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MYOCARDITIS IN CHILDREN (LITERATURE REVIEW)
Shakhzoda Rustamovna Odilova
1st year master's resident of the Department of Pediatrics and Neonatology of Samarkand
State Medical University
SAMARKAND, UZBEKISTAN
Maksim Vyacheslavovich Lim
DSс., Associate Professor of the Department of Pediatrics and Neonatology of Samarkand
State Medical University
SAMARKAND, UZBEKISTAN
Introduction
Myocarditis in children is an inflammatory disease of the heart muscle (myocardium) that
occurs in most cases as a result of infectious damage or an autoimmune process [1,2].
According to the World Health Organization (WHO), myocarditis remains one of the
important causes of hospitalizations in pediatric practice, especially in preschool and early
school-age children [3]. Meanwhile, the true prevalence of childhood myocarditis may be
underestimated due to diagnostic difficulties and frequent asymptomatic or mildly
symptomatic course [4].
In modern pediatrics, there is a wide range of diseases capable of causing inflammatory
damage to the myocardium. Etiological factors can be viruses (enteroviruses, parvovirus
B19, influenza virus, SARS-CoV-2, etc.), bacteria (streptococci, staphylococci,
mycoplasmas), as well as parasitic and fungal agents [5]. Viral etiology leads among the
causative agents of myocarditis in children, as reported by both Russian and foreign
researchers [6]. Additionally, the autoimmune component plays an important role in the
pathogenesis of myocarditis: when an infectious agent enters a child's div, the immune
system is activated, which can lead to damage of cardiomyocytes by their own antibodies [7].
The diagnosis of myocarditis in children traditionally includes a complex of clinical,
laboratory, and instrumental methods. Along with general assessment of the child's
condition, the doctor pays attention to the presence of intoxication symptoms, arrhythmias,
changes on electrocardiogram (ECG), signs of inflammation according to laboratory tests
(increased troponin levels, inflammation markers, creatine kinase-MB) [10].
Echocardiography (EchoCG) is highly informative, allowing detection of myocardial
contractility disorders, heart chamber dilation [11]. Cardiac magnetic resonance imaging
(MRI) with contrast is increasingly used in pediatric practice, providing detailed
visualization of inflammatory changes and myocardial fibrosis [12].
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Regarding treatment, it primarily aims at combating the etiological factor and reducing the
inflammatory reaction in the heart muscle. Antiviral, antibacterial, or antifungal drugs are
used (depending on the pathogen), immunotropic therapy (immunoglobulins,
corticosteroids), as well as supportive therapy (ACE inhibitors, beta-blockers, diuretics in
case of heart failure development) [13]. Timely and adequate therapy can prevent the
development of severe complications, including dilated cardiomyopathy, which can be an
outcome of recurrent or chronic myocarditis [14].
However, despite advances in diagnosis and treatment, myocarditis in children remains
difficult for timely detection and differential diagnosis with other cardiovascular system
pathologies (for example, rheumatic heart disease, congenital heart defects,
cardiomyopathies) [15]. The key importance lies in the search and verification of the
infectious agent, as well as the assessment of autoimmune mechanisms forming persistent
inflammation [16].
The scientific literature emphasizes the role of early diagnosis of childhood myocarditis,
since it is in the early stages that severe initial damage to the heart muscle can be prevented
[17]. Modern research actively studies genetic and epigenetic aspects determining the child's
response to the introduction of pathogenic agents [18]. An important direction is the
improvement of laboratory testing methods, particularly the introduction of highly sensitive
biomarkers of myocardial damage (high-sensitivity troponin, galectin-3, etc.) [19].
The purpose of this literature review is to systematize modern data on the etiology,
pathogenesis, diagnosis, and treatment of myocarditis in children, as well as to analyze
factors affecting the disease prognosis. The article presents information from domestic and
foreign sources with an emphasis on the latest achievements in the field of pediatric
cardiology and infectious diseases [20].
Below is a detailed analysis of scientific literature devoted to various aspects of myocarditis
in children, including epidemiology, main etiological factors, pathogenetic mechanisms,
clinical manifestations, diagnostic methods, therapeutic approaches, and prognosis.
