptor 4 (TLR4) and EV RNA are present in human myocarditis. Endomyocardial biopsy samples were obtained from 44 patients with myocarditis and five controls. Levels of plus- and minus-strand EV RNAs and TLR4 mRNA were measured by real-time reverse transcriptase-PCR. Immunohistochemical analysis was performed to identify the cellular source of TLR4 and the EV capsid protein VP1. EV RNA was present in 21 patients with myocarditis and these patients were defined as having either active viral replication ( n =15) or latent viral persistence ( n =6). Neither strand of EV RNA was detected in controls. TLR4 mRNA expression levels were higher in myocarditis patients than in controls (TLR4/glyceraldehyde-3-phosphate dehydrogenase ratio 1.48+/-0.17 compared with 0.08+/-0.06, P <0.001). A positive correlation was found between EV RNA and TLR4 levels (plus-strand vs TLR4: r =0.66, P <0.001; minus-strand vs TLR4: r =0.48, P <0.001). TLR4 immunostaining was observed in infiltrating cells and myocytes in patients with myocarditis. The EV capsid protein VP1 was also found in myocytes. The myocarditis group with EV replication and high levels of TLR4 showed significantly lower systolic function. The present study has shown that increased expression of TLR4 is associated with EV replication and that these RNA levels are related to cardiac dysfunction in human myocarditis.

Adult↗
PubMed1998

[Cardiac troponin T in the diagnosis and follow up of suspected myocarditis].

BACKGROUND AND OBJECTIVE: Results of routine laboratory tests for demonstrating myocardial damage in patients suspected of having myocarditis are often negative. This study was undertaken to ascertain (1) whether measuring Tropinin T (cTnT) in these patients can sensitively determine myocardial cell death, (2) to what extent this correlates with the findings of endomyocardial biopsy, and (3) whether measurement of cTnT can provide noninvasive assessment of the course of myocarditis. PATIENTS AND METHODS: 80 consecutive patients (52 men, 28 women) with clinically suspected myocarditis were investigated. The main clinical symptoms were heart failure (n = 45), angina pectoris (n = 25) or cardiac arrhythmias (n = 10). In most patients the symptoms had developed in temporal relation to a viral infection. Coronary heart disease was excluded in all by coronary angiography. Interventricular septal endomyocardial biopsies were examined histologically and immunohistologically. cTnT was measured with a highly sensitive sandwich-immunoassay. RESULTS: An increased level of cTnT (> 0.1 ng/ml) was demonstrated in 28 of the 80 patients (35%). Myocarditis was diagnosed histologically in only 5 patients, but immunohistologically in 26 of 28 (93%) with a raised cTnT level and in 23 of 52 (44%) with a normal cTnT level. The cTnT level was more frequently elevated in patients with a brief rather than a long history of myocarditis. After 6 months the cTnT level was elevated in only 4 of 28 patients with myocarditis, but the myocardial biopsy showed persisting myocarditis in 14 patients. CONCLUSION: Measurement of cTnT is a very sensitive way of demonstrating myocardial cell damage in patients clinically suspected of having myocarditis. Immunohistological analysis can often provide positive results even if the histological findings are unremarkable. The sensitivity in diagnosing of cTnT is greatest when the patient is tested shortly after the onset of symptoms.

Acute Disease↗
PubMedDate not supplied

[Suspected SIDS and diagnosis of myocarditis].

BACKGROUND: During the last years immunohistochemical techniques have improved the diagnosis of myocarditis using specific markers for quantification of leucocytes and characterization of T-lymphocytes together with the definition of MHC class II Antigens (HLA-DP, DQ, DR), known to be enhanced in cases of myocarditis. These techniques allow the diagnosis of myocarditis in an early stage of the inflammatory process in contrast to the conventional diagnostic with hematoxylin-eosin. MATERIALS AND METHODS: 20 autopsy cases were examined in a retrospective study with conventional histological and immunohistological methods. After routine investigations including toxicological and histological examination of internal organs all cases were considered as cases of Sudden Infant Death Syndrome (SIDS). RESULTS: Increased number of LCA-positive leucocytes and CD-3-positive T-lymphocytes together with enhanced expression of inflammatory marker leads to the diagnosis of a lymphomonocytic myocarditis in three cases, in one case myocarditis could be diagnosed by conventional hematoxylin-eosin staining. In one of these four cases of myocarditis a positive immunohistochemical reaction was found using a new antibody against enteroviruses. CONCLUSION: Immunohistochemical techniques improve diagnosis of myocarditis in cases of suspected sudden infant death syndrome. Further studies using immunohistochemical inflammatory markers to control the incidence of acute myocarditis are necessary.

CD3 Complex↗
PubMed2005

Favourable clinical outcome in patients with cardiogenic shock due to fulminant myocarditis supported by percutaneous extracorporeal membrane oxygenation.

AIMS: The clinical outcome of severe acute myocarditis patients with cardiogenic shock who require circulatory support devices is not well known. We studied the survival and clinical courses of patients with fulminant myocarditis supported by percutaneous extracorporeal membrane oxygenation (ECMO) and compared them with those of patients with acute non-fulminant myocarditis. METHODS AND RESULTS: Patients with acute myocarditis were divided into the following two groups. Fourteen patients who required ECMO for cardiogenic shock were defined as having fulminant myocarditis (F group), whereas 13 patients who had an acute onset of symptoms, but did not have compromised, were defined as having acute non-fulminant myocarditis (NF group). In the F group, 10 patients were weaned successfully from percutaneous ECMO. Therefore, the overall acute survival rate was 71%. Patients who were not weaned from ECMO showed smaller left ventricular end-diastolic and end-systolic dimensions, thicker left ventricular wall, and higher creatine phosphokinase MB isoform levels than those who were weaned from ECMO. When compared with patients in the NF group, the fractional shortening in the F group was more severely decreased in the acute phase [F: 10+/-4 vs. NF: 23+/-8% (mean+/-SD), P<0.001], but recovered in the chronic phase (F: 33+/-7 vs. NF: 34+/-6%). The prevalence of adverse clinical events in both groups was similar during the follow-up period of 50 months. CONCLUSION: In patients with fulminant myocarditis, percutaneous ECMO is a highly effective form of a haemodynamic support. Once a patient recovers from inflammatory myocardial damage, the subsequent clinical outcome is favourable, similar to that observed in patients with acute non-fulminant myocarditis.

