Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.
A heterogeneous group of infections produced by coxsackieviruses, including HERPANGINA, aseptic meningitis (MENINGITIS, ASEPTIC), a common-cold-like syndrome, a non-paralytic poliomyelitis-like syndrome, epidemic pleurodynia (PLEURODYNIA, EPIDEMIC) and a serious MYOCARDITIS.
A species of ENTEROVIRUS infecting humans and containing 36 serotypes. It is comprised of all the echoviruses and a few coxsackieviruses, including all of those previously named coxsackievirus B.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A form of CARDIAC MUSCLE disease that is characterized by ventricular dilation, VENTRICULAR DYSFUNCTION, and HEART FAILURE. Risk factors include SMOKING; ALCOHOL DRINKING; HYPERTENSION; INFECTION; PREGNANCY; and mutations in the LMNA gene encoding LAMIN TYPE A, a NUCLEAR LAMINA protein.
A disease of the CARDIAC MUSCLE developed subsequent to the initial protozoan infection by TRYPANOSOMA CRUZI. After infection, less than 10% develop acute illness such as MYOCARDITIS (mostly in children). The disease then enters a latent phase without clinical symptoms until about 20 years later. Myocardial symptoms of advanced CHAGAS DISEASE include conduction defects (HEART BLOCK) and CARDIOMEGALY.
A genus of the family PICORNAVIRIDAE whose members preferentially inhabit the intestinal tract of a variety of hosts. The genus contains many species. Newly described members of human enteroviruses are assigned continuous numbers with the species designated "human enterovirus".
Disease having a short and relatively severe course.
Infections caused by viruses of the genus CARDIOVIRUS, family PICORNAVIRIDAE.
The type species of CARDIOVIRUS causing encephalomyelitis and myocarditis in rodents, pigs, and monkeys. Infection in man has been reported with CNS involvement but without myocarditis.
Myosin type II isoforms found in cardiac muscle.
The innermost layer of the heart, comprised of endothelial cells.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
Infections produced by reoviruses, general or unspecified.
Inflammation of the PERICARDIUM from various origins, such as infection, neoplasm, autoimmune process, injuries, or drug-induced. Pericarditis usually leads to PERICARDIAL EFFUSION, or CONSTRICTIVE PERICARDITIS.
A diverse superfamily of proteins that function as translocating proteins. They share the common characteristics of being able to bind ACTINS and hydrolyze MgATP. Myosins generally consist of heavy chains which are involved in locomotion, and light chains which are involved in regulation. Within the structure of myosin heavy chain are three domains: the head, the neck and the tail. The head region of the heavy chain contains the actin binding domain and MgATPase domain which provides energy for locomotion. The neck region is involved in binding the light-chains. The tail region provides the anchoring point that maintains the position of the heavy chain. The superfamily of myosins is organized into structural classes based upon the type and arrangement of the subunits they contain.
A general term for diseases produced by viruses.
The hollow, muscular organ that maintains the circulation of the blood.
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
Multinucleated masses produced by the fusion of many cells; often associated with viral infections. In AIDS, they are induced when the envelope glycoprotein of the HIV virus binds to the CD4 antigen of uninfected neighboring T4 cells. The resulting syncytium leads to cell death and thus may account for the cytopathic effect of the virus.
Abnormal fluid retention by the body due to impaired cardiac function or heart failure. It is usually characterized by increase in venous and capillary pressure, and swollen legs when standing. It is different from the generalized edema caused by renal dysfunction (NEPHROTIC SYNDROME).
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The agent of South American trypanosomiasis or CHAGAS DISEASE. Its vertebrate hosts are man and various domestic and wild animals. Insects of several species are vectors.
The type species of ERYTHROVIRUS and the etiological agent of ERYTHEMA INFECTIOSUM, a disease most commonly seen in school-age children.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.

Fatal Serratia marcescens meningitis and myocarditis in a patient with an indwelling urinary catheter. (1/1509)

Serratia marcescens is commonly isolated from the urine of patients with an indwelling urinary catheter and in the absence of symptoms is often regarded as a contaminant. A case of fatal Serratia marcescens septicaemia with meningitis, brain abscesses, and myocarditis discovered at necropsy is described. The patient was an 83 year old man with an indwelling urinary catheter who suffered from several chronic medical conditions and from whose urine Serratia marcescens was isolated at the time of catheterisation. Serratia marcescens can be a virulent pathogen in particular groups of patients and when assessing its significance in catheter urine specimens, consideration should be given to recognised risk factors such as old age, previous antibiotic treatment, and underlying chronic or debilitating disease, even in the absence of clinical symptoms.  (+info)

Enteroviral RNA replication in the myocardium of patients with left ventricular dysfunction and clinically suspected myocarditis. (2/1509)

BACKGROUND: Previous studies dealing with the detection of enteroviral RNA in human endomyocardial biopsies have not differentiated between latent persistence of the enteroviral genome and active viral replication. Enteroviruses that are considered important factors for the development of myocarditis have a single-strand RNA genome of positive polarity that is transcribed by a virus-encoded RNA polymerase into a minus-strand mRNA during active viral replication. The synthesis of multiple copies of minus-strand enteroviral RNA therefore occurs only at sites of active viral replication but not in tissues with mere persistence of the viral genome. METHODS AND RESULTS: We investigated enteroviral RNA replication versus enteroviral RNA persistence in endomyocardial biopsies of 45 patients with left ventricular dysfunction and clinically suspected myocarditis. Using reverse-transcriptase polymerase chain reaction in conjunction with Southern blot hybridization, we established a highly sensitive assay to specifically detect plus-strand versus minus-strand enteroviral RNA in the biopsies. Plus-strand enteroviral RNA was detected in endomyocardial biopsies of 18 (40%) of 45 patients, whereas minus-strand RNA as an indication of active enteroviral RNA replication was detected in only 10 (56%) of these 18 plus-strand-positive patients. Enteroviral RNA was not found in biopsies of the control group (n=26). CONCLUSIONS: These data demonstrate that a significant fraction of patients with left ventricular dysfunction and clinically suspected myocarditis had active enteroviral RNA replication in their myocardium (22%). Differentiation between patients with active viral replication and latent viral persistence should be particularly important in future studies evaluating different therapeutic strategies. In addition, molecular genetic detection of enteroviral genome and differentiation between replicating versus persistent viruses is possible in a single endomyocardial biopsy.  (+info)

Chlamydia infections and heart disease linked through antigenic mimicry. (3/1509)

Chlamydia infections are epidemiologically linked to human heart disease. A peptide from the murine heart muscle-specific alpha myosin heavy chain that has sequence homology to the 60-kilodalton cysteine-rich outer membrane proteins of Chlamydia pneumoniae, C. psittaci, and C. trachomatis was shown to induce autoimmune inflammatory heart disease in mice. Injection of the homologous Chlamydia peptides into mice also induced perivascular inflammation, fibrotic changes, and blood vessel occlusion in the heart, as well as triggering T and B cell reactivity to the homologous endogenous heart muscle-specific peptide. Chlamydia DNA functioned as an adjuvant in the triggering of peptide-induced inflammatory heart disease. Infection with C. trachomatis led to the production of autoantibodies to heart muscle-specific epitopes. Thus, Chlamydia-mediated heart disease is induced by antigenic mimicry of a heart muscle-specific protein.  (+info)

From myocarditis to cardiomyopathy: mechanisms of inflammation and cell death: learning from the past for the future. (4/1509)

A progression from viral myocarditis to dilated cardiomyopathy has long been hypothesized, but the actual extent of this progression has been uncertain. However, a causal link between viral myocarditis and dilated cardiomyopathy has become more evident than before with the tremendous developments in the molecular analyses of autopsy and endomyocardial biopsy specimens, new techniques of viral gene amplification, and modern immunology. The persistence of viral RNA in the myocardium beyond 90 days after inoculation, confirmed by the method of polymerase chain reaction, has given us new insights into the pathogenesis of dilated cardiomyopathy. Moreover, new knowledge of T-cell-mediated immune responses in murine viral myocarditis has contributed a great deal to the understanding of the mechanisms of ongoing disease processes. Apoptotic cell death may provide the third concept to explain the pathogenesis of dilated cardiomyopathy, in addition to persistent viral RNA in the heart tissue and an immune system-mediated mechanism. Beneficial effects of alpha1-adrenergic blocking agents, carteolol, verapamil, and ACE inhibitors have been shown clinically and experimentally in the treatment of viral myocarditis and dilated cardiomyopathy. Antiviral agents should be more extensively investigated for clinical use. The rather discouraging results obtained to date with immunosuppressive agents in the treatment of viral myocarditis indicated the importance of sparing neutralizing antibody production, which may be controlled by B cells, and raised the possibility of promising developments in immunomodulating therapy.  (+info)

Global biventricular dysfunction in patients with asymptomatic coronary artery disease may be caused by myocarditis. (5/1509)