Epidemiology of Myocarditis in Children
Current epidemiological data indicate that the frequency of myocarditis among children can
range from 1 to 10 cases per 100,000 pediatric population, depending on the geographic
region and applied diagnostic criteria [1,2,4]. The variation in indicators is associated with
both statistical accounting peculiarities and differences in the availability of modern
diagnostic methods.
According to Russian studies, the proportion of myocarditis among all circulatory system
diseases in children ranges from 5-7% [5,16]. It is noted that during outbreaks of viral
infections (especially enterovirus or influenza nature), the number of detected myocarditis
cases increases [2,6]. This is explained by the leading role of viral etiology, where viruses
directly damage cardiomyocytes or trigger autoimmune mechanisms of inflammation [7].
The most vulnerable age group is considered to be preschool children, which is associated
with the imperfection of their immune system and higher susceptibility to infectious agents
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[8]. It is also noted that in adolescents, myocarditis may develop against the background of
severe viral infection courses, bacterial complications, or in the presence of predisposing
factors (hypovitaminosis, chronic infection foci) [9].
Etiological Factors
The main causative agents of myocarditis in children are viruses of the picornavirus family
(Coxsackie B enteroviruses, ECHO), parvovirus B19, herpesviruses (including Epstein-Barr
virus), influenza virus, respiratory syncytial virus, adenovirus, as well as SARS-CoV-2
[5,6,21]. Bacterial etiology is more often associated with diphtheria (Corynebacterium
diphtheriae),
streptococcal
and
staphylococcal
infections
[22].
Opportunistic
microorganisms (mycoplasmas, chlamydiae) and fungi (Candida spp.) usually cause
myocarditis in weakened children with comorbidities or immunodeficiencies [23].
Some parasitic diseases (Chagas disease, toxoplasmosis) in rare cases can lead to specific
myocarditis [24]. Autoimmune processes (systemic lupus erythematosus, juvenile
rheumatoid arthritis) can also cause inflammatory heart damage, although usually
accompanied by polysyndromic manifestations [25].
Pathogenesis
The pathogenesis of myocarditis in children consists of the direct cytopathic effect of the
pathogen on cardiomyocytes and immune system activation [7]. In the early stages, the virus
penetrates myocardial cells using specific receptors (e.g., Coxsackie-adenovirus receptor -
CAR), leading to cardiomyocyte necrosis and release of intracellular antigens [6].
Subsequently, innate and adaptive immunity is activated, increasing production of pro-
inflammatory cytokines (interleukin-1, interleukin-6, tumor necrosis factor-α, etc.), which in
turn attracts leukocytes, macrophages, and T-lymphocytes to the inflammation zone [7,26].
Gradually, a myocardial inflammatory infiltrate forms. At the stage of autoimmune response,
antibodies to cardiomyocyte structures form, intensifying damage to heart tissue elements
[25,27].
As a result of prolonged inflammatory process, significant numbers of cardiomyocytes may
die and be replaced by connective tissue fibers, leading to heart chamber dilation, decreased
contractile function, and progression of heart failure (formation of so-called inflammatory
dilated cardiomyopathy) [28].
Classification and Clinical Forms
In clinical practice, classification based on the duration of myocarditis course is often used:
1. Acute myocarditis: up to 1-2 months from disease onset.
2. Subacute myocarditis: 2-6 months.
3. Chronic myocarditis: over 6 months, with possible periodic relapses [8,29].
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By severity of course, mild, moderate, and severe forms are distinguished, differentiated
based on the severity of heart failure symptoms, contractile function indicators (ejection
fraction), and presence of arrhythmias [10,11]. Also identified are oligosymptomatic
variants of myocarditis, which are often diagnosed post-factum, during routine examinations
or after respiratory infections [1,17].
In young children, myocarditis may present with predominance of general intoxication
symptoms, respiratory disorders, refusal to eat, restlessness or lethargy, sometimes
complicating early diagnosis [30].
Clinical Picture
Clinical manifestations of childhood myocarditis may be nonspecific, especially in the early
stages. The most typical symptoms include [1,9,22]:
- General weakness, increased fatigue, reduced appetite;
- Tachycardia or, less frequently, bradycardia;
- Shortness of breath (especially in infants) during feeding, crying, physical activity;
- Complaints of chest pain or behind the sternum in older children;
- Heart rhythm disturbances (extrasystole, paroxysmal tachycardia, etc.);
- Possible liver enlargement, edema (with right ventricular failure).
