The aim of this study is to evaluate the blood level of anti‐heart antibodies (AHA) and its correlation with clinical outcomes in patients with severe and moderate coronavirus disease 2019 (COVID‐19). The study included 34 patients (23 males; mean age 60.2 ± 16.6 years) with COVID‐19 pneumonia. Besides standard medical examination, the AHA blood levels were observed, including antinuclear antibodies, antiendothelial cell antibodies, anti‐cardiomyocyte antibodies (AbC), anti‐smooth muscle antibodies (ASMA), and cardiac conducting tissue antibodies. Median hospital length of stay was 14 [13; 18] days. AHA levels were increased in 25 (73.5%) patients. Significant correlation (p < 0.05) of AHA levels with cardiovascular manifestations (r = 0.459) was found. AbC levels correlated with pneumonia severity (r = 0.472), respiratory failure (r = 0.387), need for invasive ventilation (r = 0.469), chest pain (r = 0.374), low QRS voltage (r = 0.415), and levels of C‐reactive protein (r = 0.360) and lactate dehydrogenase (r = 0.360). ASMA levels were found to correlate with atrial fibrillation (r = 0.414, p < 0.05). Antinuclear antibodies and AbC levels correlated with pericardial effusion (r = 0.721 and r = 0.745, respectively, p < 0.05). The lethality rate was 8.8%. AbC and ASMA levels correlated significantly with lethality (r = 0.363 and r = 0.426, respectively, p < 0.05) and were prognostically important. AHA can be considered as part of the systemic immune and inflammatory response in COVID‐19. Its possible role in the inflammatory heart disease requires further investigation.

Цель. Оценить частоту миокардита у взрослых больных с некомпактным миокардом (НКМ) левого желудочка (ЛЖ), его влияние на течение заболевания, результаты лечения и исходы. Материал и методы. В исследование включены 103 взрослых пациента с НКМ, 61 мужчина, средний возраст 45,6±14,9 лет (от 18 до 78). Средний конечный диастолический размер ЛЖ составил 6,0±0,8 см, ФВ ЛЖ 38,8±14,5%. Диагноз НКМ поставлен при помощи эхокардиографии, мультиспиральной компьютерной томографии (n=81) и магнитно-резонансной томографии (n=39). ДНК-диагностика проводилась по методу NGS с последующим секвенированием по Сенгеру. Патогенные мутации обнаружены у 9% больных в генах MYH7, MyBPC3, LAMP2, DES, DSP, TTN. Обследование включало также определение уровня антикардиальных антител, генома кардиотропных вирусов методом ПЦР, коронарографию (n=26), сцинтиграфию (n=25). Морфологическое исследование миокарда выполнено 19 пациентам (12 эндомиокардиальных биопсий (ЭМБ), 1 интраоперационная биопсия, 3 исследования эксплантированного сердца, в т. ч. два после ЭМБ, и 5 аутопсий). Средний срок наблюдения составил 12 [2; 32] месяцев. Результаты. Миокардит диагностирован в 53,4%, в т. ч. вирус-позитивный у 32,7% из них, с применением морфологического исследования миокардау 19 больных (активный у 10, пограничный у 6; с минимальными признаками активности у 3). Вирусный геном в миокарде выявлен у 8 больных (42,1%). Частота миокардита составила 44,4% при аритмическом варианте НКМ, 12,5% при хроническом ишемическом, 57,5% при дилатационной кардиомиопатии 50,0% у больных с НКМ в сочетании с другими кардиомиопатями. Особыми клиническими формами были острый/подострый миокардит у больных с НКМ (10,7% всех пациентов), острый некроз (инфаркт) миокарда (4,9%). Присоединение миокардита к НКМ привело к достоверно более тяжелой дисфункции ЛЖ (ФК ХСН 2 [1; 3] v 1,75 [0; 2], p<0,01, ФВ 33,8±13,5 v 44,7±13,6%, p<0,001), большей частоте неустойчивой желудочковой тахикардии (67,3% v 29,3%, p<0,01), оправданных срабатываний дефибрилляторов (38,9% v 0, p<0,05), смертей (16,4 и 4,2%, OШ 5,75, 95% CI 1,21-27,43, p<0,05) и трансплантации (7,3% v 2,1%, p>0,05). Только у больных с миокардитом в результате базисной (противовирусной и иммуносупрессивной) и кардиотропной терапии отмечено достоверное возрастание ФВ (при остром миокардите с 25,4±7,9 до 38,6±9,5%, p<0,01), снижение размеров ЛЖ и СДЛА. Заключение. Миокардит является типичным феноменом, который закономерно развивается у больных с первичным, в т. ч. генетически верифицированным, НКМ. Природа миокардита при НКМ может быть различна (первичный инфекционноиммунный, вторичный в ответ на генетическое/ишемическое повреждение кардиомиоцитов), однако независимо от этого он приводит к достоверному ухудшению структурно-функциональных показателей, увеличению частоты жизнеугрожающих аритмий, исходов (смерть + трансплантация, оправданные срабатывания дефибрилляторов) и требует активной базисной терапии.

