What causes myocarditis in children?

The causes of myocarditis in children vary.

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

A significant role in the chronization of inflammation in chronic myocarditis in children is assigned to the participation in the pathological process of intracellular pathogens: viruses, chlamydia, toxoplasma. The most common pathogen of viral myocarditis is considered to be the Coxsackie B virus, which is explained by the structural similarity of enteroviruses with the cell membrane of cardiomyocytes. In children, an important role is assigned to herpes viruses (cytomegalovirus, herpes simplex virus types 1 and 2, varicella zoster ). In addition to direct damage to myocardial tissue, these intracellular pathogens can persist in the body for a long time, changing the state of cellular and humoral immunity in such a way that many other infectious factors (flu, hepatitis, encephalomyelitis, Epstein-Barr, etc.) acquire the ability to induce and maintain an inflammatory process in the myocardium. Based on experimental studies on animal models, it has been 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 increasingly common.

Myocarditis in children can develop in conditions accompanied by hypersensitivity, such as 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. Burn and transplant myocarditis are distinguished separately.

Pathogenesis of myocarditis in children

The features of viral myocarditis are caused by possible direct penetration of the virus into myocytes with subsequent replication and cytotoxic effect up to cell lysis or indirect action through humoral and cellular immune responses in the myocardium. In this regard, the phase of virus replication (phase 1) is distinguished. In this phase, the pathogen can be isolated from blood and cardiac biopsies. Further, when the process becomes chronic, the presence of viral particles cannot be detected. The main significance in the pathogenesis of viral myocardial damage is given to the cellular and humoral response following virus replication, which leads to histolymphocytic infiltration and damage to elements of the heart muscle (phase 2 - autoimmune). Subsequently, the prevalence of dystrophic (phase 3) and fibrous (phase 4) changes is noted with the formation of a clinical picture of dilated cardiomyopathy (DCM).

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

The role of chronic viral infection persisting in the human body in chronic myocarditis is discussed. The possibility of long-term latent existence of viruses in myocardial tissue with their subsequent activation under the influence of various factors that reduce the body's resistance is suggested.

Experimental studies indicate that both viruses themselves and immune effector mechanisms can damage and destroy myocytes, and these different mechanisms manifest themselves differently depending on different circumstances. 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 remains one of the important issues of modern cardiology to this day, which is due to the diversity of etiological factors and pathogenetic mechanisms of their development. The unclearly defined clinical picture of myocardial disease, the possibility of the transition of individual forms of myocardial disease from one to another and their combination in the form of various combinations has led to significant terminological confusion and the absence of a single, generally accepted classification.

Pediatricians and pediatric cardiologists in our country use in their practice the classification of non-rheumatic carditis proposed by N.A. Belokon in 1984.

Classification of non-rheumatic myocarditis in children (according to Belokon N.A., 1984)

Period of onset of the disease	Congenital (early and late). Acquired
Etiological factor	Viral, viral-bacterial, bacterial, parasitic, fungal, yersiniosis, allergic
Form (by localization)	Carditis. Conduction system damage of the heart
Flow	Acute - up to 3 months. Subacute - up to 18 months. Chronic - more than 18 months (recurrent, primary chronic)
Form and stage of heart failure	Left ventricular I, IIA, PI, III stages. Right ventricular stage I, IIA, IIB, III. Total
Outcomes and complications	Cardiosclerosis, myocardial hypertrophy, rhythm and conduction disturbances, pulmonary hypertension, valve damage, constrictive myopericarditis, thromboembolic syndrome
Severity of carditis	Light, medium, heavy

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