Acute Disease↗
PubMed1996

Clinical value of echocardiographic tissue characterization in the diagnosis of myocarditis.

Inflammatory changes in the myocardium have been visually observed as alterations on echocardiograms. The goal of this study was to determine how these myocardial changes affect the texture of echocardiographic images, and how these could be described through quantitative texture analysis. The results of 142 endomyocardial biopsies were compared with those of texture analysis in echocardiograms of 106 patients suspected of having myocarditis. There were 52 cases of biopsy-proven acute myocarditis, 12 of persistent myocarditis, nine of healed myocarditis without fibrosis, 17 of healed myocarditis with fibrosis, and 35 cases of cardiomyopathy. Eight myocardial biopsies exhibited no pathological changes and nine patients had other cardiac problems. The echocardiograms of a control group of 24 healthy subjects were also evaluated by texture analysis. Three texture parameters were able to differentiate between normal and abnormal myocardium. The mean grey value, i.e. average brightness, was appreciably higher in cases of myocarditis than in control subjects, whereas one co-occurrence and one run length feature had markedly decreased. We conclude that myocarditis and fibrosis induce changes in echocardiographic image texture, i.e. increases in brightness, heterogeneity, and contrast. Performing digital image texture analysis of echocardiograms makes it possible to distinguish between myocarditis and normal myocardium.

Adult↗
PubMed1996

Reovirus-induced acute myocarditis in mice correlates with viral RNA synthesis rather than generation of infectious virus in cardiac myocytes.

The capacity for different reovirus reassortant viruses to induce acute myocarditis in mice correlates with cytopathogenic effect in primary cultures of murine cardiac myocytes. Multiple viral genes encoding proteins involved in viral RNA synthesis are determinants of this disease. We therefore evaluated the role of viral RNA synthesis in induction of acute myocarditis by infecting primary cultures of cardiac myocytes with a panel of myocarditic and nonmyocarditic viruses and quantitating RNA synthesis. RNA synthesis correlated with induction of myocarditis and with the S1 and M1 reovirus genes. Since one consequence of viral RNA synthesis is generation of infectious virus, we looked next at viral yield from cardiac myocyte cultures. Yield of infectious virus at an early time postinfection or as a final yield from primary infections did not correlate with myocarditis, but instead both correlated with the S1 gene. The S1 gene also determined the fraction of cells infected during primary infections in the culture, which varied dramatically between viruses. Viral yields per infected cell were similar for most myocarditic and nonmyocarditic reoviruses and did not correlate with induction of myocarditis or any reovirus gene. Together, the data provide two insights into reovirus-induced acute myocarditis in mice. First, while the S1 gene. which encodes the viral attachment protein sigma1 (as well as a nonstructural protein, sigma1s, of unknown function) does not determine the myocarditic potential of these viruses, it does determine the efficiency with which they infect cardiac myocytes. Second, while viral RNA synthesis is a determinant of acute myocarditis, this is not due to generation of infectious virus. This finding suggests that some other consequence of viral RNA synthesis, for example, induction of interferon, may determine reovirus-induced acute myocarditis.

Acute Disease↗
PubMed1994

Role of right ventricular endomyocardial biopsy in infants and children with suspected or possible myocarditis.

OBJECTIVES: To assess the diagnostic yield, sampling errors, risks, and therapeutic implications of right ventricular endomyocardial biopsy in children with suspected or possible myocarditis. DESIGN: Retrospective study. SETTING: Tertiary referral centre for paediatric cardiology, cardiac surgery, heart transplantation, and mechanical circulatory support. PATIENTS AND METHODS: Review of clinical and histological findings among 63 consecutive children with possible myocarditis undergoing right ventricular endomyocardial biopsy. Review of cardiac histology at subsequent necropsy or after explantation at time of transplantation. RESULTS: From January 1980 to December 1992, 76 biopsies were performed in 63 children (2 weeks to 18 years of age). In 41 cases, the biopsy was performed for evaluation of dilated cardiomyopathy. The median interval from onset of symptoms was one month. Eight children (20%; all with a history of less than six weeks duration) had biopsy proved myocarditis. Five of the eight children made a full recovery, including four who presented in cardiogenic shock. By contrast, only three of 33 children without evidence of myocarditis showed recovery of ventricular function. The whole heart was available for histological examination in 23 patients. Myocarditis was confirmed in one patient, and no evidence of myocarditis was found in the remaining 22 (all with negative biopsies). One procedure related death occurred in a 2 week old infant with dilated cardiomyopathy. In 22 cases, biopsy was performed for the evaluation of arrhythmia. Only one biopsy showed myocarditis. CONCLUSIONS: The diagnostic yield of a biopsy is low in children with arrhythmias. In children presenting with profound ventricular dysfunction, a diagnosis of acute myocarditis may avoid premature consideration of transplantation as this group has an important potential for full recovery. In less critically ill patients and in those with a longer duration of symptoms the justification for biopsy is not as clear and the procedure is not without risk.

Acute Disease↗