In severe cases, cardiogenic shock or acute heart failure develops in the child with
pronounced hypotension and organ perfusion disorders [26,31]. In some cases, myocarditis
may manifest suddenly, in the form of acute decompensation, requiring emergency
hospitalization.
Clinical and Laboratory Diagnosis
Diagnosis of myocarditis in children is based on a combination of clinical signs, physical
examination data (heart auscultation, measurement of heart rate, blood pressure), and
laboratory tests [10]. Complete blood count reveals signs of inflammation (leukocytosis,
elevated ESR), biochemical blood analysis may show increased markers of myocardial
damage (troponin I or T, creatine kinase-MB) [11].
Levels of C-reactive protein (CRP), procalcitonin, cytokines (IL-6, TNF-α) are also assessed,
allowing judgment of the degree of inflammatory process [28]. Virological and serological
studies (antidiv determination, PCR diagnostics) help identify the causative agent of
myocarditis [6,32].
Instrumental Methods
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- Electrocardiography (ECG): can detect signs of rhythm disturbances (extrasystole,
conduction blocks) and ST segment, T wave changes characteristic of inflammatory process
in the myocardium [10].
- Echocardiography (EchoCG): the main visualization method for assessing contractile
function, heart wall thickness, chamber sizes, presence of pericardial effusion [11].
- Holter ECG monitoring: allows more detailed assessment of arrhythmia episodes
throughout the day [33].
- Cardiac MRI: with gadolinium contrast provides ability to identify areas of myocardial
inflammation and fibrosis, clarify diagnosis and extent of damage [12,34].
- Endomyocardial biopsy: indicated in complex cases when morphological confirmation of
diagnosis and determination of inflammatory process activity is necessary. Dallas criteria are
used, describing histological manifestations of myocarditis (presence of inflammatory
infiltrate and cardiomyocyte necrosis) [31,35].
General Principles and Etiotropic Therapy
Treatment of myocarditis in children includes several directions: combating the causative
agent (etiotropic therapy), reducing inflammatory process activity, and supporting heart
function [13]. With confirmed viral etiology, antiviral agents (interferons, ribavirin) may be
used, though their effectiveness in the pediatric population requires further research [5,36].
For bacterial myocarditis, antibiotics corresponding to the pathogen's sensitivity spectrum
(penicillins, cephalosporins, etc.) are prescribed; for diphtheritic myocarditis -
antidiphtheritic serum and antibiotics [22]. In case of detected fungal or parasitic infection,
appropriate antifungal and antiparasitic drugs are used [23,24].
Immunotropic and Pathogenetic Therapy
In severe cases of myocarditis, with autoimmune signs or pronounced inflammatory activity,
glucocorticosteroids (prednisone, methylprednisolone) may be prescribed [7,25]. In some
cases, intravenous administration of immunoglobulin has a positive effect, helping neutralize
circulating autoantibodies and reduce inflammation [13,37].
The use of immunosuppression remains debatable and is conducted under strict control, as
suppression of the immune system during active viral replication may exacerbate the
infectious process [38].
Supportive and Symptomatic Therapy
To support heart contractile function, inotropic agents (dobutamine, dopamine) are used in
intensive care conditions for severe cases [31]. Diuretics (furosemide, spironolactone) are
prescribed for signs of congestion in the large or small circulation [39]. ACE inhibitors
(enalapril, captopril) and beta-blockers (metoprolol, bisoprolol) help reduce afterload and
improve heart remodeling in case of chronic heart failure development [13,32].
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Special importance is placed on regimen: the child should maintain relative rest, avoiding
intense physical activity until complete recovery or stabilization of heart function indicators
[9].
Prognosis and Complications
The prognosis for myocarditis in children depends on etiology, severity degree, timeliness of
diagnosis, and initiated therapy. Overall, in mild and moderate forms, especially of viral
origin, with adequate treatment, complete regression of changes and restoration of
contractile function is possible [1,37].
However, in severe myocarditis accompanied by heart failure and arrhythmias, the risk of
complications significantly increases. Among the most dangerous consequences are
[9,13,31]:
- Dilated cardiomyopathy;
- Chronic heart failure;
- Rhythm disturbances (ventricular tachycardias, complete heart blocks);
- Thromboembolic complications (with pronounced chamber dilation);
- Cardiogenic shock and fatal outcome in the acute period.
