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Objective. To evaluate the alterations of Global longitudinsl strain (GLS) and it’s value for prediction of cardiotoxicity of low to moderate cumulative doses of anthracyclines. Methods. Forty-nine women 50 ± 10 years old with breast cancer, treated with anthracyclines (cumulative dose of 251 ± 60 mg/m2) were enrolled in the study. Echocardiography with GLS measurement was performed at baseline, at the end of anthracycline treatment, then every 3 months during 1 year. Cardiotoxicity was defined as a decline in left ventricular ejection fraction (LVEF) of at least 10 % to ≤ 53 %. Results. There was a significant increase in mean LVESV and LVEDV and decrease of GLS (р < 0,05) but not LVEF at 3 month post anthracycline treatment. Cardiotoxicity was detected in 8 patients (16 %) with moderate baseline risk. Absolute ≥ 4 % reduction of GLS during follow-up, GLS andpercent of it’s reduction from baseline to 3 month post-anthracycline were predictive of cardiotoxicity (AUC = 0,822 and 0,870, respectively). The reduction in GLS of >12,5 % from baseline at 3 month post anthracyclines was predictive of cardiotoxicity with sensitivity of 80 % and specificity of 95 %. Conclusions. GLS and its reduction from baseline has shown predictive value for development of cardiotoxicity in patients with moderate risk treated with low-to moderate cumulative doses of antracyclines. Additional echocardiography with GLS assessment at 3–6 month after completion of anthracycline treatment may be recommended irrespective of cardiotoxicity risk.

Aim. To evaluate the correlation of values of left atrial (LA) strain in patients with atrial fibrillation (AF) who underwent cardioversion (CV) with AF recurrence, hospitalization or death in early and late periods after cardioversion.Material and methods. 85 patients of the University Clinical Hospital No. 1 of Sechenov University were examined: 30 men (35.3 %) and 55 women (64.7 %), the average age was 70 ± 8 years. All patients underwent speckle tracking, the parameters of LA strain and LA stiffness index were determined upon admission to the hospital after CV; after 1, 3, 6 months, a relapse of AF, the fact of hospitalization for cardiovascular reasons, and death were detected.Results. 4 people died during the follow-up, 37 hospitalizations were registered due to a relapse of AF, 7 developed a long-term persistent/permanent form of AF. The predictors associated with the onset of adverse events at the 3rd month were: reduction of the negative peak in the 4-chamber position (risk ratio (HR) 1.26, 95 % confidence interval (CI) 1.05, 1.51; p=0.009), reduction of LA strain in the 4-chamber position (HR 0.85, CI 0.75, 0.96; p=0.007), reduction of positive strain peaks in the 4-chamber (HR 0.44, CI 0.25, 0.77; pConclusion. Evaluation of LA strain parameters during speckle- tracking may be promising in patients with AF after CV, since their decrease correlates well with the risk of adverse events in the long-term periods (3 and 6 months after CV).

The aim of the study– to evaluate the parameters of left atrial myocardial strain in patients with atrial fibrillation who underwent electrical and drug cardioversion.Materials and methods.The study included 118 patients of the University Clinical Hospital No 1 of the First Sechenov Moscow State Medical University. The analysis was carried out in three groups of patients: group 1 (n=54) – patients with atrial fibrillation who underwent electrical cardioversion; group 2 (n=31) – patients with atrial fibrillation who underwent drug cardioversion; group 3 (n=43) – patients without a history of atrial fibrillation. The clinical and anamnestic data of the medical history of each patient, as well as ultrasound indicators were evaluated: global strain of the left atrial, the values of negative peaks as a reflection of the left atrial systole and the values of positive peaks as a reflection of the filling of the left atrium, LASI – the left atrial stiffness index.Results.The analysis showed that left atrial strain in patients with atrial fibrillation were reduced in all analyzed parameters: negative strain peaks (-9.00 vs. -12.6 in the control group, pConclusions.The indicators of left atrial strain were significantly reduced, and the left atrial stiffness index was significantly increased both in the group with electrical cardioversion and in the group with drug-induced cardioversion, compared with patients with similar cardiovascular pathologies, but without a history of atrial fibrillation episodes.

Giant cell myocarditis (GCM) is a rare condition. Its association with SARS‐CoV‐2 has not been described before. The 46‐year‐old female patient was admitted to the clinic on September 2020. She had 7 year adrenal insufficiency history and infarct‐like debut of myocardial disease in November 2019. After COVID‐19 in April 2020, cardiac disease progressed. The examination showed low QRS voltage, QS complexes in V1–V5 leads, atrial standstill, left ventricular systolic and restrictive dysfunction, elevated anti‐heart antibodies, and subepicardial late gadolinium enhancement by magnetic resonance imaging. Endomyocardial biopsy and pacemaker implantation were performed, but the patient died suddenly due to ventricular tachycardia or ventricular fibrillation (the resuscitation was ineffective). The autopsy revealed GCM, SARS‐CoV‐2, and Parvovirus B19 were detected in the myocardium. The role of SARS‐CoV‐2 in the pathogenesis of autoimmune myocarditis is discussed.

A procedure allowing preparation of mixed metal–carbon nanostructures from electroplating waste in a high yield was suggested. The following substances containing all the metals from the initial slime can be prepared from electroplating slimes (containing mainly iron or copper): metal phthalocyanines, phthalocyanine pyrolyzates, mixed endometallofullerenes, and their hydroxylated derivatives.

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.