BACKGROUND: The causal role of asymptomatic critical coronary artery obstruction in patients presenting with severe global biventricular dysfunction but no evidence of myocardial infarction is uncertain. METHODS AND RESULTS: Among 291 patients aged >40 years undergoing a noninvasive (2-dimensional echocardiography) and invasive (catheterization, coronary angiography, and biventricular endomyocardial biopsy, 6 to 8 samples/patient) cardiac study because of progressive heart failure (New York Heart Association functional class III or IV) with global biventricular dysfunction and no history of myocardial ischemic events, 7 patients (2.4%; 7 men; mean age, 49+/-6.9 years) had severe coronary artery disease (3 vessels in 4 patients; 2 vessels in 1 patient, proximal occlusion of left anterior descending coronary artery in 2 patients). Left ventricular end-diastolic diameter and ejection fraction by 2-dimensional echocardiography were 73+/-10.5 mm and 23+/-6.5%, respectively, and right ventricular end-diastolic diameter and ejection fraction were 39+/-7 mm and 29+/-7.2%, respectively. Biopsy specimens showed extensive lymphocytic infiltrates with focal myocytolysis meeting the Dallas criteria for myocarditis in all patients (in 5 patients with and 2 patients without fibrosis). Cardiac autoantibodies were detected with indirect immunofluorescence in the serum of 2 patients with active myocarditis. The 2 patients with active inflammation received prednisone (1 mg. kg-1. d-1 for 4 weeks followed by 0.33 mg. kg-1. d-1 for 5 months) and azathioprine (2 mg. kg-1. d-1 for 5 months) in addition to conventional drug therapy for heart failure. At 8-month overall follow-up, cardiac volume and function improved considerably in immunosuppressed patients but remained unchanged in conventionally treated patients, of whom 1 died. CONCLUSIONS: Global biventricular dysfunction in patients with severe asymptomatic coronary artery disease and no evidence of previous myocardial infarction may be caused by myocarditis. Histologic findings may influence the treatment.  (+info)

Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction. (6/1509)

BACKGROUND: The use of molecular biological techniques has demonstrated the importance of enteroviral infection of the myocardium in the pathogenesis of myocarditis and dilated cardiomyopathy in adults and adenovirus and enterovirus infection in children. The aim of this study was to determine the frequency of adenoviral infection of the myocardium of adults with impaired left ventricular function of unknown origin. METHODS AND RESULTS: Nested polymerase chain reaction (nPCR) was used to determine the frequency of detection of adenoviral DNA and enteroviral RNA in myocardial tissue samples from 94 adult patients with idiopathic left ventricular dysfunction and 14 control patients. Histological and immunohistological analyses were performed to detect myocardial inflammation. Adenoviral genomic DNA was detected by nPCR in 12 of the 94 patients with left ventricular dysfunction (in each case, adenovirus type 2), whereas enteroviral RNA was detected in another 12 patients. All control samples were negative for both viruses. In all patients, active myocarditis was excluded according to the Dallas criteria. However, there was significantly decreased CD2, CD3, and CD45RO T lymphocyte counts in the adenovirus-positive group compared with the adenovirus-negative group (P<0.05), whereas no differences were associated with enterovirus infection. CONCLUSIONS: Although enteroviruses are an important causative agent in the pathogenesis of myocarditis and dilated cardiomyopathy, this study shows that adenovirus infection is also important in the pathogenesis of left ventricular failure in adults. However, the pathogenetic basis of disease associated with adenovirus infection may be different than that after infection with other agents, particularly with respect to activation of the host immune response.  (+info)

A case of eosinophilic myocarditis complicated by Kimura's disease (eosinophilic hyperplastic lymphogranuloma) and erythroderma. (7/1509)

This report describes a patient with eosinophilic myocarditis complicated by Kimura's disease (eosinophilic hyperplastic lymphogranuloma) and erythroderma. A 50-year-old man presented with a complaint of precordial pain. However, the only abnormal finding on examinatioin was eosinophilia (1617 eosinophils/microl). Three years later, the patient developed chronic eczema, and was diagnosed with erythroderma posteczematosa. One year later, a tumor was detected in the right auricule, and a diagnosis of Kimura's disease was made, based on the biopsy findings. The patient developed progressive dyspnea 6 months later and was found to have cardiomegaly and a depressed left ventricular ejection fraction (17%). A diagnosis of eosinophilic myocarditis was made based on the results of a right ventricular endomyocardial biopsy. The eosinophilic myocarditis and erythrodrema were treated with steroids with improvement of both the eosinophilia and left ventricular function.  (+info)

Rheumatic chorea in northern Australia: a clinical and epidemiological study. (8/1509)

To describe the epidemiology and clinical features of Sydenham's chorea in the Aboriginal population of northern Australia a review was conducted of 158 episodes in 108 people: 106 were Aborigines, 79 were female, and the mean age was 10.9 years at first episode. Chorea occurred in 28% of cases of acute rheumatic fever, carditis occurred in 25% of episodes of chorea, and arthritis in 8%. Patients with carditis or arthritis tended to have raised acute phase reactants and streptococcal serology. Two episodes lasted at least 30 months. Mean time to first recurrence of chorea was 2.1 years compared with 1.2 years to second recurrence. Established rheumatic heart disease developed in 58% of cases and was more likely in those presenting with acute carditis, although most people who developed rheumatic heart disease did not have evidence of acute carditis with chorea. Differences in the patterns of chorea and other manifestations of acute rheumatic fever in different populations may hold clues to its pathogenesis. Long term adherence to secondary prophylaxis is crucial following all episodes of acute rheumatic fever, including chorea, to prevent recurrence.  (+info)

