[Acute myocarditis--various types of myocarditis and descriptions of viral, Fiedler and giant-cell myocarditis].
Explore the source record for details and available documents.
Acute Disease↗
SEARCH · PubMed Health
Results for “Myocarditis”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Abramov-Fiedler myocarditis, the most severe variant of infectious allergic myocarditis in infants].
Seven cases of Abramov-Fidler myocarditis in infants were studied. The heart affection may be considered to be an infectious-allergic process occuring in a presensitized host. The severity of the disease is due to necrotic changes in the myocardium, in some cases to the involvement of the endocardium and pericardium.
Acute Disease↗
[Pyrexia, arthralgia, thoracic pain, dyspnea and fainting spells (ECG and myocardial biopsy): (acute primary myocarditis--Fiedler's myocarditis)].
Explore the source record for details and available documents.
Acute Disease↗
[Virus-myocarditis on an example of a subsided endemic Coxsackie-virus myocarditis in the Salzburg area].
Explore the source record for details and available documents.
Austria↗
Clonal Hematopoiesis and Risk of New-Onset Myocarditis and Pericarditis.
IMPORTANCE: Clonal hematopoiesis of indeterminate potential (CHIP) is the age-related clonal expansion of hematopoietic stem cells with leukemia-associated mutations. Certain CHIP mutations promote atherosclerosis and heart failure through immune-related pathways. OBJECTIVE: To test whether CHIP is associated with the development of myocarditis and pericarditis. DESIGN, SETTING, AND PARTICIPANTS: This observational population-based cohort study used data from the UK Biobank. Enrollment occurred between 2006 and 2010. Participants with whole-exome sequencing, no prevalent cardiovascular disease or hematological malignancy, and complete covariate data were included. Follow-up occurred for a median of 13.6 (IQR, 12.8-14.2) years. Analyses were conducted from November 2024 to July 2025. EXPOSURES: Any CHIP (variant allele frequency [VAF] ≥2%) and large CHIP (VAF ≥10%) constituted coprimary study exposures. Secondary analyses considered DNMT3A and TET2 CHIP as separate exposures. MAIN OUTCOMES AND MEASURES: The primary outcome was a composite of incident myocarditis and pericarditis. Cox regression tested associations of CHIP with myocarditis and pericarditis, adjusting for age, sex, race and ancestry, and cardiovascular risk factors. Secondary analyses considered myocarditis and pericarditis as separate outcomes. Additional analyses compared associations of CHIP with myocarditis and pericarditis with those with other cardiovascular diseases, and tested the bidirectional associations between CHIP and noncardiac immune-mediated inflammatory diseases. RESULTS: Among 335 426 participants (mean age, 56.1 years; 185 429 female [55.3%] and 149 997 male [44.7%]), 11 057 had any CHIP (3.3%), 7271 had large CHIP (2.2%), and 382 developed myocarditis or pericarditis (0.11%). Any and large CHIP were associated with multivariable-adjusted hazard ratios of 1.75 (95% CI, 1.14-2.68; P = .01) and 2.07 (95% CI, 1.28-3.33; P = .003), respectively, for the primary composite outcome of incident myocarditis and pericarditis. Increased risks were observed for DNMT3A and TET2 CHIP, with hazard ratios of 2.22 (95% CI, 1.17-4.21; P = .01) for DNMT3A with pericarditis and 3.65 (95% CI, 1.16-11.49; P = .03) for TET2 with myocarditis. CHIP associated with myocarditis and pericarditis more strongly than with other cardiovascular diseases (eg, coronary artery disease and heart failure). Any CHIP was also associated with 1.27-fold risk (95% CI, 1.16-1.39; P < .001) of developing noncardiac immune-mediated inflammatory diseases, without evidence for reverse causation. CONCLUSIONS AND RELEVANCE: In this study, CHIP was a strong risk factor for myocarditis and pericarditis among middle-aged adults. Targeting CHIP and its downstream pathways may represent a strategy for preventing or treating pericarditis and myocarditis.
Adult↗
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↗
Studies on myocarditis in childhood, with special reference to the possible role of immunological process and the thymus in the chronicity of the disease.
