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PubMed1977

[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↗
PubMed1978

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↗
PubMed1976

Heart muscle performance after experimental viral myocarditis.

As part of an inquiry into possible antecedents of idiopathic cardiomyopathy, acute experimental coxsackie virus myocarditis was studied for late structural and functional sequelae. Myocarditis was induced in 12- and 22-day-old hamsters by inoculation with coxsackie virus B3. Early viremia occurred, followed by virus replication in heart muscle. Maximum peak developed tension (Tpd) of isometrically contracting isolated heart muscle was depressed 17 and 43% in the animals inoculated at 12 days, and studied 18 and 90 days later, respectively, as compared to their uninoculated controls. In both infected groups, less muscle stretch was required to reach the length at which Tpd was produced. Animals studied 180 days after inoculation did not differ from controls. The muscles from animals inoculated at 22 days of age and studied 18 days later showed a 15% depression of Tpd compared to their controls. Glycerinated muscles from this infected group developed 50% less tension than their controls. The muscles of hamsters inoculated with virus at 22 days and studied 90 and 180 days later showed no change in Tpd. The data suggest that contractility and compliance of heart muscle are decreased 18 days after inoculation, but recover by 90 days if the animals are inoculated at age 22 days. However, if the animals are inoculated at a younger age (12 days), depression of myocardial performance persists for at least an additional 90 days. It is concluded that the inflammatory stage of experimental acute coxsackie virus B3 myocarditis in the Syrian golden hamster may be followed by residual alterations in contractile proteins and myocardial function.

Animals↗
PubMed1978

[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↗
PubMedDate not supplied

Virus myocarditis: a critique of the literature from clinical, electrocardiographic, and pathologic standpoints.

Concurrent viral infection and myocarditis presumably indicate viral myocarditis. The electrocardiographic and pathologic changes developing during acute infection may, however, result from changes not produced by the infection itself, eg, fever, tachycardia, ischemia, potassium depletion, vitamin deficiencies, drugs. This qualification should be remembered in the evaluation of all alleged virus myocarditis. Viral infection seems to prefer the very young. Its localization in the heart is favored by general or local hypoxia, perhaps thus explaining a predilection for the subendocardium. It may be influenced by the strain of the organism or by the hormonal or immunologic state of the host. Intrauterine infection of the fetus with rubella, mumps, and perhaps coxsackievirus can induce congenital cardiac defects. The role of virus infection in precipitating acute myocardial infarction deserves further study. The value of treatment, including steroids, nonsteroidal immunosuppressive agents, and "antiviral" agents is not yet established.

Acute Disease↗
PubMed1978

[Toxoplasmosis-induced myocarditis].

The clinical picture of myocarditis was studied in 72 patients with toxoplasmic infection and in 44 patients not suffering from this infection. Comparison of the clinical signs of myocarditis in these two groups showed that myocarditis of toxoplasmic etiology has no characteristic features. The only distinction between these two groups was the different frequency of various symptoms. In view of this, methods of laboratory diagnosis of toxoplasmosis acquire much significance.

Diagnosis, Differential↗
PubMed1977

[Kallikrein-kinin system of the blood plasma in patients with infectious-allergic myocarditis].

The state of the blood plasma kallikrein-kinin system in infectious-allergic myocarditis was studied for the first time. Biological methods for the determination of kallikrein, kininogen, kininases, and free kinins were used. Changes in the activity of the kinin system were revealed in 92% of 38 individuals examined: activation in the first 2-4 months and exhaustion later (in 6-8 months). It was shown that the generally accepted clinico-laboratory criteria on myocarditis are not always informative. Determination of the components of the plasma kinin system is suggested as an additional diagnostic test. The use of kinin antagonists and inhibitors of the kinin system in the complex of drug therapy in infectious-allergic myocarditis is recommended.

Adult↗
PubMed1976

[Development of delayed hypersensitivity in rats with streptococcal myocarditis and arthritis].