We report the case of a patient with giant cell myocarditis who was bridged to transplantation with mechanical circulatory support and developed a fatal perioperative hyperacute rejection. The patient had received abundant transfusions that had raised her anti-HLA antibody titers. The cross-match test was positive. No pre-transplantation immunosuppressive therapy had been administered given concomitant infection. The severity and acuteness of the rejection in this case likely reflect the combined effect of preformed anti-HLA antibodies in the context of an active organ-specific immune process at the time of transplantation. This case raises the questions of the need for intensive immunosuppressive therapy before transplantation in giant cell myocarditis and of the management of patients with positive cross-match in the context of a giant cell myocarditis.
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The lymphocyte function-associated antigen 1 (LFA-1) is a member of the beta2-integrin family and plays a pivotal role for T cell activation and leukocyte trafficking under inflammatory conditions. Blocking LFA-1 has reduced or aggravated inflammation depending on the inflammation model. To investigate the effect of LFA-1 in myocarditis, mice with experimental autoimmune myocarditis (EAM) were treated with a function blocking anti-LFA-1 antibody from day 1 of disease until day 21, the peak of inflammation. Cardiac inflammation was evaluated by measuring infiltration of leukocytes into the inflamed cardiac tissue using histology and flow cytometry and was assessed by analysis of the heart weight/body weight ratio. LFA-1 antibody treatment severely enhanced leukocyte infiltration, in particular infiltration of CD11b+ monocytes, F4/80+ macrophages, CD4+ T cells, Ly6G+ neutrophils, and CD133+ progenitor cells at peak of inflammation which was accompanied by an increased heart weight/body weight ratio. Thus,
The inflammatory heart disease myocarditis leads to dilated cardiomyopathy and has been associated with a viral aetiology. The herpesvirus cytomegalovirus induces chronic myocarditis with the development of autoimmunity. Murine models of myocarditis are now well established. Murine cytomegalovirus, a natural pathogen of mice, induces both acute and chronic phases of myocarditis in the susceptible BALB/c mouse strain. Early treatment with the antiviral drugs ganciclovir and cidofovir has been shown to reduce the severity of myocarditis. However, treatment with antivirals in the late stages of infection has limited effectiveness for prevention of the chronic phase of disease. The immunological events in the progression to this chronic cardiac disease have been recently described. New knowledge of the immunopathogenesis of myocarditis can be utilized in the development of strategic antiviral and immunotherapeutic regimes.. ...
TY - JOUR. T1 - Acute Myocarditis with Infarct-like Presentation in a Pediatric Population: Role of Cardiovascular Magnetic Resonance. AU - Martinez-Villar, Maria. AU - Gran, Ferran. AU - Sabaté-Rotés, Anna. AU - Tello-Montoliu, Antonio. AU - Castellote, Amparo. AU - Figueras-Coll, Marc. AU - Ferrer, Queralt. AU - Roses-Noguer, Ferran. PY - 2018/1/1. Y1 - 2018/1/1. N2 - © 2017, Springer Science+Business Media, LLC. Chest pain is a typical symptom of acute myocarditis in adolescents. It may be indistinguishable from myocardial ischemia so it is called infarct-like pattern. Cardiovascular magnetic resonance has an important role as a non-invasive diagnostic tool. The aim of our study is to provide a description of an acute myocarditis series with infarct-like pattern and to evaluate the cardiovascular magnetic resonance role in a pediatric population. We included all pediatric patients (0-16 years) admitted to our hospital (May 2007-May 2016) with clinical diagnosis of acute myocarditis and ...
Patients with myocarditis tend to be young and outcome can be highly variable. In this analysis, the authors show that patients with biopsy-proven myocarditis warrant close clinical follow-up, especially if abnormalities on CMR are noted. Examining survival based on the presence of LGE, the survival curves separated late (more than 1 year after presentation). Because LGE represents scar, LGE likely identifies a ventricle less likely to recover after the initial viral insult. While this is a low-powered study due to the fact that it is a single-center analysis of an uncommon disease, LGE identified 97% (28 of 29) of patients who had a cardiac death from myocarditis. However, only 28% (28 of 99) of myocarditis patients with LGE died. While CMR sensitivity for the detection of myocarditis is poor (53%), it identifies higher risk myocarditis patients. Patients with myocarditis who have LGE should be watched closely for several years. However, data are insufficient to become complacent in those ...
Recent clinical studies have reinforced the importance of sex-related differences in the pathogenesis of cardiovascular diseases, with an increased incidence and mortality in men. Similar to humans, male BALB/c mice infected with coxsackievirus B3 (CVB3) develop more severe inflammation in the heart even though viral replication is no greater than in females. We show that TLR4 and IFN-gamma levels are significantly elevated and regulatory T cell (Treg) populations significantly reduced in the heart of males following CVB3 infection, whereas females have significantly increased T cell Ig mucin (Tim)-3, IL-4 and Treg. Blocking Tim-3 in males significantly increases inflammation and TLR4 expression while reducing Treg. In contrast, defective TLR4 signaling significantly reduces inflammation while increasing Tim-3 expression. Cross-regulation of TLR4 and Tim-3 occurs during the innate and adaptive immune response. This novel mechanism may help explain why inflammatory heart disease is more severe in males.
Myocarditis has an estimated incidence of 10 in 100 000 and is the most common acquired cause of cardiac failure requiring heart transplant in children.[1,2] Viruses form the main aetiological basis, with Coxsackie B virus being responsible for the majority of viral myocarditis cases.[2] The clinical presentation of myocarditis varies from mild fever, flu-like symptoms and malaise to complete cardiovascular collapse, being acute fulminant myocarditis (AFM).[3] AFM is characterised by sudden onset of severe and extensive haemodynamic compromise.[4] Complete atrioventricular heart block (CAVB) is a rare complication of myocarditis and contributes to further haemodynamic compromise.[5] Although more dramatic in its presentation, if it is managed aggressively with mechanical circulatory support, affected patients may have full recovery and less risk of developing dilated cardiomyopathy.[4] In a limited-resource setting where mechanical cardiac support is not available, immediate recognition, ...
This is an update of a previous review. Case reports and case series have described dramatic responses to intravenous immunoglobulin (IVIG) in people with presumed viral myocarditis, and its administration has become commonplace. The primary objective of this review was to compare transplant-free survival of adults and children with presumed viral myocarditis treated with IVIG versus those who did not receive IVIG. A secondary objective was to determine if a group of patients with presumed viral myocarditis could be identified (on the basis of age, duration of symptoms, acuity of onset of symptoms, cardiac function at presentation, virological results or the presence or absence of histological evidence of acute myocarditis on cardiac biopsy in patients in whom a biopsy was performed) who would be the most likely to benefit from IVIG. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (2013, Issue 12 of 12), the Database of Abstracts of Reviews of Effects (DARE) (2013, Issue ...
近五年发表SCI论文. 1. Zhang H, Yue Y, Sun T, Wu X, Xiong S. Transmissible endoplasmic reticulum stress from myocardiocytes to macrophages is pivotal for the pathogenesis of CVB3-induced viral myocarditis. Scientific reports. Feb 08 2017;7:42162.. 2. Qi X, Xiong S. Intein-mediated backbone cyclization of VP1 protein enhanced protection of CVB3-induced viral myocarditis. Scientific reports. Feb 02 2017;7:41485.. 3. Fan X, Yue Y, Xiong S. Incorporation of a bi-functional protein FimH enhances the immunoprotection of chitosan-pVP1 vaccine against coxsackievirus B3-induced myocarditis. Antiviral research. Jan 28 2017;140:121-132.. 4. Wang C, Dong C, Xiong S. IL-33 enhances macrophage M2 polarization and protects mice from CVB3-induced viral myocarditis. Journal of molecular and cellular cardiology. Dec 29 2016;103:22-30.. 5. Dong N, Dong C, Xiong S. Janus effects of ADAR1 on CVB3-induced viral myocarditis at different infection stages. International journal of cardiology. Nov 15 ...
The course and response to treatment in acute lymphocytic myocarditis are conventionally monitored by endomyocardial biopsy performed every 3-12 weeks. A patient with a short history (five days) of acute myopericarditis of unknown aetiology presented in cardiogenic shock with evidence of severe systolic dysfunction on the echocardiogram. The initial biopsy specimen showed histologically unequivocal myocarditis. Repeat endomyocardial biopsy after four days of treatment with steroids and azathioprine showed substantial histological improvement, a reduction in cellular infiltrate and myocardial necrosis, and interstitial fibrosis. Serial biopsies at 2 weeks and then 1, 2, 4, 5, 8, and 14 months after the initial biopsy showed progressive clearing of cellular infiltrate, increasing interstitial fibrosis, and compensatory myocyte hypertrophy by 4 months. At 14 months scattered lymphocytes persisted but myocyte abnormalities had resolved completely. The patient remained symptom free and systolic ...
TY - JOUR. T1 - Contribution of the innate immune system to autoimmune myocarditis. T2 - A role for complement. AU - Kaya, Ziya. AU - Afanasyeva, Marina. AU - Wang, Yan. AU - Dohmen, K. Malte. AU - Schlichting, Jens. AU - Tretter, Theresa. AU - Fairweather, DeLisa. AU - Holers, V. Michael. AU - Rose, Noel R.. PY - 2001. Y1 - 2001. N2 - Myocarditis is a principal cause of heart disease among young adults and is often a precursor of heart failure due to dilated cardiomyopathy. We show here that complement is critical for the induction of experimental autoimmune myocarditis and that it acts through complement receptor type I (CR1) and type 2 (CR2). We also found a subset of CD44hiCD62Llo T cells that expresses CR1 and CR2 and propose that both receptors are involved in the expression of B and T cell activation markers, T cell proliferation and cytokine production. These findings provide a mechanism by which activated complement, a key product of the innate immune response, modulates the induction ...
