The recommendations are dedicated to contemporary aspects of epidemiology, etiology, pathogenesis, diagnosis, etiology-based, pathogenetic and symptomatic treatment of myocarditis. Various pathogenetic mechanisms that cause the development and progression of inflammatory heart disease and cause dilatation and systolic dysfunction, lead to heart failure and the development of other complications of myocarditis are described in detail. These recommendations present the modern classification of myocarditis, approved in Ukraine, and modern algorithms for diagnosis and clinical management of patients, in particular the algorithm that justifies the appointment of glucocorticoids for patients with myocarditis. The characteristics of different variants of myocarditis are also presented with clarifications concerning diagnosis and treatment. Much attention is paid to various approaches to the etiotropic and pathogenetic treatment of myocarditis and their possible prospects. It is obvious that in order to standardize approaches to the diagnosis and management of acute and chronic myocarditis, it is necessary to conduct large-scale multicenter studies and create special registries. In addition, in the current context of the COVID-19 pandemic, the pathological effects of SARS-Cov-2 as a trigger of myocarditis need further study, in particular in terms of impact on the prognosis and approaches to pathogenetic therapy in such patients. Unification of terminology and approaches to diagnosis and clinical monitoring of patients with myocarditis can improve management tactics and increase the survival rate of such patients. To identify high-risk patients (with arrhythmias, high probability of recurrence or transformation of myocarditis into dilated cardiomyopathy) and candidates for heart transplantation, the most promising is the creation of special databases of such patients

Diagnosis and prognosis of myocarditis course remain one of the most complex and unsolved problems of contemporary cardiology, not only in Ukraine but also in the developed countries of the world. It is well known that in order to develop adequate methods of diagnosis, treatment and prevention of complications, fundamental knowledge regarding the pathogenetic mechanisms of the development and progression of a particular disease is necessary. In the pathogenesis of impaired cardiac function and its dilation in both acute and chronic stages of myocarditis, the primary role played by immunopathological reactions manifested by autoimmunization and hyperreactivity against the structural elements of the heart muscle. The pathogenetic mechanisms of viral myocarditis are based on a complex of factors – direct cytotoxic effect of virus on cardiomyocytes, activation of apoptotic processes, as well as reactions of primary and secondary immunity, microvascular lesion, remodeling of the contractile apparatus of the heart muscle. The main proinflammatory cytokines produced by immune cells in the inflammation zone are: γ-interferon, tumor necrosis factor-α, interleukin (IL) 1β, IL-2, IL-6, IL-17A, IL-23. Another mechanism of myocardial contraction is associated with the activation of immunopathological responses of the humoral type with the synthesis of cardiospecific antibodies, in particular to the β1-adrenoceptor, cardiac myosin, actin, laminin, vimentin and other structures of the heart muscle. A significant role in the pathogenesis of myocarditis is now given to stimulation of Toll-like receptors of type 2 and type 4 and activation of matrix metalloproteinases, which has a direct relationship with the production of proinflammatory cytokines. Promising to clarify some of the pathogenetic mechanisms of inflammatory heart damage is currently considered the study of different microRNAs types. Currently, the world cardiology community recognizes the relevance of further study of the various mechanisms of myocarditis pathways in order to identify those pathogenetic links, the impact of which can reduce the pathological effect of inflammatory cardiac damage and the severity of the disease and improve prognosis for patients with myocarditis. Diagnosis and prognosis of myocarditis course remain one of the most complex and unsolved problems of contemporary cardiology, not only in Ukraine but also in the developed countries of