Aim. To analyze the register of pericarditis in a therapeutic clinic, to evaluate their nosological spectrum, to optimize approaches to diagnosis and treatment. Materials and methods. For the period 2007–2018, the register includes 76 patients with the diagnosis of “pericarditis” (average age 53.1±15.7 years, 20–85 years, 46 female). Patients with hydropericardium were not included in the register. Diagnostic puncture of pericardium was carried out in 5 patients, pleural puncture – in 11 patients. Morphological diagnostics included endomyocardial/ intraoperative biopsy of myocardium ( n =4/2), thoracoscopic/intraoperative biopsy of pericardium ( n =1/6), pleural puncture ( n =5), transbronchial ( n =1), thoracoscopic biopsy of intrathoracic lymph nodes ( n =2), lung ( n =1), supraclavicular lymph node biopsy ( n =1), salivary gland ( n =1), subcutaneous fat and rectum biopsy per amyloid ( n =6/1). The genome of cardiotropic viruses, level of anti-heart antibodies, C-reactive protein, antinuclear factor, rheumatoid factor (antibodies to cyclic citrullinized peptide), antibodies to neutrophil cytoplasm were determined, extractable nuclear antigens (ENA), protein immunoelectrophoresis, diaskin test, computed tomography of lungs and heart, cardiac magnetic resonance imaging, oncologic search. Results. The following forms of pericarditis were verified: tuberculosis (14%, including in combination with hypertrophic cardiomyopathy – HCM), acute / chronic viral (8%) and infectious immune (38%), including perimyocarditis in 77%, pericarditis associated with mediastinum lymphoma/sarcoma (4%), sarcoidosis (3%), diffuse diseases of connective tissue and vasculitis (systemic lupus erythematosus, rheumatoid arthritis, diseases of Horton, Takayasu, Shegren, Wegener, 12%), leukoclastic vasculitis, Loeffler’s endomyocarditis, AL-amyloidosis, thrombotic microangiopathy (1% each), HCM (8%), coronary heart disease (constriction after repeated punctures and suppuration; postinfection and immune, 4%), after radiofrequency catheter ablation and valve prosthetics (2%). Tuberculosis was the main causes of constrictive pericarditis (36%). Treatment included steroids ( n =39), also in combination with cytostatics ( n =12), anti-tuberculosis drugs ( n =9), acyclovir/ganclovir ( n =14), hydroxychloroquine ( n =23), colchicine ( n =13), non-steroidal anti-inflammatory drugs ( n =21), L-tyroxine ( n =5), chemotherapy ( n =1). In 36 patients different types of therapy were combined. Treatment results observed in 55 patients. Excellent and stable results were achieved in 82% of them. Pericardiectomy/pericardial resection was successfully performed in 8 patients. Lethality was 13.2% (10 patients) with an average follow-up 9 [2; 29.5] months (up to 10 years). Causes of death were chronic heart failure, surgery for HCM, pulmonary embolism, tumor. Conclusion. During a special examination, the nature of pericarditis was established in 97% of patients. Morphological and cytological diagnostics methods play the leading role. Tuberculosis pericarditis, infectious-immune and pericarditis in systemic diseases prevailed. Infectious immune pericarditis is characterized by small and medium exudate without restriction and accompanying myocarditis. Steroids remain the first line of therapy in most cases. Hydroxychloroquine as well as colchicine can be successfully used in moderate / low activity of immune pericarditis and as a long-term maintenance therapy after steroid stop.

Background. A few cases of combination of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC) with left ventricular noncompaction (LVNC) have been described. Aims — to study the genetics, diagnostical features and clinical course of the combination of ARVC with LVNC. Methods. 58 patients with ARVC diagnosis (26 men; mean age 39.1 ± 14.2 years; mean follow-up period — 21.5 [6; 60] months) and 125 patients with LVNC (74 men; mean age 46.4 ± 15.1 years; mean follow-up period — 14 [3; 40] months). All patients underwent electrocardiogram (ECG), echocardiography, 24-h ECG monitoring. Heart MRI was performed in 53 (91.4%) patients with ARVC and 60 (48%) with LVNC, heart CT — in 18 (31%) patients with ARVC and 89 (71.2%) with LVNC. For all patients with combination of ARVC and LVNC DNA-diagnostic was performed using both ARVC (PKP2, DSG2, DSP, DSC2, JUP, TMEM43, TGFB3, PLN, LMNA, DES, CTTNA3, EMD, SCN5A, LDB3, CRYAB, FLNC) and LVNC (MYH7, MYBPC3, TAZ, TPM1, LDB3, MYL2, MYL3, ACTC1, TNNT2, TNI3) gene panels. Results. Combination of ARVC and LVNC was found in 9 patients (15.5% of patients form ARVC cohort and 7.2% from LVNC cohort). These patients were distinguished from patients with isolated ARVC or LVNC by aggressive ventricular arrhythmias (frequent premature ventricular beats, sustained ventricular tachycardia, significantly worse antiarrhythmic therapy effect, appropriate shocks of implanted cardioverter-defibrillators (ICD) in all patients with ICD). Patients with combination of ARVC + LVNC were also distinguished from patients with isolated LVNC by the dilatation of RV, low QRS voltage on ECG, presence of AV block, absence of signs of LV hypertrophy on ECG. LV dilatation with reduction of its ejection fraction distinguished patients with mixed cardiomyopathy from patients with isolated ARVC. Potentially pathogenic variants (IV–V classes of pathogenicity) and variants of unclear clinical significance (III class of pathogenicity) were found in both desmosomal and non-desmosomal genes in 78% of patients, including 3 (33%) — in DSP gene. Conclusions. The combination of ARVC and LVNC can be caused by mutations in both desmosomal and non-desmosomal genes and has typical features: aggressive, resistant ventricular rhythm abnormalities leading to appropriate ICD shocks and a high risk of sudden cardiac death.