Acute myocardial damage similar to that seen in human myocarditis occurs in BALB/c mice after infection with coxsackievirus B3 (CB3) or encephalomyocarditis virus (EMC). To investigate the role of antigen-specific T cells in the pathogenesis of this disorder, we compared CB3 disease expression in T cell-deficient, athymic nude (nu/nu) mice, in heterozygote (nu/+) mice with normal T cell function, and in nu/nu mice reconstituted with spleen cells from CB3- or EMC-infected nu/+ mice. Acute myocarditis occurred in both nu/nu and nu/+ mice. Severe myocarditis, however, developed only in nu/+ and nu/nu mice reconstituted with CB3-sensitized T cells, but not in those reconstituted with EMC-sensitized T cells. Myocardial virus titer and serum anti-CB3 antibody production were similar in nu/+ and nu/nu groups. Additionally, the presence of Thy 1.2 (pan T), Ly 1 (precursor of other T cell subsets), and Ly 2 (suppressor/cytotoxic T) positive cells was demonstrated in the myocardium in nu/+ and nu/nu mice ...
Myocardial T1 and T2 mapping are reliable diagnostic markers for the detection and follow up of acute myocarditis. The aim of this study was to compare the diagnostic performance of current mapping measurement approaches to differentiate between myocarditis patients and healthy individuals. Fifty patients with clinically defined acute myocarditis and 30 healthy controls underwent cardiovascular magnetic resonance (CMR). Myocardial T1 relaxation times, T2 relaxation times, left ventricular (LV) function, T2 ratio, early gadolinium enhancement ratio, and presence of late gadolinium enhancement (LGE) were analysed. Native T1 and T2 relaxation times, as well as extracellular volume fraction (ECV) were measured for the entire LV myocardium (global), within the midventricular short axis slice (mSAX), within the midventricular septal wall (ConSept), and within the remote myocardium (remote). Receiver operating characteristics analysis was performed to compare diagnostic performance. All measurement approaches
Background: Myocarditis represents an important cause of chronic dilated cardiomyopathy. Predicting the clinical course of patients with myocarditis is difficult and the prognostic value of current histological markers remains controversial. We tested whether expression of selected microRNAs (miRNAs) in endomyocardial biopsies is related to left ventricular (LV) function and clinical events in patients with myocarditis.. Methods: Endomyocardial biopsies were obtained from patients with non-inflammatory dilated cardiomyopathy (n=22) and histologically proven myocarditis (n=81). Based on literature search, we predefined a set of 6 miRNAs implicated in inflammation (miR-155, miR-146b), heart failure (miR-21, miR-133a), endothelial cell (miR-126) and skeletal muscle function (miR-206). Expression of these miRNAs in endomyocardial biopsies was quantified by RT-PCR.. Results: Expression of miR-133a, miR-206 and miR-155 was markedly upregulated in endomyocardial biopsies from patients with myocarditis ...
TY - JOUR. T1 - Fulminant Myocarditis. T2 - Epidemiology, Pathogenesis, Diagnosis, and Management. AU - Sharma, Ajay Nair. AU - Stultz, Jacob Randolph. AU - Bellamkonda, Nikhil. AU - Amsterdam, Ezra Abraham. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Fulminant myocarditis (FM) is a rare, distinct form of myocarditis that has been difficult to classify. Since 1991, the definition of FM has evolved, and it is currently considered an acute illness with hemodynamic derangement and arrhythmias due to a severe inflammatory process requiring support of cardiac pump function and/or urgent management of serious arrhythmias. Diagnosis is aided through use of biomarkers and cardiac imaging, but endocardial biopsy remains the gold standard. Recent evidence has revealed that patients with FM are significantly more likely to die or require heart transplantation than those with the nonfulminant form, refuting previous studies proposing a paradoxically low mortality in patients with FM. Acute hemodynamic derangement is ...
Fatal myocarditis is a rare complication in immunosuppressed children. Recent reports have linked human herpesvirus 6 (HHV-6) infection, typically a benign infection in childhood, with myocarditis. HHV-6 can reactivate during periods of immunosuppression. Here, we report 2 cases in which children we …
An unusual case of giant cell myocarditis presenting with cardiogenic shock that dramatically responded to conventional dose of steroids and azathioprine is reported. Cardiac recovery was rapid, complete (left ventricular ejection fraction rose to 55
Looking for primary myocarditis? Find out information about primary myocarditis. Inflammation of the myocardium. inflammation of the heart muscle . Myocarditis may be caused by infectious diseases, including viral ones, and by an... Explanation of primary myocarditis
Myocarditis is an inflammation of the myocardium, but only -10% of those affected show clinical manifestations of the disease. To study the immune events of myocardial injuries, various mouse models of myocarditis have been widely used. This study involved experimental autoimmune myocarditis (EAM) induced with cardiac myosin heavy chain (Myhc)-α 334-352 in A/J mice; the affected animals develop lymphocytic myocarditis but with no apparent clinical signs. In this model, the utility of magnetic resonance microscopy (MRM) as a non-invasive modality to determine the cardiac structural and functional changes in animals immunized with Myhc-α 334-352 is shown. EAM and healthy mice were imaged using a 9.4 T (400 MHz) 89 mm vertical core bore scanner equipped with a 4 cm millipede radio-frequency imaging probe and 100 G/cm triple axis gradients. Cardiac images were acquired from anesthetized animals using a gradient-echo-based cine pulse sequence, and the animals were monitored by respiration and pulse
Mfarrej B, Keir M, Dada S, Trikudanathan S, Sayegh MH, Sharpe AH, Guleria I. Anti-CD3 mAb treatment cures PDL1-/-.NOD mice of diabetes but precipitates fatal myocarditis. Clin Immunol. 2011;140 (1) :47-53.
Synonyms for acute isolated myocarditis in Free Thesaurus. Antonyms for acute isolated myocarditis. 1 synonym for myocarditis: myocardial inflammation. What are synonyms for acute isolated myocarditis?
The present study was designed to determine whether the wall thickening seen in acute myocarditis is caused by interstitial edema. The study group comprised 25 patients (idiopathic myocarditis, 17; eosinophilic myocarditis, 8) in whom acute myocardit
Myocarditis is a common cardiac disease. It appears to be a major cause of sudden death, and may progress to chronic dilated cardiomyopathy. From the clinical point of view, there are several challenges unique to the management of patients with myocarditis. The first challenge is to establish the diagnosis of myocarditis, which is usually based on clinical, pathological, or a combination of diagnostic criteria. The second challenge is to follow the disease activity to identify patients who may be at risk of chronic dilated cardiomyopathy development, which seems to be associated with ongoing myocardial inflammation (1) and viral persistence (2).. Cardiac magnetic resonance (CMR) has recently emerged as a noninvasive tool to diagnose myocarditis (3-6), as well as to follow its course in living patients (3,7-9). Three features potentially associated with acute myocardial inflammation may be visualized by CMR: 1) tissue edema, which may result in an elevated T2 signal; 2) capillary leakage, which ...
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Myocarditis means inflammation of the myocardium. The myocardium is the heart muscle. Myocarditis can affect anyone and occur at any age. Causes include the following:. Viral infection. The most common infections causing myocarditis are viruses called Coxsackie B and adenovirus. Other viruses which sometimes cause myocarditis include: echoviruses, influenza (flu), Epstein-Barr virus (glandular fever), rubella (german measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C.. Unknown cause (idiopathic myocarditis). In many people with myocarditis, the cause is not found. However, for the majority of these people it is likely to be caused by a virus that could not be confirmed by a test.. Other causes. Other causes of myocarditis are much less common. They include:. The heart can sometimes become infected by various bacteria, fungi, parasites and other germs. For example:. ...
Aims: Although mortality rate is very high, diagnosis of acute myocarditis remains challenging with conventional tests. We aimed to elucidate the potential role of longitudinal 2-Deoxy-2-\(^{18}\)F-fluoro-D-glucose (\(^{18}\)F-FDG) positron emission tomography (PET) inflammation monitoring in a rat model of experimental autoimmune myocarditis. Methods and results: Autoimmune myocarditis was induced in Lewis rats by immunizing with porcine cardiac myosin emulsified in complete Freunds adjuvant. Time course of disease was assessed by longitudinal \(^{18}\)F-FDG PET imaging. A correlative analysis between in- and ex vivo \(^{18}\)F-FDG signalling and macrophage infiltration using CD68 staining was conducted. Finally, immunohistochemistry analysis of the cell-adhesion markers CD34 and CD44 was performed at different disease stages determined by longitudinal \(^{18}\)F-FDG PET imaging. After immunization, myocarditis rats revealed a temporal increase in 18F-FDG uptake (peaked at week 3), which was ...
Aims: Although mortality rate is very high, diagnosis of acute myocarditis remains challenging with conventional tests. We aimed to elucidate the potential role of longitudinal 2-Deoxy-2-\(^{18}\)F-fluoro-D-glucose (\(^{18}\)F-FDG) positron emission tomography (PET) inflammation monitoring in a rat model of experimental autoimmune myocarditis. Methods and results: Autoimmune myocarditis was induced in Lewis rats by immunizing with porcine cardiac myosin emulsified in complete Freunds adjuvant. Time course of disease was assessed by longitudinal \(^{18}\)F-FDG PET imaging. A correlative analysis between in- and ex vivo \(^{18}\)F-FDG signalling and macrophage infiltration using CD68 staining was conducted. Finally, immunohistochemistry analysis of the cell-adhesion markers CD34 and CD44 was performed at different disease stages determined by longitudinal \(^{18}\)F-FDG PET imaging. After immunization, myocarditis rats revealed a temporal increase in 18F-FDG uptake (peaked at week 3), which was ...