Twenty-one cases of idiopathic myocarditis were studied. Fulminant form 1 case, acute fatal form 2 cases, acute benign form 4 cases, recurrent form 1 case. Chronic dilated form 2 cases progressive hypertrophy form 2 cases and asymptomatic and sudden death form was 10 cases. Clinical signs and symptoms of these cases were manifold. Also laboratory findings were nonspecific. Ten cases of latent myocarditis which showed sudden death syndrome were found among 47 cases, progressive hypertrophy form 2 cases and children. Early detection of latent myocarditis is considered to be necessary for preventing sudden death syndrome in school children. The relationship between cardiomyopathy and idiopathic myocarditis was discussed. Two cases of idiopathic myocarditis simulating cardiomyopathy were presented. The pathogenesis of chronicity in idiopathic myocarditis was discussed. Bound gammaglobulin in heart muscle was detected in a case showing progressive hypertrophy of the ventricles. Autopsy results showed a previously undescribed finding that the cases having normal thymus/body weight ratio tended to have markedly increased heart weight but the cases having increased thymus/body weight ratio tended to have near normal heart weight. These results are considered to suggest the possible role of immunity in the chronicity of idiopathic myocarditis.
Adolescent↗
Assessment of coxsackievirus B3 ts mutants for induction of myocarditis in a murine model.
Ten temperature-sensitive (ts) mutants isolated from a myocarditis-inducing wild-type (WT) coxsackievirus B3 parent did not induce myocarditis in adolescent CD-1 mice. An avirulent prototype ts mutant from one of the three complementation groups adsorbed to murine cardiac tissue, as did WT virus. Heart tissues from mice inoculated with WT virus contained 100- to 1,000-fold more virus than heart tissues from mice inoculated with any of the three prototype ts mutants. WT virus exhibited a greater capsid stability and a higher efficiency of replication at 37 degrees C than any of the three prototype ts mutants. All three prototype ts mutants induced less interferon in vivo than WT virus. Cell-mediated immune responses, assessed by the cell migration inhibition assay, were different in mice inoculated with WT virus when compared to ts 5 mutant virus. Peritoneal exudate cells from mice inoculated with WT but not ts 5 virus reacted specifically against antigens in WT virus HeLa cell lysates and antigens extracted with KCl from cardiac tissues of mice inoculated with WT virus. Cardiac tissues of mice inoculated with WT but not ts 5 virus contained KCl-extractable antigens which were able to specifically inhibit the migration of peritoneal exudate cells taken from mice immunized with WT virus. Therefore, ts 5 neither elicited a measurable cell-mediated immune response nor induced antigens in cardiac tissues which were immunoreactive with sensitized-(WT virus)-peritoneal exudate cells. Of 9 revertant viruses isolated from the 10 ts mutants, 5 showed covariance in ability to replicate at 39.5 degrees C and capacity for induction of myocarditis. Some revertants exhibited a reduced capsid thermostability compared to WT virus but yet retained the capacity for induction of myocarditis. The data suggest that induction of myocarditis by coxsackievirus B3 variants depends on a combination of several variables, including capsid stability, capacity for replication at 37 degrees C, and expression of the three identified genes. All three prototype ts mutants served as vaccine viruses in preventing myocarditis in adolescent mice subsequently challenged with WT virus. However, all three prototype ts mutants and their revertant variants retained partial to complete lethality in CD-1 neonates.
Animals↗
[Clinical aspects of myocarditis--symptomatology, diagnosis and pathogenesis].
On the basis of newer knowledge from literature in a survey aspects of symptomatology, diagnostics and course of the myocarditis important for practice are represented. According to the frequency of the virus myocarditis is referred to the importance of immunopathogenetic factors for prognosis and course. Own experiences confirm the transition from an acute myocarditis into a chronic cardiomyopathy which was observed by various investigators. In a 17-year-old female patient the development of a congestive cardiomyopathy after acute myocarditis could be pursued for several years. After-examination of 58 patients after acute myocarditis resulted after 3 years in 62% in cardiac residual symptoms, in which cases anamnestic data and objective findings of the examination well correlated. In 14 patients (24.1%) chronic recidivating courses were found. The importance of the biopsy of the endomyocardium for the diagnostics and differential diagnostics of cardiomyopathies is represented at the instance of a 20-year-old male with subacute rheumatic myocarditis who was hospitalised on account of symptoms of a left heart insufficiency, enlargement of the heart and a picture of a left hypertrophy in the ECG. Bioptically was found a hypertrophy with formation of a large nucleus. After 1 1/2 years clinical improvement and normalisation of size of the heart and ECG. The control biopsy now resulted in normal findings of the heart.