Aim. To analyze the difficulties of diagnosis and the clinical features of the Danon disease in women.Results. An observation of Danon disease in a woman aged 18 years with an uncomplicated family history is presented. The early development of atrial fibrillation (at the age of not more than 15 years) in combination with atrioventricular blockade against the background of regular sports was not attracted due attention for 3 years. The examination revealed: a moderate degree of left ventricular hypertrophy (up to 17 mm), its diffuse nature and simultaneous involvement of the right ventricle, signs of heart failure due to severe restrictive disorders with preserved ejection fraction. Cardiac magnetic resonance imaging data (non-specific late gadolinium enhancement) became the basis for the assumption of amyloidosis and the implementation of a myocardial biopsy. An erroneous diagnosis of cardiac amyloidosis according to myocardial biopsy was refuted during a second study, the PAS reaction revealed signs of storage disease. The diagnosis of Danon disease was verified using DNA diagnostics (c.731delG mutation was detected). Due to the presence of unsustained paroxysmal ventricular tachycardia and a high calculated risk of sudden death, cardioverter-defibrillator was implanted. The analysis of literature data on the frequency and the manifestation of Danon disease in women, the place of this disease in the structure of the causes of myocardial hypertrophy is given.Conclusion. Atrial fibrillation at a young age and left ventricular hypertrophy syndrome can develop due to primary myocardial diseases not well known in the practice of a cardiologist. They require an in-depth diagnostic search; their identification is critical for determining treatment tactics and prognosis.

A procedure was suggested for highly efficient extraction of fullerenes from electric arc carbon black, with the degree of recovery reaching 86% of the carbon black weight. Analysis by HPLC and by IR and Raman spectroscopy shows that the extracts obtained consist of a mixture of fullerenes. The possibility of preparing highly water-soluble fullerene derivatives from the extracts by hydroxylation with an aqueous solution of hydrogen peroxide was demonstrated.

Introduction Noncompact myocardium (NCM) is a cardiomyopathy with various genetic causes and clinical manifestations; its relationship with other forms of dilated cardiomyopathy (DCM) and its impact on prognosis are unclear. Objective To study the place of NCM in the structure of DCM, its clinical features and influence on prognosis in comparison with other forms of DCM syndrome. Methods The NCM registry includes 125 patients, mean age 46.4±15.1 years, 74 men and 51 women, mean follow-up 14 [4.0; 41.0] months. The DCM registry included 365 patients, mean age 46.4±15.1 years, 253 men and 112 women, mean follow-up 14 [5; 43.75] months. The examination included ECG, ECG Holter monitoring, echocardiography, blood anti-heart antibody level evaluation, and additionally cardiac CT, MRI, DNA diagnostics (in the MYH7, MYBPC3, TPM1, TNNI3, TNNT2, ACTC1, TAZ, ZASP (LDB3), MYL2, MYL3, DES, LMNA, EMD, TTR gene panel), coronary angiography, right ventricular endomyocardial biopsy. Results The proportion of patients with DCM phenotype in the NCM registry was 40% (n=49), another 11% (n=15) had DCM syndrome diagnosed simultaneously with acute/subacute myocarditis. Lethality in these subgroups was 12.2% and 33.3%, respectively, and was significantly higher than in asymptomatic, ischemic and arrhythmic variants of DCM. In the DCM registry, the proportion of patients with NCM was 21% (n=78), and increased left ventricular (LV) trabecularity was detected in another 18% (n=64). DCM patients with and without NCM did not differ by baseline echocardiographic parameters, heart failure class, and cardiotropic therapy. Pathogenic mutations were detected in 14% of DCM patients with NCM and only 3% of other patients with DCM (p Conclusion NCM is an independent form of DCM syndrome, which is characterized by higher frequency of pathogenic mutations, arrhythmic events, worse response to cardiotropic therapy, higher frequency of intracardiac thrombosis. The absence of mortality differences can be explained by the higher frequency of preventive interventions in this category of patients with DCM (prescription of anticoagulants, defibrillator implantation, heart transplantation). Funding Acknowledgement Type of funding sources: None.

Background A few cases of combination of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC) with left ventricular noncompaction (LVNC) have been described. Aims To study the genetics, diagnostical features and clinical course of the combination of ARVC with LVNC. Materials and methods 58 patients with ARVC diagnosis (26 men; mean age 39.1±14.2 years; mean follow-up period – 21.5 [6; 60] months) and 125 patients with LVNC (74 men; mean age 46.4±15.1 years; mean follow-up period – 14 [3; 40] months). All patients underwent electrocardiogram (ECG), echocardiography, 24-h ECG monitoring. Heart MRI was performed in 53 (91.4%) patients with ARVC and 60 (48%) with LVNC, heart CT – in 18 (31%) patients with ARVC and 89 (71.2%) with LVNC. For all patients with combination of ARVC and LVNC DNA-diagnostic was performed using both ARVC (PKP2, DSG2, DSP, DSC2, JUP, TMEM43, TGFB3, PLN, LMNA, DES, CTTNA3, EMD, SCN5A, LDB3, CRYAB, FLNC) and LVNC (MYH7, MYBPC3, TAZ, TPM1, LDB3, MYL2, MYL3, ACTC1, TNNT2, TNI3) gene panels. Results Combination of ARVC and LVNC was found in 9 patients (15.5% of patients form ARVC cohort and 7.2% from LVNC cohort). These patients were distinguished from patients with isolated ARVC or LVNC by aggressive ventricular arrhythmias (frequent premature ventricular beats, sustained ventricular tachycardia, significantly worse antiarrhythmic therapy effect, appropriate shocks of implanted cardioverter-defibrillators (ICD) in all patients with ICD). Patients with combination of ARVC+LVNC were also distinguished from patients with isolated LVNC by the dilatation of RV, low QRS voltage on ECG, presence of AV block, absence of signs of LV hypertrophy on ECG. LV dilatation with reduction of its ejection fraction distinguished patients with mixed cardiomyopathy from patients with isolated ARVC. Potentially pathogenic variants (IV-V classes of pathogenicity) and variants of unclear clinical significance (III class of pathogenicity) were found in both desmosomal and non-desmosomal genes in 78% of patients, including 3 (33%) in DSP gene. Conclusions The combination of ARVC and LVNC can be caused by mutations in both desmosomal and non-desmosomal genes and has typical features: aggressive, resistant ventricular rhythm abnormalities leading to appropriate ICD shocks and a high risk of sudden cardiac death. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Genetic testing of patients was supported by Grant No. 16-15-10421 of the Russian Science Foundation