Myocarditis is mainly caused by cardiotropic viruses. In recent time viruses found in endomyocardial biopsies mainly consist of parvovirus B19 (PVB19) and human herpesvirus 6 (HHV6). A definite causal link between virus-genome detection of PVB19 and/or HHV6 (via pcr techniques)and cardiac inflammation and dysfunction is however still missing.. Primary objective:. To determine the prevalence of PVB19 and HHV6 virus genome in heart muscle biopsies of cardiac surgery patients without clinical evidence of myocarditis or myocarditic sequelae. Secondary objectives:. ...
Myocarditis may present with a wide range of symptoms, ranging from mild dyspnea or chest pain that resolves without specific therapy to cardiogenic shock and death. Dilated cardiomyopathy with chronic heart failure is the major long-term sequela of myocarditis. Most often, myocarditis results from common viral infections; less commonly, specific forms of myocarditis may result from other pathogens, toxic or hypersensitivity drug reactions, giant-cell myocarditis, or sarcoidosis. Continue reading Diagnostic Criteria for Myocarditis. ...
Tumor necrosis factor (TNF) and interferon gamma (IFN-gamma) are pluripotent cytokines and have multiple functions during the inflammatory response. Using a murine model of autoimmune myocarditis, we studied the role of TNF and IFN-gamma in myocardial inflammation. Neutralizing monoclonal antibodies against TNF-alpha/beta and IFN-gamma were administered to myosin-immunized A/J mice to assess the effect on the severity of myocardial inflammation. Anti-TNF treatment significantly reduced the severity of myocarditis compared with rat immunoglobulin G or saline controls (p less than 0.0007) when given before myosin immunization. Myosin-specific lymph node T-cell proliferation studies showed no difference in the proliferative response between the anti-TNF-treated mice and controls. Administration of anti-TNF to mice after myosin immunization had no effect on the severity of inflammation. This suggests that TNF is an important mediator early in the pathogenesis of myocardial inflammation in this model ...
The present study shows an inhibitory role of IRAK4 in viral myocarditis. For the first time, we reveal IRAK4 as a double-edged sword in viral myocarditis: It acts as a proinflammatory molecule but also blocks protective cell migration and antiviral responses. The ability of the host to limit viral proliferation while minimizing tissue injury attributable to detrimental proinflammatory responses, thus protecting from autoimmune postviral cardiomyopathy, is a prerequisite of favorable outcome.. IRAK4 is a well-known proinflammatory kinase downstream of all known TLRs except TLR3. It complexes with MyD88, IRAK1, IRAK2, and IRAK-M, phosphorylates IRAK1 and IRAK2, and ultimately contributes to NF-κB and mitogen-activated protein kinase activation for inflammatory cytokine transcription.5,6,16,17 Accordingly, and as reported by our group earlier, IRAK4-deficient mice showed better survival and lower heart inflammation after experimental myocardial infarction.18 In addition, we recently found that ...
How long should viral myocarditis last - I have viral myocarditis for three weeks. At my last check-up I had sinus tachycardia and ejection fraction of 26%. Im on three different meds but Im not getting better. What is the probability for full recovery? How long does it usually take? Silly patient. The best answer for your question is provided by the treating physicians, who have the benefit of your history, exam and an understanding of the tests you have had to date. While it is understandable you want answers. We have no crystal ball with great incite based on your present ejection fraction. This is a serious illness, pay attention to your docs advise and you might do well.
Myocarditis is an inflammation of the myocardium, or middle lining. When the heart becomes inflamed, it cannot pump as well because of the damage done to its cells and swelling. The heart muscle may damage even more if the bodys immune system sends antibodies to try and fight whatever started the inflammation. Sometimes these antibodies attack the tissues of heart instead the cause of myocarditis. If too many heart muscle cells are damaged, the heart muscle weakens. In some cases, this process happens very quickly and results in heart failure or even sudden death. More often, the heart tries to heal itself; the heart muscle heals by changing the damaged or dead heart muscle cells into scar tissue. Scar tissue is not like heart muscle tissue because it does not contract and it cannot help the heart pump blood. If enough scar tissue forms in the heart, it can ultimately lead to congestive heart failure or dilated cardiomyopathy as a consequence of myocarditis.Many people with myocarditis recover ...
Dilated Cardiomyopathy is a chronic myocardial disease characterized by progressive depression of contractile function and ventricular dilatation. It is the leading cause of heart failure and the most common reason for heart transplantation. Besides genetic causes, viral infection and autoimmune response are considered to play a major role in the etiology of the disease. Among different viruses that cause the disease, Coxsackievirus B3 (CVB3) is predominantly associated with the development and progression of the disease. Moreover, Coxsackievirus induced myocarditis in the mouse mimics human myocarditis and dilated cardiomyopathy. In the murine model, the disease progresses over a period of 90 days from acute myocarditis to chronic myocarditis and further develops into dilated cardiomyopathy and congestive heart failure. Though much is known about the progression of the disease, the molecular events occurring after infection with CVB3 are not completely understood. In the current study, ...
Dilated Cardiomyopathy is a chronic myocardial disease characterized by progressive depression of contractile function and ventricular dilatation. It is the leading cause of heart failure and the most common reason for heart transplantation. Besides genetic causes, viral infection and autoimmune response are considered to play a major role in the etiology of the disease. Among different viruses that cause the disease, Coxsackievirus B3 (CVB3) is predominantly associated with the development and progression of the disease. Moreover, Coxsackievirus induced myocarditis in the mouse mimics human myocarditis and dilated cardiomyopathy. In the murine model, the disease progresses over a period of 90 days from acute myocarditis to chronic myocarditis and further develops into dilated cardiomyopathy and congestive heart failure. Though much is known about the progression of the disease, the molecular events occurring after infection with CVB3 are not completely understood. In the current study, ...
Heart failure from myocarditis may be transient or may progress to unremitting severe cardiac failure. This study was performed to determine the outcomes and prognostic features of pediatric patients with myocarditis. Patients with the diagnosis of myocarditis between 1990 and 2001 were identified t …
Major Causes of Myocarditis. Infectious agents Viral. Rickettsial Bacterial Protozoal Metazoal Allergic reactions Pharmacologic agents Systemic diseases such as vasculitis. Peripartum state (90 days before to 90 days after end of pregnancy). Toxic agents (alcohol, toxic metals such as cobalt). Describe the patient complaints and clinical findings that frequently accompany myocarditis.. The symptoms vary with the etiology, but most commonly myocarditis is subclinical, especially when it accompanies a generalized infectious processes. Patients may note fatigue, dyspnea, precordial discomfort, or palpitations. Frequently tachycardia is noted; the first heart sound may be muted and an S4 gallop is often described.. What electrocardiographic (ECG) changes are commonly seen in myocarditis?. ST-segment elevation or depression and T-wave inversions are the most frequently noted changes. Atrial arrhythmia are commonly noted, and transient heart block (first, second, or third) may be noted.. How are ...
To investigate innate immune mechanisms that lead to increased myocarditis after a single anti-Tim-3 treatment (Fig. 1⇑), we examined the level of CD80 and CD86 on APC from the heart or spleen, and CTLA-4 (intracellular) and CD28 (surface) levels on CD4+ T cells from the spleen at 6 h p.i. There is no inflammatory infiltrate in the heart at 6 h p.i., and so T cells are not present in the heart to analyze by FACS. We found that anti-Tim-3 administered during the innate immune response partially blocked Tim-3 expression and reduced CD80 levels on MC and macrophages isolated from the heart or spleen at 6 h p.i. compared with isotype controls (Fig. 3⇓A). CD80 levels were most profoundly reduced by anti-Tim-3 treatment on APC in the heart, compared with the spleen (Fig. 3⇓A). In contrast, anti-Tim-3 had little effect on MHC class II or CD86 levels on MC or macrophages (Fig. 3⇓A), which were expressed at levels similar to those induced by CVB3 infection alone (Fig. 2⇑C). Reducing Tim-3 ...
The Myocarditis Foundation raises awareness, promotes research and supports families affected by myocarditis. Learn more about our myocarditis organizations important work by visiting us online.
TY - JOUR. T1 - Myocarditis. T2 - Diagnostic value of MR imaging and CT. AU - Laissy, J. P.. AU - Bazeli, R.. AU - Benachour, N.. AU - Gaxotte, V.. AU - Schouman-Claeys, E.. AU - Serfaty, J. M.. PY - 2006/9. Y1 - 2006/9. N2 - There is a growing consensus to recognize the role of cardiac magnetic resonance (MR) imaging in the diagnosis of myocarditis. The most characteristic finding is the presence of subepicardial enhancing areas in the inferior and lateral walls in delayed-enhanced MR sequences. Segmental wall motion abnormality may be present in the myocardial segments that can be different from those exhibiting the myocardial damage in delayed enhancement sequence. These MR features provide accurate information on the type of myocardial involvement, and probably are able to assess the severity of the disease. Moreover, these MR patterns as well as others may distinguish acute myocarditis from acute myocardial infarct, both on first-pass perfusion images and on delayed-enhancement images. ...