Acute Disease↗
Secondary myocardial disease. Virus myocarditis and cardiomyopathy.
In an attempt to prove the hypothesis that virus myocarditis may be a cause of idiopathic cardiomyopathy, clinical and experimental studies were performed. Eleven patients with a presumptive or proven diagnosis of virus myocarditis were followed for one and a half to 13 years after the acute illness. One patient died in the acute stage, six recovered completely and one continued to have bifascicular block without subjective symptoms. Three patients had exertional dyspnea, cardiomegaly and an abnormal ECG three to 13 years after the onset, and two of them had an enlarged LV cavity with reduced EF and histological changes in myocardial biopsies. The clinical picture in these three cases was similar to that seen in congestive cardiomyopathy. Clinical observations of the heart in an epidemic of coxsackie B 3 virus infection among school children revealed that 49 (19%) of 263 infected children had abnormal chest-X ray, electrocardiographic or echocardiographic findings one to 10 months after the onset, however none of them developed cardiomyopathy. In experimental infection of weanling golden hamsters with coxsackie B 3 virus (Nancy strain), all animals developed acute and severe myocarditis, and the virus was detected in the myocardium. Hemodynamic data suggested decreased contractility of the left ventricle in the acute stage. Histologically the heart showed focal myocardial necrosis and cellular infiltration without calcification, findings which resemble those in human doxsackie B virus myocarditi. Thus, the golden hamster is a better animal model than the mouse in studies on virus myocarditis and postcarditic cardiomyopathy.
Acute Disease↗
Histopathology of the conducting tissue of the heart in Chagas' myocarditis.
The conducting tissue of the heart was studied in 25 human cases of Chagas' myocarditis with a method which employs complete serial sections mounted on continuous transparent plastic tape. The pathological changes were correlated with electrocardiographic findings. The inflammation of the acute phase of Chagas' myocarditis, as seen in one single case, did not seem to interfere with conduction through the AV system. In chronic Chagas' myocarditis the conducting tissue showed extensive and variable changes: chronic inflammation, fibrosis, atrophy and fragmentation of specific fibers, extreme dilatation and tortuosity of veins, capillaries and lymphatics, fatty infiltration, and arterial medial and intimal fibrosis. A preferential involvement of the right bundle branch and the anterior fascicles of the left branch was observed and an excellent correlation with electrocardiographic abnormalities was found. There was also evidence presented that bundle branch block may be caused by disease proximal to the bundle branches. Complete AV block seemed to be the final result of the progressive inflammatory and degenerative changes involving the conduction system in chronic Chagas' myocarditis. Inflammation and fibrosis did also involve the sinoatrial node, Purkinje fibers, intracardiac nervous ganglia, and the contractile myocardium.
Acute Disease↗
Coxsackie myocarditis complicating treatment of Hodgkin's lymphoma.
A fatal case of Coxsackie B4 myocarditis complicating treatment of Hodgkin's lymphoma in an adult is reported. The virus was isolated from the myocardium obtained at autopsy and light microscopy confirmed a myocarditis with involvement of the conduction system. Electron-microscopy showed dense mitochondrial inclusions. Coxsackie myocarditis rarely results in death of affected adults. It is postulated in this case that the treatment of the Hodgkin's lymphoma resulted in B lymphocyte depletion, allowing a more virulent infection to occur with resultant fatal myocarditis.
Adult↗
Testosterone-induced focal myocarditis in rats. I. Morphological and biochemical studies with special reference to pathogenetical mechanism and species differences.
Focal myocarditis characterized by interstitial edema, round cell infiltration and fibrosis occurred in rats given a subcutaneous administration of testosterone propionate in a dose of 50 mg/kg for 30 consecutive days or longer. Biochemical analysis showed a two to five time increase of deoxycorticosterone and a moderate decrease of corticosterone in blood plasma of these rats as well as in those treated with 50 mg/kg of testosterone propionate for 15 days. It was also shown that myocarditis did not occur in adrenalectomized rats after administration of testosterone propionate 50 mg/kg for 30 days, while subcutaneous injections of deoxycorticosterone acetate in a dose of 15 mg/kg for 30 days invariably produced cardiac lesions in both adrenalectomized rats and sham-operated rats. Regarding species difference, administration of testosterone did not produced either a high blood level of deoxycorticosterone or focal myocarditis in guinea pigs or rabbits. From these results, it is concluded that focal myocarditis in rats after administration of large amounts of testosterone propionate is related to the elevation of deoxycorticosterone in blood plasma but not to the direct effects of testosterone propionate on the myocardium.