the world. It is well known that in order to develop adequate methods of diagnosis, treatment and prevention of complications, fundamental knowledge regarding the pathogenetic mechanisms of the development and progression of a particular disease is necessary. In the pathogenesis of impaired cardiac function and its dilation in both acute and chronic stages of myocarditis, the primary role played by immunopathological reactions manifested by autoimmunization and hyperreactivity against the structural elements of the heart muscle. The pathogenetic mechanisms of viral myocarditis are based on a complex of factors – direct cytotoxic effect of virus on cardiomyocytes, activation of apoptotic processes, as well as reactions of primary and secondary immunity, microvascular lesion, remodeling of the contractile apparatus of the heart muscle. The main proinflammatory cytokines produced by immune cells in the inflammation zone are: γ-interferon, tumor necrosis factor-α, interleukin (IL) 1β, IL-2, IL-6, IL-17A, IL-23. Another mechanism of myocardial contraction is associated with the activation of immunopathological responses of the humoral type with the synthesis of cardiospecific antibodies, in particular to the β1-adrenoceptor, cardiac myosin, actin, laminin, vimentin and other structures of the heart muscle. A significant role in the pathogenesis of myocarditis is now given to stimulation of Toll-like receptors of type 2 and type 4 and activation of matrix metalloproteinases, which has a direct relationship with the production of proinflammatory cytokines. Promising to clarify some of the pathogenetic mechanisms of inflammatory heart damage is currently considered the study of different microRNAs types. Currently, the world cardiology community recognizes the relevance of further study of the various mechanisms of myocarditis pathways in order to identify those pathogenetic links, the impact of which can reduce the pathological effect of inflammatory cardiac damage and the severity of the disease and improve prognosis for patients with myocarditis. Diagnosis and prognosis of myocarditis course remain one of the most complex and unsolved problems of contemporary cardiology, not only in Ukraine but also in the developed countries of the world. It is well known that in order to develop adequate methods of diagnosis, treatment and prevention of complications, fundamental knowledge regarding the pathogenetic mechanisms of the development and progression of a particular disease is necessary. In the pathogenesis of impaired cardiac function and its dilation in both acute and chronic stages of myocarditis, the primary role played by immunopathological reactions manifested by autoimmunization and hyperreactivity against the structural elements of the heart muscle. The pathogenetic mechanisms of viral myocarditis are based on a complex of factors – direct cytotoxic effect of virus on cardiomyocytes, activation of apoptotic processes, as well as reactions of primary and secondary immunity, microvascular lesion, remodeling of the contractile apparatus of the heart muscle. The main proinflammatory cytokines produced by immune cells in the inflammation zone are: γ-interferon, tumor necrosis factor-α, interleukin (IL) 1β, IL-2, IL-6, IL-17A, IL-23. Another mechanism of myocardial contraction is associated with the activation of immunopathological responses of the humoral type with the synthesis of cardiospecific antibodies, in particular to the β1-adrenoceptor, cardiac myosin, actin, laminin, vimentin and other structures of the heart muscle. A significant role in the pathogenesis of myocarditis is now given to stimulation of Toll-like receptors of type 2 and type 4 and activation of matrix metalloproteinases, which has a direct relationship with the production of proinflammatory cytokines. Promising to clarify some of the pathogenetic mechanisms of inflammatory heart damage is currently considered the study of different microRNAs types. Currently, the world cardiology community recognizes the relevance of further study of the various mechanisms of myocarditis pathways in order to identify those pathogenetic links, the impact of which can reduce the pathological effect of inflammatory cardiac damage and the severity of the disease and improve prognosis for patients with myocarditis.