The finding of normal coronary arteries in patients admitted with chest pain and positive troponin is well recognized. Owing to its ability to provide tissue characterization, cardiovascular magnetic resonance imaging allows a diagnosis of myocarditis in 50% of patients with this presentation (1). The displayed images are from such a patient, who had no prior history of cardiac disease, and provide in vivo histological insight into the process of myocarditis. In the acute phase, evidence of extensive myocardial inflammation is seen in the lateral left ventricular (LV) wall using a short inversion time inversion recovery sequence (A)with corresponding late gadolinium enhancement (B). Follow-up images at 3 months show resolution of the inflammation (C), correlating with clinical recovery, and the development of localized myocardial fibrosis (D). RV = right ventricle.. ...
Background/Purpose: To establish EGPA/Churg Strauss inflammatory heart disease prevalence and develop an algorithm for heart disease screening in EGPA patients. Methods: An audit of all EGPA patients attending Addenbrookes was performed. Clinical presentation, cardiac studies, disease outcome measures and clinical course was noted. Values are given as percentages and median (IQR). Mann Whitney U was used. Results: 131 EGPA patients (47% men) were followed of whom 96 (73%) underwent cardiac evaluation. Median age was 50 years (38 - 58), 37% were ANCA +ve and asthma preceded diagnosis in most by a median of 97 months (36 - 240). 41 of those screened (43%) were symptomatic for heart disease with: dyspnoea (47%), chest pain (29%), limb oedema (24%), palpitations (13%), syncope (4%), abdominal discomfort (2%) and shock (2%). 27/96 (28%) patients had EGPA-related heart disease in 20 of whom this was present at EGPA diagnosis, 5 developed it at time of EGPA flare and it preceeded EGPA diagnosis in ...
TY - JOUR. T1 - Cannabidiol limits T cell-mediated chronic autoimmune myocarditis. T2 - Implications to autoimmune disorders and organ transplantation. AU - Lee, Wen Shin. AU - Erdelyi, Katalin. AU - Matyas, Csaba. AU - Mukhopadhyay, Partha. AU - Varga, Zoltan V.. AU - Liaudet, Lucas. AU - Haskó, G.. AU - Čiháková, Daniela. AU - Mechoulam, Raphael. AU - Pacher, Pal. PY - 2016. Y1 - 2016. N2 - Myocarditis is a major cause of heart failure and sudden cardiac death in young adults and adolescents. Many cases of myocarditis are associated with autoimmune processes in which cardiac myosin is a major autoantigen. Conventional immunosuppressive therapies often provide unsatisfactory results and are associated with adverse toxicities during the treatment of autoimmune myocarditis. Cannabidiol (CBD) is a nonpsychoactive constituent of marijuana that exerts antiinflammatory effects independent of classical cannabinoid receptors. Recently, 80 clinical trials have investigated the effects of CBD in ...
Idiopathic inflammatory myopathy (IIM) is a group of autoimmune diseases with systemic myositis which may involve the myocardium. Cardiac involvement in IIM, although often subclinical, may mimic clinical manifestations of acute viral myocarditis (AVM). Our aim was to investigate the usefulness of the combined analysis of cardiovascular magnetic resonance (CMR) T1 and T2 mapping parameters measured both in the myocardium and in the thoracic skeletal muscles to differentiate AVM from IIM cardiac involvement. Sixty subjects were included in this retrospective study (36 male, age 45 ± 16 years): twenty patients with AVM, twenty patients with IIM and cardiac involvement and twenty healthy controls. Study participants underwent CMR imaging with modified Look-Locker inversion-recovery (MOLLI) T1 mapping and 3-point balanced steady-state-free precession T2 mapping. Relaxation times were quantified after endocardial and epicardial delineation on basal and medial short-axis slices, as well as in different
Looking for online definition of myocarditis in the Medical Dictionary? myocarditis explanation free. What is myocarditis? Meaning of myocarditis medical term. What does myocarditis mean?
Objective: To investigate the association of a wide QRS-T angle on the surface ECG and late gadolinium enhancement on contrast-enhanced cardiovascular magnetic (CMR) imaging in patients with clinically suspected myocarditis.. Background: Diagnosis and risk stratification in patients with suspected myocarditis is particularly challenging due to a great spectrum of clinical presentations. Late gadolinium enhancement (LGE) visualizes myocardial necrosis and fibrosis in patients with biopsy-proven myocarditis. The presence or absence of late gadolinium enhancements in these patients is prognostically meaningful. The QRS-T angle from the surface ECG, on the other hand, may serve as a simple and easily available risk marker in suspected myocarditis.. Methods: We enrolled 97 consecutive patients that were referred to CMR imaging for a clinical suspicion of myocarditis. All patients obtained a standardized digital 12-lead ECG for the calculation of the QRS-T angle and underwent contrast-enhanced CMR ...
Once the diagnosis of Lyme carditis is made, antibiotics effective against Borrelia burgdorferi should be initiated. Although there is good evidence that disseminated Lyme disease should be treated with parenteral antibiotics, there is no consensus regarding treatment for isolated Lyme carditis. The Infectious Diseases Society of America recommends oral therapy with doxycycline or amoxicillin for asymptomatic 1st or 2nd degree heart block. Furthermore, there is no evidence that treatment with antibiotics alters the course of the conduction abnormalities seen in Lyme carditis. It seems prudent in patients with high-grade AV block caused by Lyme disease, however, that parenteral antibiotic therapy should be administered in a monitored setting.. Parenteral antibiotic choices include ceftriaxone 2 g QD, cefotaxime 2 g BID, or penicillin G 200,000 to 400,000 units/kg/day divided into six doses. Duration of treatment for disseminated disease should be for four weeks. Oral regimens include doxycycline ...
Thanks to Liora Pearlman from Beijing, China - a mom of 3: 1 vaccine injured child, and 2 healthy unvaccinated children - for her excellent research and literature compilation as follows:. Vaccination causes myocarditis in 3% of healthy patients (Helle, Koskenvuo, Heikkilaet al.1978; Amsel, Hanukoglu, Friedet al.1986) . Part of this can be explained by circulating antigen precipitating in the heart tissue however people often develop autoantibodies to myocardial tissue after damage to the heart (Rose, Herskowitz, Neumannet al.1988) and this response may be exacerbated by a vaccine draining into a lymph node where the autoimmune process is developing. In either case the myocarditis induced by vaccination can lead to chronic autoimmune destruction of the myocardial tissue. . Case study: Rare association: possible myocarditis secondary to influenza vaccination. (thefreelibrary.com). More studies, about myocarditis and various vaccines.. Helv Paediatr Acta 1976 OCT;31(3):257-60 ...
Leptospirosis is caused by the spirochetes belonging to genus leptospira [1]. This is a zoonotic disease which can cause multi-system involvement [1,6,7]. The pathogenesis of this organ dysfunction is not yet fully understood.. Our patient had exposure history with clinical symptoms and signs strongly consistent with leptospirosis with positive IgM antibodies by enzyme-linked immunosorbent assay (ELISA). Therefore this can be considered a probable case of leptospirosis according to case definition [8-10].. Myocarditis is one of the known cardiac complications of leptospirosis infection [11,12]. But myocarditis is an underestimated complication of leptospirosis due to the fact that it is frequently asymptomatic. Leptospirosis myocarditis can have a severe evolution and at times prove even fatal [13]. During the leptospirosis outbreak in 2008 in Sri Lanka, myocarditis was reported in 7.1% of patients and heart failure in 3.9% [13]. Navinan et al have shown that myocardial inflammation and ...
OBJECTIVES--To elucidate the potential role of cytokines in the pathogenesis of cardiomyopathy and myocarditis. BACKGROUND--Experimental studies show that certain cytokines depress myocardial contractility and that tumour necrosis factor-alpha plays an important part in the pathogenesis of myocardial injury in animal models of viral and autoimmune myocarditis. METHODS--Plasma interleukin 1-alpha, interleukin 1-beta, interleukin-2, interleukin-6, tumour necrosis factor-alpha, tumour necrosis factor-beta, granulocyte-macrophage colony stimulating factor, granulocyte colony stimulating factor, macrophage colony stimulating factor, interferon-alpha and interferon-gamma were measured in 13 patients with acute myocarditis, 23 patients with dilated cardiomyopathy, 51 patients with hypertrophic cardiomyopathy, nine patients with acute myocardial infarction, 18 patients with angina pectoris, 12 patients with essential hypertension and 17 healthy controls. RESULTS--Increased concentrations of cytokines ...
TY - JOUR. T1 - Echocardiographic observation of acute myocarditis with systemic lupus erythematosus. AU - Ueda, Takashi. AU - Mizushige, Katsufumi. AU - Aoyama, Tohru. AU - Tokuda, Michiaki. AU - Kiyomoto, Hideyasu. AU - Matsuo, Hirohide. PY - 2000/2/1. Y1 - 2000/2/1. N2 - Although myocarditis from a series of autopsies of patients with systemic lupus erythematosus was frequently observed, the incidence of clinically apparent myocardial dysfunction was low. A 30-year-old woman with systemic lupus erythematosus was examined by echocardiography. An acoustic densitometry was followed at the left ventricular posterior wall throughout the clinical course. A decrease in the magnitude of cyclic variation of integrated backscatter (IB) was observed before treatment. Following the combined treatment, steroid and cyclophosphamide, a repeated ultrasonic tissue characterization showed an increase in the magnitude of cyclic variation of IB. It is thought that ultrasonic tissue characterization may be a ...
On Monday February 29 th, Candace Moose, Co-Founder of the Myocarditis Foundation, attended New Jersey Rare Disease Day. Rare Disease Week is a global event sponsored in the US by the National Organization for Rare Diseases. It is designed to bring awareness of the unique needs of victims of rare diseases and to advocate for legislation affecting of our diseases. Candace met with Senator Ronald Riser who serves on the Health and Human Services Committee, in his NJ State Capitol office in Trenton, to make him aware of myocarditis, the Myocarditis Foundation, and how this disease can impact the lives of NJ residents. The NJ Rare Disease group asked for Senator Risers support for Assembly Bill #2337 which requires health insurers to limit chronic rare disease patients out of pocket costs for certain prescription drugs. Senator Riser was receptive to supporting this bill when it reaches the Senate floor.. ...