Цель. Изучить спектр клинических форм некомпактного миокарда (НКМ) у взрослых, особенности их проявления, течения и прогрессирования в процессе проспективного наблюдения. Материал и методы. В исследование включены 116 взрослых пациентов с НКМ левого желудочка (ЛЖ), 67 мужчин, средний возраст 46,3±15,1 года) и 42 больных с повышенной трабекулярностью (ПТ) ЛЖ (24 мужчины, средний возраст 43,5±15,2 лет). Средний конечный диастолический размер ЛЖ составил 6,0±0,8 и 5,9±1,1 см, фракция выброса (ФВ) ЛЖ 38,6±14,0% и 44,6±18,3%, соответственно. Диагноз НКМ поставлен при помощи эхокардиографии, мультиспиральной компьютерной томографии (n=77) и магнитно-резонансной томографии (n=51), диагноз ПТ -по данным эхокардиографии, магнитно-резонансной томографии (n=11), мультиспиральной компьютерной томографии (n=24). ДНК-диагностика проводилась по методу NGS с последующим секвенированием по Сенгеру. Обследование включало определение антикардиальных антител, генома кардиотропных вирусов методом ПЦР, коронарографию (n=29/2), сцинтиграфию (n=27/4). Морфологическое исследование миокарда выполнено 22/6 больным с НКМ/ПТ (14/6 эндомиокардиальных, 1 интраоперационная биопсия, 3 исследования эксплантированного сердца, 6 аутопсий). Средний срок наблюдения при НКМ составил 15 [5;40] мес., при ПТ -6 [2;19] мес. Результаты. Патогенные мутации обнаружены у 12 (10,3%) больных в генах тяжелой цепи бета-миозина (MYH7), миозин-связывающего белка С (MyBPC3), лизосом-ассоциированного мембранного протеина 2 (LAMP2), десмина (DES), десмоплакина (DSP), титина (TTN), варианты с неустановленным клиническим значением (VUCS) -еще у 5 (4,3%); при ПТ у 1 больного выявлен VUCS. О наличии семейной кардиомиопатии можно думать у 24 пациентов (22%). Сочетание НКМ с врожденными пороками сердца диагностировано у 11 (9,5%) больных. Выделены 6 клинических вариантов (форм, сценариев диагностики) НКМ: бессимптомный (2% всех больных регистра), аритмический (15%), ишемический (7%), НКМ у больных с дилатационной кардиомиопатией (42%), НКМ у больных с острым/подострым миокардитом (12%) и в сочетании с другими первичными кардиомиопатиями (22%)гипертрофической кардиомиопатией, аритмогенной дисплазией правого желудочка, рестриктивной кардиомиопатией, первичной миодистрофией, саркоидозом сердца, болезнью Данона. Миокардит диагностирован у 51,7% больных с разными формами НКМ и у 59,5% больных с ПТ. Час тота основных клинических проявлений НКМ (хроническая сердечная недостаточность, различные нарушения ритма сердца, тромбоэмболические осложнения) и исходов варьировали в группах больных с разными вариантами течения НКМ. У больных с ПТ ЛЖ (не достигающей критериев НКМ) отмечены сходные клинические варианты при менее выраженной степени дисфункции миокарда, более редких жизнеугрожающих аритмиях и эмболиях. Диагностированные исходно клинические формы отличались стабильностью во времени. При анализе динамики ФВ и конечного диастолического размера ЛЖ отмечено достоверное улучшение только в группе больных с острым/подострым миокардитом (ФВ возросла с 27,3% до 39,2%, p<0,05), большинству ...