Aim. To study the nosological spectrum in the syndrome of primary left ventricle hypertrophy (PLVH) using morphological and genetic diagnostics and to compare the clinical course of true hypertrophic cardiomyopathy (HCM) and its phenocopy.Material and methods. Fifty five adult patients (29 men, 48.2±17.0 years) with PLVH (12 mm and more) were included. The exclusion criteria were athletic heart, hypertensive heart disease, severe valvular disease and other causes of secondary left ventricle (LV) hypertrophy. We performed 11 endomyocardial biopsy, 8 intraoperative biopsy, 1 study of explanted heart, 1 autopsy with virus investigation (real-time polymerase chain reaction) of the blood and myocardium. Mutational screening had included simultaneous sequencing of the MYBPC3, TAZ, TPM1, LDB3, MYL2, ACTC1, MYL3, MYH7, TNNI3 and TNNT2 genes based on NGS technology (Ion Torrent PGMTM) with following Sanger resequencing of potentially significant genetic variants. For patients with a phenotype of particular genetic syndrome the Sanger sequencing of target gene(s) for performed first. Clinical examination had included electrocardiography, Holter monitoring, echocardiography, coronary angiography, computer tomography/magnetic resonance imaging (by indication). The mean follow-up was 8 [3;32] month.Results. Isolated HCM was found in 28 patients, and 10 have a combination of HCM and noncompaction myocardium (NCM). Mutations in the MYH7 and MYBPC3 genes were detected in six cases. In 17 cases (30.9%) the non-sarcomeric causes of LVHS were detected. Three patients had Fabry disease, 2 ‒ had Danon disease, in 10patients we found amyloidoses, in 1 – Friedreich ataxia, and 1 patient was diagnosed with LEOPARD syndrome (all cases were confirmed by DNA diagnostics). Genotype-positive diagnosis was established in 23.6% of patients. In patients with HCM were significantly more frequent asymmetric septal hypertrophy with obstruction and muscle bridges, in other forms of primary hypertrophy – right ventricular hypertrophy, low QRS voltage, QS complexes and increasing of ejection fraction (EF) (55.7±12.5% vs 62.5±10.1% in HCM, p=0.08). The morphologic signs of myocarditis were in 46.7% of patients with HCM detected: in 3 patients with NCM and in 4 patients with isolated HCM. The viral genome in the myocardium was in 11 patients with HCM (73.3%) detected, previously human herpes virus type 6 (it was correlation with myocarditis) and parvovirus B19. Eleven patients died due to a stroke/heart failure without no significant differences between patients with HCM and phenocopy.Conclusion. The spectrum of causes of the primary left ventricular hypertrophy is very wide. The frequency of myocarditis associated with sarcomeric HCM was 46.7%. When lower EF and heart failure in patients with HCM can be result of myocarditis, in patients with storage disease they are the result of disease itself.

The nuclear magnetic resonance (NMR)-relaxation characteristics of protons in pure aqueous and buffer solutions of highly hydroxylated endofullerenols with paramagnetic gadolinium ions at ambient temperature have been studied. These systems were thoroughly characterized by SANS and examined by NMR at various resonance frequencies: f = 2 kHz–500 MHz. In all the cases, we have discovered much higher longitudinal and transversal relaxation rates as compared to the reference salt solutions with Gd+3 ions in the same range of concentrations (0.1–10.0 mM/l). We suppose that this effect is due to the fact that the objects studied reveal well-manifested abilities to the self-assembly in acidic conditions. As a result, the transversal relaxation rate (1/T2) increases greatly, and also the longitudinal relaxation rate (1/T1) demonstrates a broad maximum at resonant frequencies f ~ 20–100 MHz that are determined by the time of fullerenol diffusive rotations. The relaxation rates, which increase linearly with fullerenol content (0.1–10.0 mM/l), testify the stable assembly. The studied features of fullerenol assembly and its strong influence on the proton relaxation make it possible to suppose good prospects of these metal–carbon structures for biomedical applications, in particular, as contrast agents in MRI.