With adherence to rehabilitation principles and regular dynamic monitoring, a significant
portion of children can avoid severe complications and maintain satisfactory or nearly
normal heart function [40].
Prevention
There is no specific prevention for myocarditis, but it is important to take measures to
reduce infection risks and timely treat chronic inflammation foci. In particular [16,25]:
- Conducting vaccinations against influenza and other respiratory infections;
- Observing sanitary-hygienic standards in children's groups;
- Timely treatment of acute respiratory and bacterial diseases (especially sore throat,
sinusitis, pneumonia);
- Monitoring chronic infection foci (caries, tonsillitis, etc.);
- Using personal protective equipment (masks, antiseptics) during epidemics;
- Healthy lifestyle, balanced nutrition, and adequate physical activity.
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Early diagnosis of myocarditis in children, especially with symptoms indicating heart
pathology after an infection, is crucial in preventing disease progression [17,35].
Discussion
Analysis of modern research shows that myocarditis in children should be considered a
multifactorial disease, based on both infectious and autoimmune mechanisms [1,7]. Viral
agents play a leading role in initiating the inflammatory cascade, however, subsequent
autoimmune reorganization may sustain the pathological process even after pathogen
elimination [6,25].
Improvement of laboratory methods (PCR, high-sensitivity biomarkers, serology) and
visualization technologies (contrast-enhanced cardiac MRI) expands possibilities for early
diagnosis and allows individualization of therapeutic tactics [12,34,36]. However, questions
of differential diagnosis between myocarditis and some forms of idiopathic dilated
cardiomyopathy remain unresolved, especially when there are no obvious signs of infectious
process [28].
The literature emphasizes the need for an interdisciplinary approach: involvement of
pediatrician, cardiologist, infectious disease specialist, rheumatologist, and immunologist for
comprehensive patient assessment [16,22]. Close collaboration of specialists helps timely
identify secondary autoimmune reactions, select optimal immunotherapy regimens, and
assess the need for antiviral treatment [13,38].
An important aspect is the problem of residual myocardial changes and risk of developing
dilated cardiomyopathy in the long term. According to some foreign sources, up to 30% of
children who have experienced clinically expressed myocarditis may show signs of chronic
heart failure within 5-10 years [7,31]. Therefore, monitoring cardiovascular system status
during remission, active rehabilitation, and prevention of repeated infection episodes
become crucial [39,40].
Conclusion
1. Myocarditis in children is a multifactorial inflammatory lesion of the heart muscle, most
often caused by viral agents.
2. Etiological factors include enteroviruses, parvovirus B19, adenoviruses, influenza viruses,
bacteria (diphtheria, streptococci), etc.; pathogenesis is based on direct cytopathic and
autoimmune effects on cardiomyocytes.
3. Clinical manifestations vary from oligosymptomatic forms to severe conditions with heart
failure and arrhythmias; non-specific symptoms (shortness of breath, lethargy, feeding
refusal) are often observed in young children.
4. Diagnosis is based on combination of clinical picture, laboratory data (troponins,
inflammation markers), visualization methods (EchoCG, cardiac MRI), electrocardiography;
endomyocardial biopsy is performed if necessary.
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5. Treatment includes etiotropic (antiviral or antibacterial) therapy, immunotherapy
(corticosteroids, immunoglobulins), and supportive heart failure therapy (ACE inhibitors,
beta-blockers, diuretics).
6. Prognosis depends on timeliness of diagnosis and adequacy of treatment; some children
fully recover, others may progress to chronic form with risk of developing dilated
cardiomyopathy.
7. Prevention is based on reducing infection spread (vaccination, sanitation of chronic
infection foci), healthy lifestyle, and increased physician vigilance regarding myocarditis,
especially after viral diseases.
Thus, for improving outcomes of myocarditis in childhood, a comprehensive approach is
necessary, including early detection, personalized therapy, strict disease course monitoring,
and adequate rehabilitation. Further research should focus on improving objective diagnostic
methods, clarifying pathogenetic mechanisms, and developing new therapeutic strategies
considering genetic and immunological characteristics of a child's organism.
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