Adrenalectomy↗
[Problems of the clinical diagnosis of myocarditis].
Anamnesis, clinical findings, changes of the ECG, findings of X-ray examinations and biological reactions in 39 patients with myocarditis are discussed. For the diagnosis of myocarditis are discussed. For the diagnosis of myocarditis changes of the ECG, enlargement of the heart, cardiac insufficiency and disturbances of rhythm are of greatest importance. Changes in the ST-T-segment are non-specific. An exact anamnesis and a comparison with previous findings (X-ray serial examination, ECG) may give decisive hints. Biological reactions are often unreliable in making the diagnosis. There are no typical symptoms and findings for the diagnosis of the inflammatory disease of the myocardium. In the individual case the diagnosis of a myocarditis may be a tentative or excluded diagnosis.
Adolescent↗
[Differential diagnosis of myocarditis from a number of cardiovascular system diseases].
The work is based on the analysis of 206 patients with myocarditis of whom 168 had infectious allergic myocarditis and 38 had idiopathic myocarditis. A wide variety of clinical laboratory and instrumental methods of examination was used and intravital puncture biopsy of the myocardium was conducted. The article discusses the criteria of differential diagnosis which make it possible to distinguish the form of myocarditis from a large group of cardiovascular diseases following a similar course, i.e. primary rheumatic carditis, ischemic heart disease, valvular diseases, pericarditis and others.
Adult↗
[Serum concentrations of proteinase inhibitors, complement components and of acid alpha-1-glucoprotein in children with myocarditis (author's transl)].
We examined 4 panels of children and 40 control patients for their serum levels of the complement components C3, C4 and the C3 activator, the proteaseinhibitors alpha-1-antitrypsin, alpha-2-macroglobulin and acid alpha-1-glycoprotein. Children of the group with active myocarditis revealed the consumption of the complement system, increased protease inhibitors and elevated acid alpha-1-glycoprotein. Group 2, children with the clinical diagnosis chronic myocarditis or status post myocarditis showed in six of seven cases low complement levels and elevated alsGP. 4 children showed increased A1AT and five increased A2MG. In the third panel: status post myocarditis, we estimated in five of eight patients complement activation, 4 children showed increased A2MG and alsGP and in 3 cases elevated A1AT levels were detected. Group 4 children revealed no complement consumption and showed no increased levels for the other proteins estimated, with the only exception of 1 case with increased alsGP. The children of the control group showed normal levels for the six proteins. By means of the examinations an inflammatory process can be detected, tissue injury can be indicated and the participation of the immune system can be shown.
Adolescent↗
Necrotizing myocarditis in mice infected with Western equine encephalitis virus: Clinical, electrocardiographic, and histopathologic correlations.
Western equine encephalitis (WEE) virus was found in myocardial tissue of adult mice during the first five days after inoculation of the virus, with a peak titer (5.0 log plaque-forming units/g) at 24 hr. Light microscopy revealed a multifocal necrotizing myocarditis with a prominent inflammatory response and hyaline and granular degeneration of myofibers. Electron microscopy showed cytoplasmic viral nucleoids and budding and free mature WEE viral particles. Serial electrocardiograms showed the development of disturbances of rate and rhythm, defects in conduction, marked elevation in the ST segment, and low voltage. Myocarditis has not been previously recognized as a complication of alphavirus infection in humans. and we found no evidence for myocardial damage in 11 persons with acute WEE virus infections studied electrocardiographically in 1975. Demonstration of myocarditis in the WEE virus-infected mouse, however, suggests the need to monitor human patients for possible cardiac involvement during future epidemics of WEE virus infection.
Animals↗
[Change in the index of neutrophil damage in infectious allergic myocarditis and its sequelae].
The reaction of damage to the blood neutrophils (the IND test) by a soluble cardiac antigen was studied in 10 healthy individuals, in 15 persons with infectious-allergic myocarditis and in 13 persons with myocarditic cardiosclerosis. Autoallergic shifts in relation to the cardiac antigen were revealed in half of the patients with infectious-allergic myocarditis and in one third of persons with myocarditic cardiosclerosis. The shifts were more marked in patients with infectious-allergic myocarditis.
Adolescent↗