Myocarditis is a focal or diffuse inflammatory lesion of the heart muscle that clinically manifests with symptoms and/or signs of heart failure (HF). It is caused by infectious agents (viruses, bacteria, parasites, protozoa) and non-infectious factors (toxins, poisons, heavy metals, burns, radiation, metabolic disorders, allergens, pesticides, medications), as well as systemic connective tissue diseases (CTDs). Clinically, myocarditis can present in fulminant, subacute, or chronic forms (active or persistent), and also as giant cell or eosinophilic myocarditis. The main pathogenetic mechanisms include the entry of pathogens through portals such as the respiratory tract, gastrointestinal tract, or genitourinary system; viral penetration into cardiomyocytes; viral replication; disruption of the multiprotein complex within the cell; activation of the inflammasome cascade; apoptosis, necrobiosis, and necrosis of cardiomyocytes; formation of inflammatory cellular infiltration; chemokine and cytokine production; and autoimmune damage to cardiomyocytes, leading to structural and functional remodeling of the heart. Diagnosis of myocarditis is based on anamnesis (acute onset, association with infection), clinical symptoms (dyspnea, palpitations, fever, chest pain), electrocardiographic findings (conduction and/or excitability disturbances), echocardiographic findings (reduced systolic function, chamber dilatation), laboratory tests (leukocytosis, lymphopenia, elevated ESR, increased levels of brain natriuretic peptide, C-reactive protein, fibrinogen, procalcitonin, ferritin, D-dimer, immunoglobulin E), and serological tests (identification of viruses, bacteria, etc.). Additional diagnostic tools include measurements of troponins, lactate dehydrogenase, CK-MB, interleukin-6 titers, myocardial autoantibodies, assessment of CTD activity, and viral load quantification via polymerase chain reaction (PCR). In cases of acute myocarditis, cardiac MRI with gadolinium shows subepicardial and transmural contrast enhancement. The gold standard for diagnosis remains endomyocardial biopsy with light microscopy of formalin-fixed paraffin-embedded sections, immunohistochemical analysis, molecular tests (PCR), and transmission electron microscopy. Modern treatment of myocarditis includes etiological and pathogenetic therapy. In the majority of patients, especially in milder cases, myocarditis resolves spontaneously without active intervention, with spontaneous recovery occurring as the infection subsides. Severe and extremely severe cases often progress to post-myocarditic cardiosclerosis, leading to dilated cardiomyopathy and the potential need for heart transplantation. This article presents the results of a clinical case of acute myocarditis in a 38-year-old patient with bilateral pneumonia. The diagnosis of acute myocarditis was established based on medical history, clinical presentation, echocardiographic findings, and laboratory and serological data.
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