The level and significance of anticardiac antibodies (ACA) in patients with COVID-19 infection have not yet been studied.Aim. To assess the level of various ACA in patients with severe and moderate COVID-19 infection and to identify the correlation of antibody profile with the clinical performance and prognosis.Material and methods. The study included 86 (38 women and 48 men) patients aged 20-90 years (60,2±16,6 years) who were hospitalized for moderate and severe COVID-19 infection in April-June 2020. Nasopharyngeal swab confirmed the disease in 59,3% of patients. In addition to the standard examination, electrocardiography and chest scan, level of antinuclear antibodies (ANA), antiendothelial cell antibodies (AECA), anti-cardiomyocyte antibodies, antibodies to anti-smooth muscles (ASMA) and cardiac conduction system fibers. Echocardiography was performed in 17 patients. Mean length of stay was 14 [12; 18] days. Death was considered as the primary endpoint.Results. Prevalence of heart disease and symptoms (including hypertension and coronary artery disease) was 45,3%. The manifestations of coronavirus heart damage include arrhythmias (supraventricular premature beats, 3,6%; atrial fibrillation, 9,3%), heart failure (9,3%), low QRS voltage (11,4%), repolarization abnormalities (41,9%), pericardial effusion (30%). An increase in troponin levels was observed in low number of patients. All types of cardiovascular disease correlated with the maximum D-dimer level (AUC, 0,752, p<0,01). Titers of two or more types of ACA were increased by 3 or more times in 25 (73,5%) patients. Significant (p<0,05) correlations of ANA level with cardiovascular symptoms/diseases in general (r=0,459), anti-cardiomyocyte antibodies — with the prevalence of pneumonia (r=0,472), shortness of breath severity (r=0,370), respiratory failure (r=0,387), oxygen therapy (r=0,388) and mechanical ventilation (r=0,469), as well as the presence of chest pain (r=0,374), QRS voltage decrease (r=0,415), maximum level of CRP (r=0,360) and LDH (r=0,360). ANA and anti-cardiomyocyte antibody levels strongly correlated with pericardial effusion (r=0,721 and r=0,745, respectively, p<0,05). The mortality rate was 9,3%. Heart failure was one of the death causes in 37,5%. The level of anti-cardiomyocyte antibodies and ASMA correlated with mortality (r=0,363, and r=0,426, p<0,05) and had a predictive value. Mortality in patients with cardiovascular disease was 17,9%, without — 2,2% (p<0,05). The most powerful predictive model for COVID-19 adverse outcomes includes age, diabetes, oxygen therapy extent, maximum leukocyte, C-reactive protein and D-dimer levels. However, a model that includes only age, diabetes, and cardiovascular disease also has sufficient predictive power (correlation coefficient, 0,568, p<0,001).Conclusion. An increase in ACA titers was detected in 73,5% of patients, correlated with mortality, in most cases reflects the general activity and severity of the disease and can be regarded as part of response in COVID-19. At the same time, a direct correlation with signs of myocardial damage, the presence and volume of pericardial effusion confirms the direct role of ACA in the development of myopericarditis.