Loeffler's endocarditis remains is a very rare disease, develops due to eosinophilic inflammation predominantly of the endocardium with an outcome in fibrosis and massive thrombus formation and. He is generally characterized by an unfavorable prognosis. Clinical case of a 42-year-old patient with Loeffler endocarditis is presented. The development of the disease was preceded by a polyvalent allergy, mild dry eye syndrome and pansinusitis with a single eosinophilia of blood up to 16%. The reason for the hospitalization was the appearance of biventricular heart failure. During the previous year, the level of blood eosinophils remained normal, a threefold increase in the level of eosinophilic cationic protein was observed once. A 20-fold increase in the pANCA level, a 2.5-fold increase in the level of antibodies to DNA, an antibody to the nuclei of cardiomyocytes 1:160 were detected. The diagnosis was made on the basis of electrocardiography data (low QRS voltage, atrial hypertrophy), echocardiography, multispiral computed tomography and magnetic resonance imaging of the heart (thickening and delayed contrasting of the endocardium, massive thrombosis of the left ventricular apex with obliteration of its cavity, encapsulated fluid in the pericardium with compression of the right ventricle). Systolic dysfunction, severe signs of restriction and arrhythmias were absent. Trombectomy, tricuspid valve plasty, pericardial resection, suturing of an open oval window were performed. Signs of active inflammation with single eosinophils, vasculitis, perimuscular sclerosis, endocardial sclerosis were detected in morphological and immunohistochemical studies of endo-, myo-, pericardium. Viral genome was not found. The therapy with methylprednisolone 24 mg/day, azathioprine 75 mg/day was started. Six months after the operation, the symptoms of heart failure are completely absent, the thrombosis did not recur.

Purpose of the study. Evaluation of the value of the results of the use of cardiac functional examination methods for the stratification of the risk of developing cardiovascular complications in planned abdominal surgical interventions in patients over 65 years of age or with cardiac pathology.Materials and methods. The study included 179 patients over 65 years of age or with a history of heart disease who underwent elective abdominal surgery. The median age was 70 years. During the operation and for 30 days after it, cardiac complications were recorded: severe (myocardial infarction, stroke, death from cardiovascular disease), others (strokes of exertional angina, ischemic dynamics of the ST segment on the electrocardiogram – ECG – rest, paroxysmal fibrillation / flutter atrial). All patients underwent basic examination – examination, anamnesis, ECG, blood test, assessment of respiratory function, ECG monitoring. Additionally, echocardiography (EchoCG) and ergospirometry (ESM) were performed.Results. In 30 (16.8 %) patients, various MTRs were detected: 6 (3.4 %) of fatal myocardial infarctions, 2 (1.1 %) of fatal strokes; 3 (1.7 %) cases of sudden cardiac death, angina attacks were recorded in 4 (2.2 %) patients, 7 (3.9 %) had ischemic ECG dynamics, 11 (6.1 %) had fibrillation episodes or atrial flutter. Chronic obstructive pulmonary disease, intervention on the colon, blood hemoglobin level 103 μmol / l, presence of any pathological changes in the resting ECG were associated with the development of SSO; according to EchoCG – VTI (linear velocity integral) in the outflow tract of the left ventricle (LV) 57 ml, global LV myocardial deformity is less than 18 %, increase in heart rate (HR) at the 1st minute load test> 27 %, peak oxygen consumption at ESM Conclusion. The risk of perioperative MTS during planned abdominal operations in patients older than 65 years or with a history of heart disease is relatively high – 16.8 %. When assessing the risk associated with the operation, it is advisable to additionally conduct echocardiography with VTI assessment in the LV outflow tract and myocardial deformity indicators, as well as ESM with the determination of HR increase in the 1st minute of the test and peak oxygen consumption.

The additional atomic occupancy in the octahedral and the tetrahedral voids of the face-centered cubic lattice (fcc) of fullerene C

Endohedral metallofullerenes Me@C2n (n = 30–50), their hydroxylated derivatives Me@C2n(OH)38–40 (Me = Tm, Ho, Eu, Sm, Co), and fullerenol С60(OH)38 have been synthesized The radiation resistance of these structures under irradiation in reactor by thermal and fast neutron fluxes in the fluence range of 1018–1019 cm–2 (cadmium ratio of ~10) has been analyzed. Endofullerenols are shown to be more stable in comparison with initial endohedral fullerenes; the molecules containing Eu and Sm (atoms characterized by the largest slow-neutron absorption cross section) turned out to be most stable. The mechanism of the formation of secondary Eu and Sm endofullerenols is discussed taking into account the neutron capture and emission of γ quanta by excited nuclei, which acquire the recoil energy.