The aim of the study - to evaluate the efficacy of glucocorticoids (GC) in patients with acute myocarditis (AM) after COVID-19 infection. Material and methods We included 60 pts with severe AM and heart failure (HF) with reduced (<40%) left ventricular (LV) ejection fraction (EF) who had COVID-19 infection 1–2 months before the enrollment. According to the results of cardiac magnetic resonance (CMR) included pts had ≥2 Lake Louise criteria for myocarditis. All pts on the background of HF therapy (β-blockers, ACE-inhibitors, MRA antagonists, diuretics) were prescribed GC: 0.25 mg/kg per day methylprednisolone for 3 months, followed by a gradual dose reduction of 1–2 mg per week until complete discontinuation after 6 months. Evaluation before the start of GC therapy and after 6 months included CMR, 2D- and speckle-tracking echocardiography. Results After 6 months according to the results of CMR the number of LV segments with inflammatory lesions decreased to (3,58±0,42) from (6,32±0,77) segments in average (p=0,001). This was followed by improvement of LV systolic function: increase of LV EF in average to (43,5±2,6) from (32,2±2,4) % (p=0,003), longitudinal global systolic strain (LGSS) absolute value to (11,3±1,1) from (7,9±0,5) % (p=0,012) and circumferential global systolic strain (CGSS) to (12,1±1,0) from (8,9±0,6) % (p=0,023). Also we observed LV volume reduction: decrease of LV end-diastolic (from 118,9±8,6 to 95,3±7,2 ml/m2, p=0,033) and LV end-systolic (from 80,1±5,1 to 59,1±4,4 ml/m2, p=0,027) volume indexes. Wherein in 24 of 60 pts (41,6%) on the background of significant decrease in the number of LV segments with inflammatory lesions (to 1,34±0,21 from 6,12±0,73 segments, p=0,0001) after 6 months we observed the recovery of LV EF ≥50%, followed by an improvement of LGSS and CGSS on 42,1 and 39,4% respectively (p=0,001). According to multivariate regression analysis, predictors of LV EF recovery (≥50%) after 6 months of GC treatment were established: presence of inflammatory lesions in ≤5,0 LV segments, values of LGSS and CGSS ≥9.0% and ≥9.5% respectively before the start of GC. Conclusions The use of GC in pts with severe AM after COVID-19 was followed by the decrease of LV segments number affected by inflammation, improvement of LV systolic function and reduction of LV volume indexes. In 41,6% of pts GC therapy was associated with LV EF recovery after 6 months and predictors of its effectiveness were found: presence of inflammatory lesions in ≤5,0 LV segments, values of LGSS and CGSS ≥9.0% and ≥9.5% respectively before the start of GC. Funding Acknowledgement Type of funding sources: None.

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The aim – to establish differences in the structural and functional state of the heart in patients with chronic myocarditis and dilated cardiomyopathy and to investigate their associations with the presence of cardiac rhythm disorders. Materials and methods. We included 95 patients who were divided into two groups: the first group consisted of 55 patients with chronic myocarditis (CM), the second group included 40 patients with dilated cardiomyopathy (DCM). All patients had heart failure (HF) II or higher functional class (FC) according to the classification of the New York Heart Association (NYHA) and a reduced left ventricular (LV) ejection fraction (EF). All patients underwent the echocardiography (EchoCG) with speckle tracking (ST), Holter electrocardiogram monitoring and cardiac magnetic resonance (CMR) imaging. Results and discussion. A comparative analysis of the EchoCG data revealed that CM was characterized by lower values of LV end-diastolic and end-systolic volume indexes (by 21.7 and 28.6 %, respectively, p<0.01) and by 16.8 % (p<0.05) higher value of LV EF compared to DCM; when studying the results of ST EchoCG, it was found that in patients with CM, the absolute values of the longitudinal, circumferential and radial global systolic LV strain were by 25.0; 23.7 and 28.5 %, respectively, higher compared with patients with DCM (p<0.05–0.01). The obtained data were confirmed by the results of 6-minute walking test, so patients with DCM demonstrated the lower tolerance to physical exercise comparing with CM. When performing CMR in patients with CM, along with inflammatory changes in the myocardium (edema and hyperemia), fibrotic changes were present, while DCM was characterized only by diffuse fibrotic changes of the heart. The association between the presence of delayed enhancement on CMR and episodes of unstable ventricular tachycardia was proved for both CM and DCM – the result of Fisher’s exact test was p=0.019 and p=0.027 respectively. Conclusions. In patients with DCM compared with CM we found more significant impairment of the structural and functional state of the heart, that was manifested by the presence of the worst heart failure functional class and a lower tolerance to exercise test. It has been established that fibrotic changes of the myocardium both in CM and in DCM are associated with the presence of ventricular arrhythmias, including such potentially dangerous ones as episodes of unstable ventricular tachycardia.