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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.
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.
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.
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.
Sudden death of pups in the 4- to 6-week age range has recently been occurring in western Canada as a result of severe, primary, nonsuppurative myocarditis. At necropsy, the prominent macroscopic lesion was pulmonary edema, and microscopically, characteristic intranuclear inclusion bodies were found within cardiac myofibers in association with myocarditis. Ultrastructurally, numerous small particles resembling parvoviruses were found within the intranuclear inclusion bodies, which were positive by direct fluorescent antibody test for canine parvovirus. Of three pups inoculated with homogenate from affected myocardium, one developed lesions resembling canine parvoviral enteritis.
Surviving puppies from three separate litters in which deaths had occurred from suspected viral myocarditis were examined clinically and electrocardiographically. Of 11 puppies examined, 5 subsequently died or were euthanised within 11 days of initial examination. ECG changes present in these puppies for 1 to 11 days prior to death were small R waves (less than 0.4 mV in lead II), S-T segment elevation, QRS notching and paroxysmal ventricular tachycardia (PVT). No clinical signs referable to the ECG changes were present before the terminal episodes of apparent sudden death or death following a brief period of dyspnoea. Multifocial subacute myocarditis was present on post-mortem examination. A sixth puppy with small R waves remained clinically normal for a further 4 weeks. It then developed severe dyspnoea which persisted for 24 hours before euthanasia. Extensive fibrosis of the left ventricle was present on post-mortem examination.
In oral infection with cysts and oocysts of strain 131 Toxoplasma gondii, specific interstitial productive myocarditis with involvement of the endo- and pericardium developed in albino mice and guinea pigs in the acute stage of the process. Toxoplasmic myocarditis terminated in focal cardiosclerosis. The intensity of cardiac affection was higher in oral infection with toxoplasm oocysts than in infection with cysts than in infection with cysts. Unabating persistence of toxoplasms in the myocardium of the infected animals after subsidence of acute inflammatory phenomena was revealed (cysts in the myocardium).
Five patients with hypertension died as a result of myocarditis. Three were treated with methyldopa and hydrochlorothiazide, two with methyldopa alone. Their ages ranged from 30 to 71 years. In all instances death occurred suddenly, and myocarditis was not suspected clinically. The inflammatory changes in the hearts of these patients were most consistent with a hypersensitivity reaction. Additionally, there was hepatitis consistent with hypersensitivity in four of the cases.
The work is based on observations over 168 patients with infectious-allergic myocarditis. The principal clinical, instrumental-laboratory, and morphologic criteria of this disease are discussed. The contractile function of the myocardium and central hemodynamics were studied. Intravital puncture biopsy of the myocardium was employed for the first time in this disease. Clinico-morphologic variants of infectious-allergic myocarditis are distinguished.
Trichinellosis myocarditis with the presence of juvenile forms of the parasite in the myocardium is an extremely rare pathology, according to the literature. The present observation refers to a woman of 43 who had been treated for a long time for rheumatism. In 1974, aortic valve failure was diagnosed and in September, 1976, she was sent for operative treatment. Three hours after admission she developed acute cardiac insufficiency and died. Trichinellosis myocarditis was diagnosed at autopsy.
Two children with typhoid myocarditis have been presented. Although the mortality rate with this complication particularly in presence of heart block is high both patients survived. Heart block was successfully treated with isoproterenol and xylocaine. The possibility of myocarditis must be considered in any child with typhoid.
This is a report of 6 single cases of prenatal virus myocarditis originated from an endemic region around Salzburg. The cardiac involvement showed different grades dependent too on time of infection and on transfer of maternal antibodies to the child. Infections immediately before delivery cause severe illness, but infections some weeks before birth less severe damage. Symptoms of meningitis were not noticed. The diagnosis of myocarditis by Coxsackie virus was certain in two deceased newborns (Patient 1 and 2), very probable in one decreased baby (Patient 3) and probable in the surviving children (Patient 4, 5 and 6).
A 19 year old woman presented with chest pain after a dental extraction for a dentoalveolar abscess. Electrocardiographic and serum isoenzyme changes were consistent with acute anterior myocardial infarction. At autopsy bacteria were demonstrated, within the myocardium in the absence of a myocardial abscess or endocarditis. This case illustrates the occurrence of isolated acute bacterial myocarditis after a dental extraction.
Two patients are reported with hypersensitivity myocarditis. One, a 71-year-old female, was being treated with methyldopa at the time of her death and the second, a 67-year-old female, was receiving tetracycline for a respiratory tract infection.
A 44-year-old white female with chronic rheumatic heart disease and mitral insufficiency was admitted to the hospital for cardiac catheterization and mitral valve replacement. On the ninth postoperative day the patient experienced a sudden onset of chest pain, hypotension, and died shortly therafter. Autopsy revealed multiple mural thrombi of the left atrium, one of which occluded the mitral orifice. Histologic examination showed a granulomatous and non-specific interstitial myocarditis involving all chambers of the heart. In the granulomas, both inside and outside giant cells, rounded foreign bodies were noted which stained light blue with hematoxylin and eosin, red with the periodic acid Schiff reagent, dark bluish-black with Gram's iodine, and showed Maltese cross birefringence under polarized light. These particles were identical with starch granules from surgical glove powder. The cause of death was acute mitral occlusion form a flapping mural thrombus.
In a 34-year-old patient asthma had developed as an allergy to infection. He died suddenly from cardiac and respiratory arrest following parenteral penicillin and sulphonamides. At autopsy necrotizing angiitis of the myocardial vessels as well as eosinophilic myocarditis were shown. These findings are probably the expression of a drug allergy.
Suckling, weanling, and adult HaM/ICR and Swiss-Webster mice were inoculated intraperitoneally with the TC631 and Dowell strains of coxsackievirus B4. Vero cell-inoculated and uninoculated control mice were also studied under code. An intense, necrotizing myopericarditis was produced in suckling mice; it was less severe in weanlings. Myocarditis did not occur when coxsackievirus B4 was inoculated into adult mice. Progressive sclerosis and thickening of all valves in both strains of mice were observed with equal frequency in infected and control mice. There was no evidence that coxsackievirus B4 induced a specific valvular or endocardial lesion.
A 3 1/2-year-old boy, during the course of acute lymphocytic leukemia presented clinical, roentgenological and ECG signs of myocarditis, which disappeared completely within 1 1/2 month. ECHO type 7 virus was isolated from the faeces during the acute stage of the disease and rise in ECHO 7 neutralizing antibodies was demonstrated in paired sera of the patient. This unusual pathogenicity of ECHO 7 virus could be explained with the impairment of the host resistance induced by leukemia and immunosuppressive therapy.