To investigate whether intravenous contrast-enhanced multislice spiral computed tomography (computed tomography) (MSCT) versus myocardial morphological examination can diagnose myocarditis and the non-inflammatory causes of dilated cardiomyopathy (DCM) and evaluate prognosis in patients with the latter.A study group consisted of 130 patients, including 95 men (46.8±11.9 years), with DCM (mean left ventricular (LV) end-diastolic dimension (EDD), 6.6±0.8 cm; mean LV ejection fraction (EF), 29.8±9.3%; NYHA functional class (FC) III (II; III)). All the patients underwent intravenous contrast-enhanced 320-slice CT of the heart; myocardial morphological examination was made in 48 patients (endomyocardial biopsy in 29 patients, intraoperative biopsy in 7, and autopsy in 9, and study of the explanted heart in 3). In addition, cardiotropic viral DNA in the blood and myocardium and the level of anticardiolipin antibodies were determined; echocardiography (in all the patients), scintigraphy (n = 45), magnetic resonance imaging (MRI) (n = 21), and coronary angiography (CG) (n = 46), and a genetic consultation were performed. A comparison group comprised 20 patients, including 14 men (69.3±9.2 years), with coronary atherosclerosis (40% or more stenoses) according to MSCT findings in the absence of criteria for DCM (mean LV EDD, 4.8±0.5 cm; mean LV EF, 59.4±4.6%).Morphological/comprehensive examination showed that myocarditis as a cause of DCM was diagnosed in 76 (65%) patients; its concurrence with genetic cardiomyopathies was in 17 more patients (17%). MSCT of the heart revealed lower accumulation areas in 2 (1.5%) patients (type 1 based on the proposed rating scale), delayed myocardial contrast agent accumulation (DMCAA) in 81 (62.3%): subendocardial accumulation (type 2) in 8, intramyocardial accumulation in 4 (type 3), subepicardial accumulation in 52 (type 4), and transmural accumulation in 15 (type 5); DMCAA was not noted in 49 patients. DMCAA was not found in the comparison group. As compared with biopsy, the sensitivity, specificity, predictive value of positive and negative results of the tests in detecting active myocarditis for all the types of DMCAA were 77.4, 47.1, 72.7, and 53.3%, respectively; those for types 3-5 of DMCAA were 77.4, 52.9, 75.0, and 56.3%; those in detecting all the morphological types of myocarditis were 68.3, 28.6, 84.8, and 13.3%, and those for types 3-5 were 65.9, 28.6, 84.4, and 12.5%, respectively. Comparison of the data of MSCT and those of comprehensive examination in all the patients with DCM, the diagnostic significance in detecting myocarditis for all the types of DMCAA was 70.6, 67.9, 88.9 and 38.8%, respectively; that for DMCAA types 3-5 was 60.8, 67.9, 87.3, and 32.3%. In the study group, MSCT also identified the non-compacted myocardium (n = 31 (23.8%)), coronary atherosclerosis (n = 31 (23%)), which is confirmed by CG findings in 15 patients. The patients with DMCAA significantly more frequently showed a relationship with previous infection, acute onset, significantly higher NYHA FCs, end-diastolic and end-systolic LV volumes, and insignificantly lower LV EF. During a mean follow-up periods of 12 (6; 37.25) months, the overall mortality rate was 17.7% (23 deaths); the death + transplantation index was 20% (n = 26). All the types of DMCAA were found to be significantly related to prognosis: in the DMCAA group, the mortality rate was 21.5% versus 7.8% in the non-DMCAA group (odds ratio 3.22; 95% confidence interval, 1.02 to 10.21; p0.05).MSCT with the assessment of delayed contrast enhancement (and simultaneous CT coronary angiography) can be used for the non-invasive diagnosis of myocarditis in patients with DCM, including that in the presence of contraindications to MRI. DMCAA correlates with the presence of myocarditis, its activity, the degree of functional disorders, and prognosis.Цель исследования. Изучение возможности мультиспиральной компьютерной томографии (МСКТ) сердца с внутривенным контрастированием у больных с синдромом дилатационной кардиомиопатии (ДКМП) в диагностике миокардита (в сопоставлении с морфологическим исследованием миокарда), невоспалительных причин ДКМП и оценке прогноза. Материалы и методы. В основную группу вошли 130 пациентов (95 мужчин, средний возраст 46,8±11,9 года) с синдромом ДКМП: средний конечный диастолический размер (КДР) левого желудочка (ЛЖ) 6,6±0,8 см, средняя фракция выброса (ФВ) 29,8±9,3%; III (II; III) функциональный класс (ФК) по классификации NYHA. Всем проведена 320-срезовая МСКТ сердца с внутривенным контрастированием; 48 пациентам выполнено морфологическое исследование миокарда (эндомиокардиальная биопсия у 29, интраоперационная у 7, аутопсия у 9, исследование эксплантированного сердца у 3). Кроме того, определяли ДНК кардиотропных вирусов в крови и миокарде, уровень антикардиальных антител, проводили эхокардиографию (всем пациентам), сцинтиграфию (у 45), магнитно-резонансную томографию - МРТ (у 21), коронарографию - КГ (у 46), консультацию генетика. Группу сравнения составили 20 пациентов (14 мужчин, средний возраст 69,3±9,2 года) с коронарным атеросклерозом (стенозы 40% и более) по данным МСКТ в отсутствие критериев ДКМП (средний КДР ЛЖ 4,8±0,5 см, средняя ФВ 59,4±4,6%). Результаты. По данным морфологического комплексного обследования, миокардит как причина синдрома ДКМП диагностирован у 76 (65%) пациентов, его сочетание с генетическими кардиомиопатиями - у 17 (17%). При МСКТ сердца участки пониженного накопления выявлены у 2 (1,5%) больных (1-й тип по предложенной шкале оценки), отсроченное накопление контрастного препарата (ОНКП) в миокарде - у 81 (62,3%): у 8 субэндокардиальное (2-й тип), у 4 интрамиокардиальное (3-й тип), у 52 субэпикардиальное (4-й тип), у 15 трансмуральное (5-й тип); у 49 больных ОНКП не отмечено. В группе сравнения ОНКП не выявлено. В сопоставлении с биопсией чувствительность, специфичность, прогностическая ценность положительного и отрицательного результатов тестов всех типов ОНКП в выявлении активного миокардита составили 77,4, 47,1, 72,7 и 53,3%, 3-5-го типа ОНКП - 77,4, 52,9, 75 и 56,3%, в выявлении всех морфологических типов миокардита - 68,3, 28,6, 84,8 и 13,3%, 3-5-го типов 65,9, 28,6, 84,4 и 12,5% соответственно. При сопоставлении данных МСКТ и комплексного обследования у всех больных с ДКМП диагностическая значимость всех типов ОНКП в выявлении миокардита составила 70,6, 67,9, 88,9 и 38,8%, 3-5-го типа ОНКП - 60,8, 67,9, 87,3 и 32,3%. При МСКТ в основной группе выявлены также некомпактный миокард (n=31, или 23,8%), коронарный атеросклероз (n=31, или 23%), который подтвержден данными КГ у 15 пациентов. У больных с ОНКП достоверно чаще определялись связь дебюта с перенесенной инфекцией, острое начало, достоверно более высокие ФК по классификации NYHA, конечный диастолический и конечный систолический объемы ЛЖ, недостоверно более низкая ФВ ЛЖ. Общая летальность при среднем сроке наблюдения 12 (6; 37,25) мес составила 17,7% (умерли 23 больных), показатель смерть + трансплантация - 20% (26 больных). Выявлена достоверная связь всех типов ОНКП с прогнозом: в группе ОНКП летальность составила 21,5% по сравнению с 7,8% в группе без ОНКП (отношение шансов 3,22 при 95% доверительном интервале от 1,02 до 10,21; p0,05). Заключение. МСКТ с оценкой отсроченного контрастирования (и одновременной КТ-ангиографией коронарных артерий) может использоваться для неинвазивной диагностики миокардита у пациентов с синдромом ДКМП, в том числе при наличии противопоказаний к проведению МРТ. ОНКП в миокарде коррелирует с наличием миокардита, его активностью, степенью функциональных нарушений и прогнозом.