The authors induced streptococcal myocarditis and arthritis in rats by means of three methods. They proved the development of late hypersensitivity in the experimental animals by determining skin sensitivity and by transfer of lymphocytes and leucocytes from animals with myocarditis and arthritis of healthy recipients. The maximal percentage of animals with late hypersensitivity was obtained in the groups, in whom leucocytes from rats with arthritis were transfered. The arthritis was caused by administration of alive streptococcal culture (at 14 days intervals) three times. Recipients of leucocytes from rats with adjuvant arthritis and streptococci were next. The smallest percentage of successful transfer of late hypersensitivity was obtained in recipients of leucocytes, isolated from animals with streptococcal arthritis and myocarditis, induced after single contamination with alive streptococcal culture.

Animals↗
PubMed2026

Red Flags for Differentiating Desmosomal "Hot-Phase" Cardiomyopathy From Acute Myocarditis.

BACKGROUND: Desmosomal "hot-phase" cardiomyopathy (HPC), characterized by bursts of myocardial inflammation mimicking acute myocarditis (AM), carries relevant risks of adverse outcomes. This study aimed to identify diagnostic "red flags" favoring HPC over AM. METHODS: Patients (n=134) receiving a first diagnosis of AM, proven by endomyocardial biopsy or cardiac magnetic resonance plus troponin elevation, were retrospectively identified at a referral center. HPC was defined by presence of pathogenic desmosomal gene variants (DGVs). Clinical, imaging, and electrical features were compared between HPC cases and controls with gene-negative AM to identify red flags. Diagnostic algorithms were derived and tested in an external multicenter cohort of DGV carriers (n=30). RESULTS: Patients with HPC (n=22; 91% DSP+) were more frequently female (73% versus 24%, P<0.001) and younger than unmatched controls with AM (32&#xb1;14 versus 41&#xb1;14&#x2009;years, P=0.007). When matched 1:1 by age, sex, and presentation, DGV carriers showed distinctive red flags: family history of cardiomyopathy/AM/sudden death; recurrent troponin peaks; persistent left ventricular systolic dysfunction; right ventricular involvement; ring-like late gadolinium enhancement; late gadolinium enhancement persistence or extension; low QRS voltages; life-threatening ventricular arrhythmias at <45&#x2009;years; persistent >1000/24&#x2009;hours ventricular ectopy; and recurrent nonsustained ventricular tachycardia. A "first-contact" algorithm based on female sex and age <30&#x2009;years achieved 77% accuracy, identifying 63% of DGV carriers in the external cohort. An alternative algorithm incorporating ring-like late gadolinium enhancement, right ventricular involvement, and family history showed higher accuracy (93%) and yield (93%). CONCLUSIONS: Myocarditis in DGV carriers predominantly affects young women. A red flag-based approach improves recognition of desmosomal HPC over classic AM.

Humans↗
PubMed1977

Myocarditis in juvenile rheumatoid arthritis.

Three children are described who have had myocarditis as part of juvenile rheumatoid arthritis (JRA). The diagnosis was established by the appearance of cardiomegaly or congestive heart failure or both in the absence of substantial pericardial effusion or extra cardiac cause. Myocarditis, in these cases, occurred on a background of severe, active systemic disease. No pathologic specimens from hearts of acute cases are available, but an autopsy specimen of one child who died after two months of treatment with high doses of steroids showed diffuse changes typical of the "dilated ventricle" type of cardiomyopathy. Treatment with high doses of adrenocorticosteroids has been rapidly successful in controlling the acute phase, while digoxin must be used with extreme care because of high incidence of toxicity to glycosides.

Adolescent↗
PubMed1979

Myocarditis with microabscess formation caused by Listeria monocytogenes associated with myocardial infarct.

Myocardial infarction complicated by bacterial infection is rare. The present case is an instance in which the infecting organism, Listeria monocytogenes, is also rare--an instance not previously reported. The clinical findings were fever without localized infection, severe atherosclerotic heart disease, a myocardial infarct of indeterminate age, and a left ventricular aneurysm. Additional electrocardiographic findings include left bundle branch block, intraventricular conduction defect, and multiple episodes of ventricular tachycardia, all of which may be associated with myocardial infarction and none of which is specific for suppurative myocarditis. Myocardial enzyme abnormalities were absent. Listeria monocytogenes was identified from blood cultures on the day following the patient's death. This case illustrates the difficulty in diagnosing suppurative myocarditis complicating myocardial infarction and the dire consequence of such infection. A review of the literature is included.

