Associate professor Masyuta D. I icon

Associate professor Masyuta D. I

НазваAssociate professor Masyuta D. I
Розмір445 b.

M.Gorky Donetsk National Medical University Department No. 2 of Pediatrics Head of the Department Dr. Churilina A.V., Ph.D. VIRAL MYOCARDITIS, INFECTIVE ENDOCARDITIS, AND THE PRIMARY CARDIOMYOPATHIES IN CHILDREN

  • Associate professor Masyuta D.I.

Viral Myocarditis

  • Myocarditis refers to inflammation, necrosis, or myocytolysis that may be caused by many infectious, connective tissue, granulomatous, toxic, or idiopathic processes affecting the myocardium with or without associated systemic manifestation of the disease process or involvement of the endocardium or pericardium.

Viral Myocarditis

  • Practically, endocardium and pericardium are involved in the process as well, so the term "carditis" is preferable.

  • Coronary pathology is uniformly absent.

  • The most common manifestation is congestive heart failure, although arrhythmias and sudden death may be the first detectable signs.

  • Viral infections are the most common etiology.

Etiology And Epidemiology

  • The incidence of viral myocarditis in children is unknown, as many mild cases may go undetected.

  • The incidence of viral myocarditis in children is unknown, as many mild cases may go undetected.

Etiology And Epidemiology

  • Its manifestations are to some degree age dependent.

  • In early infancy, viral myocarditis often occurs as an acute, fulminant disease.

  • In toddlers and young children, it occurs as an acute but less fulminant myopericarditis.

  • In older children and adolescents, it is often asymptomatic and comes to clinical attention primarily as a precursor to idiopathic dilated cardiomyopathy.


  • Acute viral myocarditis may produce a fulminant inflammatory process characterized by

  • ellular infiltrates,

  • cell degeneration and necrosis, and

  • subsequent fibrosis.


  • Viral myocarditis may also become a chronic process with persistence of viral RNA or DNA (but not infectious virus particles) in the myocardium.

  • Chronic inflammation is then perpetuated by the host immune response, which includes T lymphocytes activated against viral-host antigenic alterations.

  • Such cytotoxic lymphocytes and natural killer cells, together with persistent and possibly defective viral replication, may impair myocyte function without obvious cytolysis.


  • Alternatively, the persistent viral infection may alter major histocompatibility complex antigen expression, with resultant exposure of neoantigens to the immune system.

  • In addition, some viral proteins may share antigenic epitopes with host cells, resulting in autoimmune damage to the antigenicaly related myocyte.

  • The net final result of chronic viral-associated inflammation is often dilated cardiomyopathy.

Clinical Manifestations

  • The presentation depends on the age and acute or chronic nature of the infection.

  • Connection between the onset of the disease and acute respiratory infection sometimes is clear.

  • Interval between acute respiratory infection and the onset of carditis is short (2-9 days) or it is absent.

Clinical Manifestations In The Neonates

  • The neonate may present with

    • fever,
    • severe heart failure,
    • respiratory distress,
    • cyanosis,
    • distant heart sounds,
    • weak pulses,
    • tachycardia out of proportion to the fever,
    • mitral insufficiency caused by dilatation of the valve annulus,
    • a gallop rhythm,
    • acidosis, and
    • shock.

Clinical Manifestations In The Neonates

  • In the most fulminant form, death may occur within 1 -7 days of the onset of symptoms.

  • The chest roentgenogram demonstrates an enormously enlarged heart and pulmonary edema.

  • The electrocardiogram reveals sinus tachycardia, reduced QRS complex voltage, and ST segment and T wave abnormalities. Arrhythmias may be the first clinical manifestation and in the presence of fever and a large heart strongly suggest acute myocarditis.

Clinical Manifestations In The Older Patients

  • The older patient with acute myocarditis may also present with acute congestive heart failure; however, more commonly patients will present with the gradual onset of congestive heart failure or the sudden onset of ventricular arrhythmias.

  • In these patients, the acute infectious phase has usually passed and an idiopathic dilated cardiomyopathy is present.


  • The sedimentation rate and heart enzymes (creatine phosphokinase (CPK), lactate dehydrogenase (LDH)) may be elevated in acute or chronic myocarditis.

  • Echocardiography will demonstrate poor ventricular function and often a pericardial effusion, mitral valve regurgitation.

  • The use of the polymerase chain reaction (PCR) to identify viral RNA or DNA has allowed the viral etiology of many of these formerly "idiopathic" cases to be determined.


  • The approach to treating acute myocarditis involves supportive measures for severe congestive heart failure.

  • Dopamine or epinephrine may be helpful if there is poor cardiac output with systemic hypotension.

  • However, all inotropic agents, including digoxin, should be used with caution as patients with myocarditis may be more susceptible to the arrhythmogenic properties of these agents.

  • Digoxin is often started at half the normal dosage.


  • Arrhythmias should be treated in the normal fashion.