The additional atomic occupancy in the octahedral and the tetrahedral voids of the face-centered cubic lattice (fcc) of fullerene C60was detected by neutron and x-ray powder diffraction. The observed occupancy exactly tracks the rearrangement of the orientation order with temperature decreases and results from the large atomic vibrations of the carbon atoms constituting the fullerene molecules. This motion assumes a small but finite probability to find the carbon atoms in the fcc interstitial voids, which is modeled by the detected 'phantom' occupancies.

Aims To evaluate safety and efficacy of moderate intensity interval exercise training early after heart failure decompensation on exercise tolerance and health-related quality of life (HRQoL). Methods and results This is a prospective randomized controlled study. We screened 234 consecutive patients admitted with decompensated heart failure; 46 patients (42 men/4 women; 61 ± 12 years of age) were randomized to a moderate intensity aerobic interval training ( n = 24) or to a control group ( n = 22). Patients underwent cardiopulmonary exercise testing, echocardiography and Minnesota Living with Heart Failure questionnaire (MLHFQ) at baseline, after three weeks and after three months. After three weeks, peak-VO2 increased by 17% in the training group ( p = 0.003) with further increase by 10% after three months ( p Conclusions Interval exercise training early after an episode of heart failure decompensation is safe and effective in improving exercise tolerance and health-related quality of life in selected patients after achievement of clinical stability. Positive effects remained sustained after three months. Further studies are needed to define role and indications for interval exercise training early after heart failure decompensation.

Purpose To study the predictors of death, transplantation and appropriate shocks (AS) of defibrillators in patients with dilated cardiomyopathy (DCM) depending on its etiology. Methods In 300 patients with DCM syndrome (206 males, 47.6±12.7 years, the average left ventricle (LV) end-diastolic diameter 6.4 [5.9; 7.1] cm, LV ejection fraction (EF) 32 [25; 40] %) were performed viral genome (real-time PCR) and anti-heart antibodies investigation, ECG, Holter, Echo-CG, cardiac CT, MRI, coronary angiography, and also morphological study of myocardium in 103 (34%) patients. Defibrillators were implanted in 80 (26.7%) patients: 47 ICD, 33 CRTD. The follow-up was 15 [6; 42] months. Results The following causes of DCM syndrome have been identified: the isolated myocarditis (n=164, 54.7%), the primary/genetic DCM (n=58, 19.3%), the genetic DCM with myocarditis (n=71, 23.7%), peripartum (n=1, 0.3%) and chemotherapy-induced cardiomyopathy (n=5, 1.7%), arteriovenous malformation (n=1, 0.3%). Genetic forms of DCM were represented by noncompact myocardium (n=64), ARVC (n=12), TTR-amyloidosis (n=1), myopathy (n=6). The pathogenic mutations in the genes LMNA (n=1), DES (n=2), DSP (n=2), EMD (n=2), PKP2 (n=1), MUH7+MyBPC3 (n=2), MyBPC3 (n=4) were detected. The AS rate was 23.8%. The only predictor of AS was identified the genetic/primary nature of DCM, that is diagnosed in 100% of patients with AS in comparison with 57% in patients without AS, p0.05). The mortality in patients with DCM was 19.7%, rate of transplantation 4.3%, death + transplantation 23.0%, SCD 2.7%. There were no differences depending on devises implantation due to adequate selection to procedure. The following factors were associated with mortality: high NYHA class and severe heart dysfunction, absence of improvement after start of therapy, acute debut of symptoms, viral genome in the myocardium, absence of anti-heart antibodies, absence of immunosuppressive therapy, beta-blockers and ACE inhibitors and MRA. The predictors of transplantation were genetic/primary DCM, younger age (38.3±10.3 vs 48.0±12.7, p Conclusions The etiology of DCM syndrome plays a key role in the prognosis and should be considered when selecting patients for ICD and heart transplantation. The genetic nature of DCM is the more important predictor of shocks than EF. The total mortality is clearly associated with resistant myocardial dysfunction.