Patients with chronic myocarditis have a high risk of an unfavorable course of the novel coronavirus disease (COVID-19) due to the ability of the SARS-Cov-2 virus to independently cause acute myocarditis, to have a direct and cytokine-mediated cytopathic effect on the myocardium, as well as immunosuppressive therapy. At the same time, the features of the interaction of chronic myocarditis and COVID-19 have not been studied. The article describes a 31-year-old patient with a 10-year history of chronic recurrent infectious-immune myocarditis, who was on long-term immunosuppressive therapy (methylprednisolone and azathioprine in the past, then hydroxychloroquine). In May 2020, a serologically confirmed COVID-19 diagnosis was made. There were risk factors for the unfavorable course of coronavirus infection: heart failure and a history of persistent atrial fibrillation, male sex. Basic therapy with hydroxychloroquine (with an increase in its dose to 800-400 mg/day), ceftriaxone, and levofloxacin was carried out. The severity of pneumonia was moderate, despite febrile fever and severe intoxication. No relapses of arrhythmias, respiratory or heart failure were observed. Minimal laboratory (some increase in anticardial antibody titers) and echocardiographic signs of exacerbation of myocarditis without an increase in troponin T levels were revealed, which quickly regressed. It can be assumed that the maintenance immunosuppressive therapy of myocarditis with hydroxychloroquine had a positive effect on the course of coronavirus pneumonia and made it possible to avoid recurrence of myocarditis. Further study of the features of the course of the pre-existing myocarditis and pneumonia in COVID-19 is necessary.

Purpose: To evaluate the clinical features, laboratory and instrumental tests results and the effectiveness of complex treatment in a patient with multiple etiologies of dilated cardiomyopathy (DCM) with a high risk of sudden cardiac death. Methods: Female patient was 34 years old. Follow up period was seven years. Since the age of 23 (after a respiratory infection), chest pains and shortness of breath appeared. Coronary arteries were intact. After syncope in 2013, Holter-ECG was performed: 2048 premature ventricular beats (PVBs)/day and episode of sustained ventricular tachycardia (VT, 1 min) were registered. MRI was performed, and a cardioverter defibrillator (ICD) was implanted. Results: ECG showed low QRS voltage and negative T waves in leads V2-V6, III, aVF. In signal-averaged ECG, late potentials were detected. Echocardiography (EchoCG) demonstrated left and right ventricular dilatation, diffuse reduction of left ventricular (LV) contractility and multiple pseudochordae in LV. MRI showed LV noncompaction (LVNC), thickening of the epicardial fat and hypo-/dyskinesia of the anterior wall of the right ventricular (RV), dilatation of both ventricles with decrease of their ejection fraction and subepicardial gadolinium enhancement in the early and late phase in the LV, intraventricular septum and the free walls of the RV. The presence of LVNC was confirmed by cardiac computed tomography (CT). Late contrast enhancement in the middle and subendocardial layer of the LV was observed as well. The level of anticardiac antibodies was high (1:160–1:320). The reasons for statement of a possible diagnosis of myocarditis in this case were the connection of the onset of symptoms with viral infection, high titers of anticardiac antibodies, and early and late subepicardial contrast enhancement by MRI and CT. The endomyocardial biopsy was obtained, and subendocardial lipomatosis, separation of myocardium by fibrous septa, lymphocytic infiltrates (more than 14 cells/mm2) and vasculitis were found. Viral genome in myocardium was not detected. A new splicing mutation in the desmoplakin (DSP) gene was found (NM_004415.4: c.1141-2A>G/N (rs794728111)). Combination of arrhythmogenic right ventricular cardiomyopathy (ARVC), LVNC and myocarditis was diagnosed. Immunosuppressive therapy (prednisone and azathioprine) was prescribed, LV ejection fraction stabilized at the level of 40%. The appropriate shocks of the ICD due to sustainedVT (HR 210/min) with transformation into ventricular fibrillation were recorded twice. For this reason, sotalol was temporarily replaced with amiodarone. After the suppression of myocarditis activity, sustained VT and ICD interventions were not observed. Conclusions: In a young patient with arrhythmogenic syncope and DCM syndrome, a combination of ARVC (two major and three minor criteria, definite diagnosis) and LVNC with the biopsy proved virus-negative chronic myocarditis was diagnosed. DCM as a syndrome can have multiple causes, and the combination of myocarditis and primary cardiomyopathy is not rare. LVNC can be observed in patients with typical desmosomal protein mutations. The use of immunosuppressive therapy led to the stabilization of heart failure and decreased the risk of arrhythmic events.

