What causes myocarditis in children?

The causes of myocarditis in children are different.

• Infectious causes of myocarditis.
  • Viruses - Coxsackie A and B, ECHO, adenoviruses, influenza A and B viruses, poliomyelitis, rubella, measles, mumps, PC viruses, varicella zoster, herpes simplex, hepatitis, HIV, cytomegalovirus, parvovirus B19, Epstein-Barr.
  • Bacteria - Mycoplasma pneumoniae. Chlamydia, Rickettsia, Borrelia burgdorferi, Staphylococcus aureus, Enterococci spp., Corinebacteria diphtheriae.
  • Mushrooms - Criptococcus neoformans.
  • Protozoa - Toxoplasma gondii, Tripanosoma cruzi.
  • Parasites - Trichinella spiralis, echinococcus.
• Noninfectious causes of myocarditis.
  • Endocrine disorders - thyrotoxicosis, pheochromocytoma.
  • Allergic reactions - sulfonamides, penicillins, tetracyclines, insect bites.
  • Toxic effect - aminosalicylic acid, paracetamol, procainamide, streptomycin, doxorubicin, cyclophosphamide, etc.
  • Other diseases are Kawasaki disease, rheumatoid arthritis, systemic vasculitis, connective tissue diseases.
  • Other causes are radiation therapy, transplant rejection.
  • It is universally recognized that inflammatory myocardial lesions can develop in any infectious diseases, at any age, including the fetal period.

An important role in the chronicization of inflammation in chronic myocarditis in children is involved in the pathological process of intracellular pathogens: viruses, chlamydia toxoplasma. The most frequent causative agent of viral myocarditis is the Coxsackie B virus, which is explained by the structural similarity of enteroviruses to the cell membrane of cardiomyocytes. In children, an important role is assigned to the herpes group viruses (cytomegalovirus, herpes simplex virus types 1 and 2, varicella zoster ). In addition to direct damage to myocardial tissue, these intracellular pathogens can persist for a long time in the body, changing the state of cellular and humoral immunity in such a way that many other infectious factors (influenza, hepatitis, encephalomyelitis, Epstein-Barr, etc.) acquire the ability to induce and support inflammatory process in the myocardium. Based on experimental studies in animal models, it was shown that herpes simplex viruses in combination with other pathogens cause pronounced inflammatory and autoimmune reactions. Recently, cases of myocarditis associated with parvovirus B19 have become more common.

Myocarditis in children can develop in conditions accompanied by hypersensitivity, for example, in acute rheumatic fever, or be a consequence of exposure to radiation, chemicals, drugs, physical effects. Myocarditis often accompanies systemic diseases of connective tissue, vasculitis, bronchial asthma. Separately, burn and transplant myocarditis have been identified.

Pathogenesis of myocarditis in children

The features of viral myocarditis are due to the possible direct penetration of the virus into the myocytes, followed by replication and cytotoxic effect, up to cell lysis or mediated action through humoral and cellular immune responses in the myocardium. In this connection, the virus replication phase is isolated (phase 1). In this phase, the causative agent can be isolated from the blood and cardiac biopsies. Further, when the process is chronicized, the presence of virus particles can not be detected. The main significance in the pathogenesis of myocardial viral damage is attached to the cellular and humoral response following the replication of the virus, which leads to histo-lymphocytic infiltration and damage to the elements of the cardiac muscle (phase 2-autoimmune). Further, the prevalence of dystrophic (phase 3) and fibrotic (phase 4) changes is noted with the formation of a clinical picture of dilated cardiomyopathy (DCMP).

With non-viral infectious myocarditis, the leading role in the pathogenesis of the disease, apart from the direct introduction of the pathogen or its toxins, is allergic and autoimmune mechanisms. The morphological substrate of various types of myocarditis is the combination of dystrophic-necrobiotic changes in cardiomyocytes and exudative-proliferative changes in interstitial tissue.

Discuss the role of chronic viral infection, persistent in the human body in myocarditis with chronic course. Assume the possibility of a long latent existence of viruses in myocardial tissue with their subsequent activation under the influence of various factors that reduce the resistance of the organism.

The results of experimental studies indicate that both viruses and immune effector mechanisms themselves can damage and destroy myocytes, and these various mechanisms manifest themselves in different ways depending on various circumstances. The genetic predisposition, the presence of antiviral protective factors and the immunogenicity of viruses play an important role in viral myocarditis.

Classification of myocarditis in children

Classification of myocarditis to the present day remains one of the important issues of modern cardiology, which is due to the diversity of etiological factors, pathogenetic mechanisms of their development. An indistinctly outlined clinical picture of myocardial disease, the possibility of switching certain forms of myocardial diseases to one another and combining them in the form of various combinations led to considerable terminological confusion and the absence of a single universally recognized classification.

Pediatricians and children's cardiologists in our country use in their practice the classification of non-rheumatic carditis, proposed by NA. Belokon in 1984

Classification of non-rheumatic myocarditis in children (according to Belokon NA, 1984)

Period of onset of disease	Congenital (early and late). Acquired
Etiological factor	Viral, viral-bacterial, bacterial, parasitic, fungal, iersiniosis, allergic
Form (for localization)	Carditis. Damage to the conduction system of the heart
Flow	Acute - up to 3 months. Podostroye - up to 18 months. Chronic - more than 18 months (relapsing, primarily chronic)
The form and stage of heart failure	Left ventricular I, IIA, PB, III stage. Right ventricular I, IIA, IIB, III stage. Total
Outcomes and complications	Cardiosclerosis, myocardial hypertrophy, rhythm and conduction disorders, pulmonary hypertension, valve damage, constrictive myopericarditis, thromboembolic syndrome
The severity of carditis	Light, medium, heavy

[1], [2], [3], [4], [5], [6]