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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±14 versus 41±14 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 years; persistent >1000/24 hours ventricular ectopy; and recurrent nonsustained ventricular tachycardia. A "first-contact" algorithm based on female sex and age <30 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↗

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↗

PubMed1979

Clinical aspects of nonrheumatic myocarditis in children.

Sixty-eight patients of clinically diagnosed myocarditis, 0--15 years of age, were followed up and analyzed. Forty (58.8%) were males. The majority were older than 5 years. Clinical courses were rather mild, chronic and self-limiting at large. Only 1 case had a relation to chronic cariomyopathy. Exertional symptoms (chest pain, chest distress, syncope) were seen in 25 (36.8%). ECG changes were very common: the majority were nonspecific ST elevation, depression or both, mainly in leads II, III, V5 and V6. Positive Master' test, prolonged QTc, widened mean spatial QRS-T angle and various arrhythmias were also observed. Cardiac performance, estimated by echocardiogram and phono-mechanocardiogram was lowered in 41 (60.3%). Large IV sound and large A wave in apexcardiogram were also frequently found. All but 3 patients showed continuous elevation of serum enzymes, namely, LDH, LDH-1/LDH-2, CPK, CPK-MB, HBD and GOT. Etiological evidences were obtained by serological study in 11 cases (16.2%): 2 of Coxsackie B-1, 3 of Coxsackie B-2, 1 of Coxsackie B-4, 2 of mycoplasma pneumoniae, 1 of cytomegalovirus, 1 of ECHO-7 and 1 of rubella. We proposed a criteria for diagnosis of myocarditis as follows: (1) Exertional symptoms. (2) ECG findings. (3) Serum enzyme abnormality. (4) Lowered cardiac performance. (5) Cardiomegaly. (6) Changing character of all signs and symptoms.

Adolescent↗

PubMed1979

Clinical features of acute coxsackie B viral myocarditis.

Clinical features of 11 patients of acute Coxsackie B viral myocarditis diagnosed by neutralizing antibody titers were reported. All patients had a flu-like symptom and 8 patients had fever. Initial cardiac manifestations were congestive heart failure in 9 patients, and syncopal attack in 4 patients. Electrocardiographic abnormalities frequently observed were non-specific ST-T changes, low voltage, and intraventricular conduction, disturbances including 4 patients of complete A-V block due to trifascicular block. Ten patients had a rise of serum enzymes. It seemed that in severe patients the serum enzymes rose markedly. From the analysis of laboratory and histological findings. Coxsackie B viral myocarditis were often complicated by hepatitis.

Adolescent↗

PubMed1978

The myocarditis of systemic lupus erythematosus: association with myositis.

Five patients with clinically overt myocarditis in the setting of systemic lupus erythematosus were analyzed in terms of associated clinical and serologic features. Myositis and antibodies to nuclear ribonucleoprotein (RNP) were present in all. A retrospective review in 140 consecutive patients with systemic lupus erythematosus, including three of these five, showed a highly significant association of myocarditis with myositis (P less than 0.0005). The presence of antibodies to RNP in this small group did not attain statistical significance (P less than or equal to 0.10). The pathologic findings in the one patient who died showed similar patterns of inflammation in both cardiac and skeletal muscle, suggesting the possibility of a generalized inflammatory process directed against striated muscle. Furthermore, although anti-RNP antibodies were found uniformly in these patients, their significance remains to be defined.

Adolescent↗

PubMed1976

[Effect of antikinin agents on the course of experimental myocarditis].

The therapeutic action of 5 preparations: specific antikinin substances -- anginin and contrical, and nonspecific -- epsilon-aminocapronic acid, aspirin and indometacine, was tested in 71 rabbits with allergic myocarditis. It has been concluded that in the allergic distruction of the myocardium plasma kinins, which are formed and accumulated in large quantities, take part in the pathogenesis of the disease serving as mediators of the tissue distruction, therefore specific antagonists of kinins and inhibitors of the kinin system should be included as pathogenetic agents into the complex of allergic myocarditis treatment.

Aminocaproates↗

PubMed1979

Trials of treating myocarditis in mice infected with coxsackie B3 viruses.

On the assumption of an immunologic background of chronic myocarditis after infection with Coxsackie B3 viruses, mice were treated with prednisolone or cyclophosphamide, starting 18 days after infection, for periods of three months. The favorable therapeutic effect indicates that chronic myocarditis is an immunologic disease.

Animals↗

PubMed1979

Preliminary report on an unidentified virus from infantile myocarditis.

A preliminary report on an unidentified virus from two cases of infantile myocarditis is presented. The virus isolated from two separate occasions showed characteristics of an enterovirus. The significance of this virus in its association with infantile myocarditis requires further investigation.

Enterovirus↗

PubMed1977

Occurrence of myocarditis in sudden death in children.

This study suggests that the prevalence of "silent" myocarditis may be higher in the pediatric population than is generally suspected and may contribute to a significant number of sudden and unexpected deaths in children, particularly those older than one year of age. The incidence of histologic myocarditis in children dying a violent death is similar to that reported as an incidental finding in adults.

Adolescent↗

PubMed1979

Analysis of sudden unexpected death in southern Ontario, with emphasis on myocarditis.

The records of all 2427 autopsies performed at the Brantford (Ont.) General and Paris (Ont.) Willett hospitals from Jan. 1, 1969 to Aug. 15, 1978 were reviewed. Of the 1299 cases of sudden unexpected death investigated by a coroner almost 28% were due to unnatural causes--violence or poisoning. The main cause of natural sudden death was coronary artery disease, which accounted for 43.3% of all the sudden unexpected deaths. In 20 cases the cause of death was thought to be viral myocarditis, and in 9 of the 20 there was serologic evidence of at least previous coxsackievirus disease. Two of the nine cases were of special interest because of the finding of giant-cell myocarditis in one and aortic valve disease in the other. Eleven of the 20 persons were aged 13 to 46 years. These findings support the view that the most serious manifestation of enterovirus infection today is cardiac damage by coxsackieviruses.

Adolescent↗