<b><i>Purpose:</i></b> The aim of this study is to evaluate the frequency of cardiac involvement in patients with coronavirus disease 2019 (COVID-19), possible immune mechanisms of myocardial injury, and the place of cardiovascular pathology among other prognostic factors. <b><i>Methods:</i></b> The study included 86 patients (48 male, 60.2 ± 16.6 years) with COVID-19. In addition to common investigation, examination of troponin T (<i>n</i> = 18) and anti-heart antibodies (AHA, <i>n</i> = 34) were used. The average hospital period was 14 [12; 18] days. <b><i>Results:</i></b> The incidence of cardiovascular disease and symptoms was 45.3%. Arrhythmias, heart failure, low-QRS voltage, repolarization disorders, and pericardial effusion were the typical for coronavirus cardiac injury. The level of AHA was increased in 73.5%. Significant (<i>p</i> &#x3c; 0.05) correlations of AHA level with inflammatory activity, pneumonia, respiratory failure, cardiac symptoms, and death were found. D-dimer &#x3e;0.5 μg/mL had a sensitivity of 79.2% and specificity of 60% in the prediction of cardiovascular manifestations. Cardiac failure was one of the causes of death in 3/8 patients (37.5%). Lethality in the presence of cardiovascular pathology was 17.9 versus 2.2% without it, <i>p</i> &#x3c; 0.05. The most powerful prognostic model includes age, diabetes, oxygen therapy volume, maximum leukocyte level, C-reactive protein, and D-dimer (correlation coefficient 0.871, <i>p</i> &#x3c; 0.001). The model with only age, diabetes, and cardiovascular disease included also had predictive power (correlation coefficient 0.568, <i>p</i> &#x3c; 0.001). <b><i>Conclusions:</i></b> The cardiovascular pathology is frequent in patients with COVID-19 and strong correlates with the D-dimer. It indicates the high significance of prothrombotic and ischemic mechanisms. High AHA levels may reflect an inflammatory heart injury. The cardiovascular pathology is associated with higher lethality.

Chronic infectious-immune myocarditis of severe course can potentially be considered as a factor that aggravates the course of new coronavirus disease (COVID-19) and increases the risk of adverse outcomes. The interaction of chronic myocarditis and COVID-19 during long-term immunosuppressive therapy has not been studied. We present a description of a 35-year-old female patient with chronic infectious-immune myocarditis (morphologically confirmed, with a history of infarction-like onset and thromboembolic complications), who had continuous immunosuppressive therapy with methylprednisolone and mycophenolate mofetil. The patient also received new oral anticoagulants and tenofovir (for chronic HBV infection). COVID-19 (SARS-Cov-2 RNA+) was diagnosed in May 2020. Risk factors for the adverse course of coronavirus infection included severe obesity, heart failure, and life-threatening ventricular arrhythmias. Correction of immunosuppressive therapy (withdrawal of the cytostatic agent, administration of hydroxychloroquine) and therapy with levofloxacin, an interleukin-17 inhibitor (netakimab) were performed. The severity of pneumonia and respiratory failure was moderate despite high fever and high levels of inflammatory markers in the blood (including interleukin-6). Signs of exacerbation of myocarditis, increased levels of troponin T and anticardial antibodies (compared with the initial ones) were not found. It can be assumed that supportive immunosuppressive therapy for myocarditis has a positive effect on the course of coronavirus pneumonia and avoids exacerbation of myocarditis. Careful continuation of immunosuppressive therapy with temporary withdrawal of aggressive cytostatics can be recommended in chronic myocarditis. Further study of the features of the course of previous myocarditis and COVID-19 pneumonia is necessary.