Aged↗
PubMed1977

[Rapidly fatal myocarditis due to group B streptococci (author's transl)].

The case of acute purulent group B streptococcal myocarditis in a 29-year-old Turk is described, no similar case having previously been published. He fell ill suddenly with gastro-intestinal symptoms, high fever and pain in arms and legs. The ECG had low voltage in the limb leads and signs of a large acute myocardial infarct. The sedimentation rate was slightly raised, an initial leukopenia was followed by leukocytosis and high enzyme activity. He died in cardiogenic shock on the third day of illness. The post-mortem examination revealed acute purulent myocarditis, and numerous group B streptococci (Strept. agalactiae) were found in the myocardium.

Adult↗
PubMed1977

Fatal myocarditis associated with acute tonsillitis.

A case of myocarditis, hepatic necrosis, and acute anuria associated with acute tonsillitis was described. The previously reported relation between myocarditis and tonsillitis not of diphtheritic or beta-hemolytic streptococcal origin was discussed, as well as the implications for management.

Acute Disease↗
PubMed1976

Phaeochromocytoma with myocarditis managed with alpha-methyl-p-tyrosine.

A case of bilateral phaeochromocytoma with catecholamine-induced myocarditis is described. The two operations needed allowed comparison of the use of alpha-methyl-p-tyrosine alone and in conjunction with adrenergic blocks in the management of the patient. The combination of both drugs was particularly successful in the relief of symptoms and reduction of catecholamine metabolism as monitored by 4-hydroxy-3-methoxymandelic acid (HMMA) excretion. As myocarditis is a potentially fatal complication, further investigation of the combined use of alpha-methyl-p-tyrosine and adrenergic blocking drugs is suggested in the pre-operative management of patients with phaeochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1979

Ventricular aneurysms complicating coxsackievirus group B, types 1 and 4 murine myocarditis.

Suckling Swiss Webster mice were inoculated with 10(4)TCD50 of coxsackieviruses, group B types 1 or 4. Virulent necrotizing myocarditis resulted in 185 infected mice. Of the latter group, three (14.3%) nurslings on the 17th and 23rd day after inoculations had left ventricular aneurysms postmortem. None of 61 concurrently matched control mice developed aneurysms. Ventricular aneurysm is a suggested but previously undocumented complication of murine, and possibly human necrotizing transmural coxsackievirus myocarditis.

Animals↗
PubMed1978

Experimental Coxsackie virus B-3 and B-4 myocarditis in mice.

Mice were inoculated with recently isolated Coxsackie virus B-3 and B-4 intraperitoneally. Severest lesions in the hearts were observed in mice between the age of 7 and 14 days. Grossly yellow-white patches were seen on the hearts of mice from the 7th day to the 6th month after virus inoculation. Microscopically, the heart showed extensive myocardial necrosis, inflammation with small mononuclear cells and calcification on the day of 7. There were myocardial fibrosis and calcification at the 6th month after inoculation with Coxsackie virus B-3, and at the 3rd month after inoculation with Coxsackie virus B-4, but generally pathologic changes were less severe in the latter. Myocardial fibrosis in the present experiment was most prominent among the experiments we have studied. It was confirmed that chronic myocardial fibrosis follows acute Coxsackie virus myocarditis in mice. Possible role of Coxsackie virus myocarditis in the development of cardiomyopathy was briefly discussed.

Animals↗
PubMed1979

Experimental study of virus myocarditis in culture.

In this present paper, the authors would like to present here two points of results from the experimental study concerning virus myocarditis in culture. One is the direct delicate features of heart cells affected with Coxsackie B3 (Cox. B3) virus viewed through both light microscope and electron microscope. The other is the fact that marked proliferation of fibroblastic cells take place to replace the heart cells impaired by the virus suggesting to us the possibility of one of the genesisses, revealing fibroblastic involvement in the Idiopathic Cardiomyopathy (ICM) which could be followed by the residual of the virus myocarditis.

Animals↗