Pericarditis and myocarditis are diseases of a similar etiology and clinical image, and they often overlap. Depending on the clinical manifestation, there is pericarditis with simultaneous involvement of the heart muscle (myopericarditis), or myocarditis with pericardial involvement (perimyocarditis). The paper presents a case of a young patient with myopericarditis, with attention to the electrocardiographic image and parameters of myocardial damage ...
Figure 6: Inferoseptal thinning (left panel) and LGE (right panel) of the left ventricular myocardium (arrows). Perspective:. LGE is correlated with inducible ventricular tachycardia and sudden death in many myocardial diseases, such as ischemic, hypertrophic, dilated, or arrhythmogenic right ventricular cardiomyopathy as well as in chronic Chagas heart disease (Mavrogeni 2013). The presence and the extent of LGE is also associated with recurrent tachyarrhythmia and even sudden cardiac arrest (Neilan 2015). New onset left bundle branch block has been described in patients with myocarditis (Mavrogeni 2014).. We report a case of acute lymphocytic myocarditis with a pattern of LGE correlating with conduction disturbances such as total AV Block, and with ventricular arrhythmia. This case illustrates the occurrence of right bundle branch block, left anterior hemi-block, and even transient complete atrioventricular block in myocardial inflammation and its visibility by CMR.. This case proves that CMR ...
Figure 6: Inferoseptal thinning (left panel) of the left ventricular myocardium and LGE (right panel) in the inferior, inferoseptal, and anteroseptal segments (arrows). Perspective:. LGE is correlated with inducible ventricular tachycardia and sudden death in many myocardial diseases, such as ischemic, hypertrophic, dilated, or arrhythmogenic right ventricular cardiomyopathy as well as in chronic Chagas heart disease [2]. The presence and the extent of LGE is also associated with recurrent tachyarrhythmia and even sudden cardiac arrest [3]. New onset left bundle branch block has been described in patients with myocarditis [4].. We report a case of acute lymphocytic myocarditis with a pattern of LGE correlating with conduction disturbances such as total AV Block, and with ventricular arrhythmia. This case illustrates the ability of CMR to demonstrate the acute changes occurring during myocarditis and by using LGE to show the substrate of electrophysiological disturbances caused by myocardial ...
AbstractIn humans, it is acknowledged that dilated cardiomyopathy is also caused by infection-induced myocarditis. To evaluate whether the occurrence of lesions of dilated cardiomyopathy in cattle may be triggered by myocarditis, an adult Holstein-Friesian dairy cow which showed dilated cardiomyopathy associated with myocarditis was examined by histopathology. Traumatic pericarditis or idiopathic ...
Leptospirosis has a varied clinical presentation with complications like myocarditis and acute renal failure. There are many predictors of severity and mortality including clinical and laboratory parameters. Early detection and treatment can reduce complications. Therefore recognizing the early predictors of the complications of leptospirosis is important in patient management. This study was aimed at determining the clinical and laboratory predictors of myocarditis or acute renal failure. This was a prospective descriptive study carried out in the Teaching Hospital, Kandy, from 1st July 2007 to 31st July 2008. Patients with clinical features compatible with leptospirosis case definition were confirmed using the Microscopic Agglutination Test (MAT). Clinical features and laboratory measures done on admission were recorded. Patients were observed for the development of acute renal failure or myocarditis. Chi-square statistics, Fishers exact test and Mann-Whitney U test were used to compare patients with
On Tuesday, the Health Ministry of Israel said that cases of heart inflammation are reported in some young men who took the Pfizer (NYSE: PFE) vaccine. However, Pfizer said it found no relationship between these heart inflammations cases found in Israel to its vaccine.. In its statement, Pfizer said it has thoroughly reviewed adverse events, and it reviews data regularly with the help of the Israeli Ministry of Healths Vaccine Safety Department. Israel ministrys statement said it found 275 cases of myocarditis among over 5 million vaccinated people from December 2020 to May 2021 in Israel.. According to the study conducted by health experts, the ones who got heart inflammation spent less than four days in health centers. The study also mentions a link between the second and myocarditis cases among men between 16 and 30. In fact, according to the study, myocarditis cases were more reported in men aged between 16 and 19 than in other age groups.. ...
PubMedID: 27502060 | Noninvasive Contrast-Enhanced Ultrasound Molecular Imaging Detects Myocardial Inflammatory Response in Autoimmune Myocarditis. | Circulation. Cardiovascular imaging | 8/1/2016
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Each patient will be randomized to receive either standard care and immunosuppression therapy (treatment group) or standard care alone (control group). To prevent bias, randomization will be stratified by recency of symptom onset to ensure that both the treatment and control groups are balanced with respect to it. Within each of these 2 strata, permuted-block randomization will be done to keep the number of treatment and control patients balanced. Due to the necessary monitoring of the patients randomized to receive immunosuppression therapy, treatment cannot be blinded. Approximately 1 year after the last patient has been randomized, the observed times from randomization to the composite endpoint (death, transplantation, or LVD placement) will be compared in the treatment and control groups.. Completion date provided represents the completion date of the grant per OOPD records ...
Another major physiologically relevant function of immunoproteasomes found during viral infection is a more efficient generation of viral peptides resulting in improved antigen presentation of MHC class I epitopes (Schwarz et al, 2000; Kincaid et al, 2012). Although facilitated antigen processing by the immunoproteasome is also evident for coxsackievirus peptides in vitro (Jakel et al, 2009; Voigt et al, 2010; Respondek et al, 2017), this immunoproteasome‐dependent improvement of epitope liberation has no effect on the course of CVB3 infection in vivo (Opitz et al, 2011). Interestingly as shown in this study, ONX 0914 treatment in C57BL/6 mice with hereditary resistance to viral cardiomyopathy slightly deteriorated disease parameters like viral load without affecting overall long‐term course. Such effects could be at least partially attributed to the solid T1IFN response this host induces to combat CVB3 infection (Jakel et al, 2009; Rahnefeld et al, 2011), and which was significantly reduced ...
TY - JOUR. T1 - Expression of natriuretic peptide in ventricular myocardium of failing human hearts and its correlation with the severity of clinical and hemodynamic impairment. AU - Arbustini, Eloisa. AU - Pucci, Angela. AU - Grasso, Maurizia. AU - Diegoli, Marta. AU - Pozzi, Roberto. AU - Gavazzi, Antonello. AU - Graziano, Gabriella. AU - Campana, Carlo. AU - Goggi, Claudio. AU - Martinelli, Luigi. AU - Silini, Enrico. AU - Specchia, Giuseppe. AU - Vigano, Mario. AU - Solcia, Enrico. PY - 1990/10/15. Y1 - 1990/10/15. N2 - Atrial natriuretic peptide (ANP) was immunohistochemically investigated in (1) right ventricular endomyocardial biopsy specimens from 87 apparently healthy donor hearts taken from victims of cerebral accidents; (2) 1 normal heart not suitable for transplantation (HBsAg carrier); (3) right ventricular endomyocardial biopsy specimens from 151 patients with dilated cardiomyopathy (DC); and (4) 57 explanted hearts, 26 with DC and 31 with ischemic heart disease. No ANP ...
A man died of cardiac arrest after eating too much licorice. (New England Journal of Medicine). Kids hearts are literally working harder during the pandemic. (STAT). Autopsies of COVID-19 cases showed lymphocytic myocarditis in 14% but increased macrophage infiltration into the heart in 86%, perhaps because of systemically elevated proinflammatory cytokines. (European Heart Journal). Abdominopelvic ultrasound or CT showed thromboembolism in 11% of COVID-19 patients in one large series. (American Journal of Roentgenology). Mayo Clinic reported a 5.2% rate of symptomatic thromboembolic events in its hospitalized COVID-19 patients. (Arteriosclerosis, Thrombosis, and Vascular Biology). Prone positioning for severe COVID-19 changes ECG readouts in a way that can be interpreted as anteroseptal infarct, so notation is critical and vectorcardiograms are useful. (JAMA Internal Medicine). It may be moot given hydroxychloroquines lack of proven efficacy, but a modest-sized study suggested arrhythmic ...
TY - JOUR. T1 - Epitope Mapping of SERCA2a Identifies an Antigenic Determinant That Induces Mainly Atrial Myocarditis in A/J Mice. AU - Krishnan, Bharathi. AU - Massilamany, Chandirasegaran. AU - Basavalingappa, Rakesh H.. AU - Gangaplara, Arunakumar. AU - Rajasekaran, Rajkumar A.. AU - Afzal, Muhammad Z.. AU - Khalilzad-Sharghi, Vahid. AU - Zhou, You. AU - Riethoven, Jean-Jack M. AU - Nandi, Shyam S.. AU - Mishra, Paras Kumar. AU - Sobel, Raymond A.. AU - Strande, Jennifer L.. AU - Steffen, David J. AU - Reddy, N R Jayagopala. PY - 2018/1/15. Y1 - 2018/1/15. N2 - Sarcoplasmic/endoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA)2a, a critical regulator of calcium homeostasis, is known to be decreased in heart failure. Patients with myocarditis or dilated cardiomyopathy develop autoantibodies to SERCA2a suggesting that they may have pathogenetic significance. In this report, we describe epitope mapping analysis of SERCA2a in A/J mice that leads us to make five observations: 1) SERCA2a ...
Myocarditis is simply inflammation of the heart muscle. The etiology is varied and may be secondary to a variety of infections, systemic diseases, drugs, and toxins, Viral myocarditis is usually self limited but can lead to chronic dilated cardiomyopathy and sudden cardiac death. Patients often present with chest pain, elevated cardiac enzyme levels, and ECG changes, making differentiation from acute infarction difficult. On contrast enhanced MRI, the presence of focal delayed enhancement in a non-coronary artery distribution together with wall motion abnormalities correlates strongly with acute or subacute myocarditis. The enhancement becomes less intense and more diffuse over time. Myocarditis lesions occur predominantly in the lateral free wall. Contrast enhancement does not typically affect the subendocardium like infarction. Myocardial necrosis of myocarditis is also usually less confluent than infarction.. ...