Purpose To estimate the frequency of myocarditis in adult patients with noncompact myocardium (NCM) of the left ventricle (LV), its influence on the disease, the outcome and results of treatment. Methods We included 103 adult patients with NCM (61 males, 45.6±14.9 years). The average EDD LV was 6.0±0.8 cm, LV EF 38.8±14.5%. To diagnose NCM were performed Echo-CG, CT (n=81) and MRI (n=39). We performed NGS sequencing, followed by Sanger sequencing of detected variants (revealed in 9% of patients in the genes MYH7, MyBPC3, LAMP2, DES, DSP, TTN). The examination also included anti-heart antibodies and viruses (PCR) study and morphological study in 19 patients (endomyocardial biopsy in 14, intraoperative biopsy in 1, explanted heart study in 1 and autopsy in 3). The mean follow-up was 12 [2; 32] months. Results The myocarditis was diagnosed in 55 (53.4%) patients with NCM: in 19 patients by morphological study (active in 10 and borderline in 9 patients) and in 36 patients on the basis of a complex examination (the relationship with a respiratory infection, a 3–4-fold increase in the anti-heart antibodies, the viral genome in the blood, pericardial effusion, subepicardial LGE). The myocarditis was virus-positive in 17 patients (36.1%). The parvovirus B19, human herpes virus type 6, cytomegalovirus, herpes simplex virus and Epstein-Barr virus were detected in the myocardium in 8 patients (42.1%), and in 14 patients (25.5%) in the blood. Pathogenic genetic variants were revealed in four patients with morphologically verified myocarditis. The rate of myocarditis depended on the clinical form of NCM: 44.4% in arrhythmic form, 12.5% in chronic ischemic form, 57.5% in dilated pattern and 50.0% in association of NCM with other cardiomyopathies. In 10% of all patients, acute myocarditis was the first manifestation of the disease. In 5% the myocardial necrosis was the main manifestation of the myocarditis. The association of NCM with myocarditis led to more severe myocardial dysfunction (NYHA class 2 [1; 3] v 1.75 [0; 2], p0.05). Only in patients with myocarditis, there was a significant increase in EF (in acute myocarditis from 25.4±7.9 to 38.6±9.5%, p Morphological verification of myocarditis Conclusion Myocarditis is a regular phenomenon that develops in half of patients with primary NCM. The nature of myocarditis in NCM may be different (primary infectious and immune, secondary in response to genetic/ischemic damage to cardiomyocytes). However, it leads to a significant deterioration of structural and functional parameters, an increase in life-threatening arrhythmias, unfavorable outcomes and requires basic therapy.

Background Left ventricular noncompaction (LVNC) is characterized by high frequency of heart failure, arrhythmias, thromboembolism and ischemia. Purpose To estimate frequency, predictors, outcomes of adverse events in patients with LVNC. Methods 120 patients with LVNC were included (male, 58.3%); mean age, 45.9±15.0 years. To diagnose LVNC EchoCG (n=120), CT (n=85), MRI (n=55) were performed. The mean LV EF was 39.0±13.9%, LV EDV 155.5±65.0ml, LV EDD 6,03±0.8cm, LA volume 96.3±38.4ml. The median follow-up was 15 [4.0; 41.0] months. We also performed NGS sequencing, followed by Sanger sequencing. Results Pathological mutations in genes MYH7, MyBPC3, LAMP2, DES, DSP, TTN were found in 10% of patients. The main clinical manifestations were chronic heart failure NYHA II-III (66.7% of patients), ventricular arrhythmias (PVCs>500/day in 46.7%, sustained/unsustained VT in 49.2%), AF 30.8% (paroxysmal, n=18; persistent, n=11; permanent, n=9), ischemia (angina pectoris in 20%, myocardial necrosis in 13.3%), intracardiac thrombosis without anticoagulants (19.2%), embolism (6.7%), AV block degree II-III (11.7%), bundle branch blocks (37.5%), sinus node dysfunction (10%). VT frequency was associated with lower LV EF (34.6±13.4 v 42.8±13.1 p=0.001), higher NYHA functional class (class 2.5 [2.0; 3.0] v class 2 [0.75; 3.0], p Conclusion Thromboembolic events, arrhythmias and ischemia are typical adverse events of LVNC. Non-sustained/sustained ventricular tachycardia, myocardial infarction is significantly associated with increased mortality. LV dilation, systolic and diastolic dysfunction increases the frequency of thromboembolism in these patients. Low voltage ECG, poor R-wave progression, QRS duration and myocarditis should considered predictors for arrhythmias in LVNC patients.

AIM To develop an algorithm for optimization of rate-adaptive pacing settings in heart failure patients with preserved ejection fraction (HFpEF) and permanent cardiac pacing. METHODS This is a prospective randomized controlled study. A total of 54 patients with HFpEF, permanent atrial fibrillation (AF), and VVIR pacing were randomized to an intervention group with optimization of rate-adaptation parameters by using cardiopulmonary exercise testing (CPET) and pacemaker stress echocardiography (PASE), and to a control group with conventional programming. CPET, 6-min walk test (6-mwt), echocardiography (echo), Duke Activity Status Index (DASI), and Minnesota questionnaire (MLHFQ) were performed at baseline and after 3 months. PASE was used to exclude exercise-induced ischemia and to determine safe upper sensor rate. Pacing parameters were corrected to achieve optimal heart rate increments of 3-6 bpm for 1 mL/min/kg of VO2 (oxygen uptake). RESULTS After 3 months, the intervention group demonstrated significant improvement of VO2 peak by 1.64 ± 1.6 mL/min/kg, anaerobic threshold by 1.33 ± 1.3 mL/min/kg, exercise time by 170 ± 98 s, 6-mwt distance by 75 ± 63 m (P