  • The role of corticosteroids for treatment of acute viral myocarditis is still controversial. In a small series of pediatric patients, treatment with prednisone (2 mg/kg daily; tapered to 0.3 mg/kg daily over 3 mo.) was effective in reducing myocardial inflammation and in improving cardiac function.

  • Corticosteroids are administered in diffuse process with cardiac failure, subacute onset, with affection of conductive system.

  • However, relapse may occur when immunosuppression is discontinued.


  • Antibiotics are given during 2-3 weeks and more for prevention of complications.

  • Trials are currently under way evaluating the efficacy of intravenous gamma globulin.

  • Improvement of myocardial metabolism includes prescription of riboxin, panangine, vitamins, polarizing mixture i.v.


  • The outcome of the symptomatic neonate with acute viral myocarditis remains poor, with a mortality between 50 % and 70 %.

  • Patients with lesser symptoms may have a somewhat better prognosis, and complete resolution has been described.


  • The outcome of older patients with chronic dilated cardiomyopathy associated with prior viral infection is also poor without therapy.

  • These patients continue to have inflammation, fibrosis, and deteriorating cardiac function.

  • Although spontaneous resolution may occur in 10-20 %, as many as 50 % of untreated older patients will die within 2 yr. of presentation and 80 % within 8 yr. without cardiac transplantation.


  • This condition has been called

    • fetal endocarditis,
    • endocardial fibrosis,
    • prenatal fibroelastosis,
    • elastic tissue hyperplasia, and
    • endocardial sclerosis.


  • In primary endocardial fibroelastosis (EFE) there is no apparent predisposing valvular lesion or other congenital heart abnormality.

  • In secondary EFE severe congenital heart disease of the left-sided obstructive type (e.g., aortic stenosis or atresia, forms of hypoplastic left heart syndrome, or severe coarctation of the aorta) is present.


  • In secondary EFE the ventricular cavity is often contracted, whereas in the primary disease a dilated left ventricular chamber is seen, usually during infancy.

  • However, in young adults a contracted form of primary EFE has been observed.

  • No etiology for primary EFE has been established.


  • Pathologically, there is a white fibroblastic thickening of the endocardium, virtually always in the left ventricle, which frequently obscures the trabeculation of the inner surfaces of the cardiac chamber.

  • The lesion may spread to involve the valves.


  • Microscopically, the lesion consists of a fibroelastic thickening of the endocardium and may result in subendocardial degeneration or necrosis of muscle with vacuolation of muscle fibers.

  • The involved valve leaflets are characterized by a myxomatous proliferation with an increase in collagenous elements.


  • The endocardium may be 5-6 times thicker than normal and there is subsequent narrowing of the ventricular chamber.

  • The poor diastolic filling leads to a low cardiac output resulting ultimately in forward failure and features of coronary ischemia.

Clinical manifestations

  • The clinical manifestations are variable.

  • Infants, usually younger than 6 mo. of age, who apparently had been in good health, develop severe congestive heart failure, often precipitated by a respiratory infection.

Clinical manifestations

  • Affected infants may manifest

    • dyspnea,
    • cough,
    • anorexia,
    • hepatomegaly,
    • edema,
    • failure to thrive, and
    • recurrent pulmonary infections.

Clinical manifestations

  • Chronic congestive heart failure can be controlled for some time by digitalis and diuretics; however, most patients eventually succumb.

  • Infants in whom valvular lesions or associated congenital cardiovascular defects are predominant usually expire in the 1st mo. of life.

Clinical manifestations

  • Roentgenograms confirm significant cardiac enlargement.

  • The electrocardiogram is abnormal, with changes indicative of left atrial and left ventricular hypertrophy with strain.

  • The echocardiogram shows a bright-appearing endocardial surface and a dilated, poorly functioning left ventricle.


  • It is directed toward alleviation of congestive heart failure and prevention of intercurrent infections.

  • End-stage EFE, with signs of heart failure despite a maximal medical regimen, is an indication for cardiac transplantation.


  • There is a cardiac affection of non-inflammatory character.

  • Myocardiodystrophies are the disorders of physico-chemical structure of the cardiac muscle and its metabolism.

  • Anamnestic diagnostic criterion is connection with previous disease.


  • Clinical diagnostic criteria are as follows:

    • cardialgias,
    • felling of unsatisfactory inspiration,
    • dispnea on physical exertion,
    • vegetative symptoms.


    • Considerable cardiomegaly,
    • steady diastolic murmur,
    • severe degree of processes,
    • atrio-ventricular tachycardia,
    • arrhythmia,
    • chronic disorders of blood circulation
  • testify against myocardiodystrophy.

Infective endocarditis

  • Clinical signs

  • Fever

  • Anaemia and pallor

  • Splinter haemorrhages in nailbed

  • Clubbing (late)

  • Necrotic skin lesions

  • Changing cardiac signs

  • Splenomegaly

  • Neurological signs from cerebral infarction

  • Retinal infarcts

  • Arthritis/arthralgia

  • Haematuria (microscopic).


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