Gene expression differences.Gene expression that was significantly different in both arms of the study was predominantly decreased in the ARF group after in vitro stimulation with Rh+ GAS, corresponding to failure to respond in the same way as both control individuals and the ARF group after stimulation with Rh− GAS. These genes are involved in cytokine activity, chemokine signaling, leukocyte extravasation, cell-mediated cytotoxicity, and apoptosis.. The genes with decreased expression included IFN-γ and IL-10, which play a central role in cell-mediated immunity. The role of these cytokines in ARF/RHD has been explored in other studies. In the animal model of ARF (cardiac myosin-induced autoimmune myocarditis and valvulitis in the Lewis rat), protection is conferred by IL-10-producing lymphocytes (17). In our study, a decrease in expression or the number of such lymphocytes may account for the decrease in measurable IL-10 expression. In a different mouse model of autoimmune myocarditis, the ...
Targeting CD40L-CD40 interaction could be useful in clinical applications for curing autoimmune diseases, providing treatment following transplantation and treating tumors [15]. One strategy to disrupt this interaction is to use an anti-CD40L monoclonal antibody: this approach has been shown to be effective in mouse models of RA, SLE, MS, IBD, T1 diabetes, and inflammatory heart disease [29]. The humanized CD40L monoclonal antibody BG9588 (hu5c8) has shown therapeutic effects on SLE patients in clinical trials [17, 30]. Another humanized monoclonal antibody, IDEC-131, was tested in a phase II clinical study in ITP patients [31]. However, they were not approved for clinical use because of thrombotic complications when BG9588 was used in some SLE patients and IDEC-131 was used in treating Crohns disease [27]. A third humanized anti-CD40L antibody, ABI793, targeted a different epitope and was found to have the same thrombotic complications, suggesting that these complications are a common effect ...
TY - JOUR. T1 - Recognizing and treating myocarditis in recent-onset systemic sclerosis heart disease: potential utility of immunosuppressive therapy in cardiac damage progression. AU - Crea, Filippo. AU - Pieroni, Maurizio. AU - Smaldone, Costantino. AU - Campioni, Mara. AU - Bellocci, Fulvio. AU - Bonomo, Lorenzo. AU - Ferraccioli, Gianfranco. PY - 2014. Y1 - 2014. N2 - Scleroderma heart disease is a major risk of death in systemic sclerosis (SSc). Mechanisms underlying myocardial damage are still unclear. We performed an extensive study of SSc patients with recent-onset symptoms for heart disease and examined the efficacy of immunosuppressive therapy.. AB - Scleroderma heart disease is a major risk of death in systemic sclerosis (SSc). Mechanisms underlying myocardial damage are still unclear. We performed an extensive study of SSc patients with recent-onset symptoms for heart disease and examined the efficacy of immunosuppressive therapy.. KW - ANCA. KW - Adult. KW - Aged. KW - Disease ...
Patient: Female 57 Final Diagnosis: Coxsackie myocarditis and hepatitis Symptoms: Fever ? headache ? general SEDC malaise ? sob. GSK1120212 and generalized malaise. Her white blood cell count was 13×103 cells/mm3. Interestingly lumbar puncture ruled out meningitis. An echocardiogram to evaluate elevated troponin revealed an GSK1120212 ejection portion of 30% with severe left ventricular global hypokinesis without valvular vegetations consistent with new-onset systolic heart failure. Cardiac MRI showed a small pericardial effusion with bilateral pleural effusion. As she continued to be febrile a viral panel was ordered exposing coxsackie B4 antibody titer of 1 1: 640 (reference: >1: 32 indicates recent contamination) with positive Epstein-Barr computer virus deoxyribonucleic acid by PCR consistent with viral myocarditis. Conclusions: Coxsackie B computer virus myocarditis is usually rarely acknowledged and reported by the general internist in clinical practice so we would like present our ...
BACKGROUND Fulminant lupus myocarditis is usually a uncommon but fatal manifestation of systemic lupus erythematosus. pneumonia. Ultrasound uncovered an enlarged center with a minimal still left ventricular ejection small percentage. Fulminant lupus myocarditis with cardiogenic shock was taken into consideration initially. Because of the associated pneumonia, intense immunosuppression was contraindicated. Her cardiac function continued to be vital following the preliminary therapy of intravenous immunoglobulin and corticosteroids at a typical dosage, but she responded well to later on PE therapy plus corticosteroids administration. The patient fully recovered with normal cardiac function. Summary This case shows that PE is definitely a valuable treatment choice without adverse effects of immunosuppression in individuals with fulminant lupus myocarditis and coexisting illness. strong class=kwd-title Keywords: Plasma exchange, Cardiogenic shock, Lupus myocarditis, Systemic lupus erythematosus, ...
Immunotherapy is a powerful weapon in the fight against cancer, but inflammation of the heart muscle (myocarditis) is one of its most serious side effects. This has been highlighted in a review article on the immunological causes and processes of myocarditis, which has just been published by an international research team. Autoimmune reactions are in fact among the most common causes of myocarditis. And such reactions can be triggered by cancer immunotherapies due to their specific modes of action. The increasing use of these treatments could therefore lead to an increase in cases of myocarditis.. Inflammation of the heart muscle is extremely dangerous, but often remains undetected due to a lack of simple diagnostic options. Although the inflammation is often caused by infections, autoimmune responses are also a common trigger. A team of experts from Karl Landsteiner University of Health Sciences in Krems (KL Krems), Charité university hospital in Berlin and Columbia University in New York have ...
Learn more about Myocarditis -- Adult at Medical City Dallas DefinitionCausesRisk FactorsSymptomsDiagnosisTreatmentPreventionrevision ...
The Advisory Committee on Immunization Practices (ACIP) COVID-19 Vaccine Safety Technical (VaST) Work Group has reviewed post-authorization COVID-19 vaccine safety data on a weekly basis since the start of the U.S. vaccination program, the CDC said in a statement.. The VaST session on May 17, 2021, included several presentations on myocarditis following mRNA vaccines, from the Department of Defense (DoD), the Vaccine Adverse Event Reporting System (VAERS), and Vaccine Safety Datalink (VSD), the statement continued. There were also brief updates from the Veterans Administration (VA) and the Clinical Immunization Safety Assessment (CISA) groups about their plans for future investigation of myocarditis.. The report noted that reports of vaccine-induced myocarditis have occurred predominantly in adolescents and young adults, more often in males than females, more often following dose 2 than dose 1, and typically within 4 days after vaccination.. VaSt went on to recommend that Further ...
Direct Gene Transfer with IP-10 Mutant Ameliorates Mouse CVB3-Induced Myocarditis by Blunting Th1 Immune Responses. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
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List of causes of Anorexia and Epidural abscess and Fever and Myocarditis, alternative diagnoses, rare causes, misdiagnoses, patient stories, and much more.
The ICD-10 Code A38.1 is the code used for Scarlet fever with myocarditis .An alternative description for this code is Scarlet fever with ...
The infectious etiology of myocarditis often remains unidentified. We report a case of myocarditis associated with human parechovirus (HPeV) infection in an adult. HPeV is an emerging pathogen that can cause serious illness, including myocarditis, in adults. Testing for HPeV should be considered in differential diagnosis of myocarditis ...
阿部 美保1, 福田 信夫2, 井形 次郎1, 稲山 久美1, 福田 保1, 篠原 尚典2, 添木 武2, 酒部 宏一2, 小野瀬 由紀子2, 田村 禎通2. Miho ABE1, Nobuo FUKUDA2, Ziro IKATA1, Kumi INAYAMA1, Tamotsu FUKUDA1, Hisanori SHINOHARA2, Takeshi SOEKI2, Kouichi SAKABE2, Yukiko ONOSE2, Yoshiyuki TAMURA2. 1公立学校共済組合四国中央病院内科, 2国立善通寺病院循環器科・臨床研究部. 1Depertment of Internal Medicine Shikoku Central Hospital, 2Division of Cardiology, and Clinical Research, Zentsuji National Hospital. キーワード : acute myocarditis, diastolic dysfunction of the ventricle, echocardiography, mitral annular velocity, left ventricular inflow velocity A man aged 27 years was admitted to the hospital because of fever and general fatigue. The electrocardiogram showed abnormal Q wave in leads II, III, and aVF, and poor R-wave progression in leads V3 through V6 at time of admission. The chest roentgenogram showed cardiac enlargement and no ...
Looking for diphtheritic paralysis? Find out information about diphtheritic paralysis. or , complete loss or impairment of the ability to use voluntary muscles, usually as the result of a disorder of the nervous system. The nervous tissue that... Explanation of diphtheritic paralysis
J Am Heart Assoc 2020 Aug 18;9(16)e015351, S Greulich, A Seitz, KAL Müller, S Grün, P Ong, N Ebadi, KP Kreisselmeier, P Seizer, R Bekeredjian, C Zwadlo, C Gräni, K Klingel, M Gawaz, U Sechtem, H ...
Coronary artery disease or CAD - This is caused by the reduced supply of blood to the heart muscles. Chest pain due to CAD is referred to as angina. Experts say that having CAD puts you at risk of having a heart attack.. • Heart attack - Also known as myocardial infarction or MI, it happens when death of the heart muscle cells occurs. Chest pain due to a heart attack is commonly accompanied by nausea, sweating and shortness of breath.. • Myocarditis - This is characterized by the inflammation of the heart. Chest pain brought about by myocarditis is similar to that which is experienced during a heart attack. Fever, fatigue, and palpitation are other symptoms.. • Pericarditis - Unlike myocarditis, this condition is the inflammation of the membrane surrounding the heart. Someone with this medical problem may experience worsening of chest pain when breathing or swallowing food.. • Mitral valve prolapse - This happens when the mitral valve of the heart fails to close properly. Dizziness, ...

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