Репозиторий Университета

© 2020 Purpose: to study the effect of immunosupressive therapy (IST) in the virus-negative and virus-positive patients with immune-mediated myocarditis. Methods: in 60 patients (45 male, 46.7 ± 11.8 years, mean LV EDD, 6.7 ± 0.7 cm, EF 26.2 ± 9.1%) active/borderline myocarditis was verified by endomyocardial biopsy (n = 38), intraoperative biopsy (n = 10), examination of explanted heart (n = 3) and autopsy (n = 9). Indications for IST determined based on histological, immune activity. The follow-up was 19.0 [7.25; 40.25] months. Results: The viral genome in the myocardium was detected in 32 patients (V+ group), incl. parvovirus B19 in 23. The anti-heart antibody level was equally high in the V+ and V- patients. Antiviral therapy was administered in 24 patients. IST (in 22 V+ and 24 V- patients) include steroids (n = 40), hydroxychloroquine (n = 20), azathioprine (n = 21). The significant decrease of LV EDD (6.7 ± 0.7 to 6.4 ± 0.8), PAP (48.9 ± 15.5 to 39.4 ± 11.5 mm Hg, р<0,01), increase of EF (26.5 ± 0.9 to 36.0 ± 10.8), and lower lethality (23.9% and 64.3%; RR 0.37, 95% CI 0.19–0.71), p<0.01, were found only in IST group. Significant improvement due to IST were achieved not only in V-, but also in V+ patients. Conclusions: IST in patients with immune-mediated lymphocytic myocarditis is effective and is associated with lower lethality both in virus-negative and virus-positive patients.

© 2018 Stolichnaya Izdatelskaya Kompaniya. All rights reserved. Bolshaya Pirogovskaya ul. 2-4, Moscow, 119435 Russia Pericarditis is not enough researched and described in literature despite the emergence of a large quantity of up-to-date laboratory and instrumental methods of verification. The main problem is that pericarditis might be a sign of many infectious and non-infectious diseases. It is quite difficult to define the etiopathogenetic reason of process. The article presents a clinical observation of a 53 years old mail patient with paroxysms of atrial flutter, non-symptomatic febrile fever, arthralgia and signs of exudative pericarditis, which were manifested after the acute viral infection. The symptoms have been lasting for 8 months before the patient's hospitalization. In lab tests anemia, leucopenia, increase level of platelets and increase antinuclear antibody level were found. Several conceptions were considered: cancer with paraneoplastic syndrome, systemic disease, infectious process, myeloma, which were subsequently excluded. Due to the fact that pericardial effusion may often be associated with tuberculosis Diaskin test and T-SPOT were performed and they appeared to be positive. After several months of antituberculous treatment temperature normalized, atrial flutter episodes and arthralgia diminished. So empirically and laboratory tuberculous pericarditis with atypical manifestation was confirmed. The particularity of this observation is a nontypical clinical picture and the absence of a primary focus of infection. That is why the clinicians could not define the diagnosis rapidly.

© 2018 by the MediaSphere. A case of thyrotoxic myocarditis in a 60-year-old female patient is oresented. With the diagnosis of «Unstable angina» she was admitted to the intensive care unit for patients with myocardial infarction at the Yudin city clinical hospital in Moscow. Earlier, the patient had been treated with tyrosol for thyrotoxicosis, but she independently abolished the drug. She ecperienced pain in the chest for the first time in her life. Emergency, coronaroangiography was performed. No hemodynamically significant damage to the blood vessels of the heart was detected. Later, according to the outpatient blood test for thyroid hormones, a diagnosis was established — «severe thyrotoxicosis». The next day after hospitalization, treatment with tyrosol was started at a dose of 30 mg per day. Sinus tachycardia persisted. A reliable increase in cardiospecific enzymes was detected. The pain in the chest did not recur. Echocardiography did not reveal impairment of local or global myocardial contractility. On the fifth day of hospital treatment the patient suddenly died of cardiac and respiratory arrest. The autopsy study revealed autoimmune thyroiditis, thyrotoxic serous-lymphocytic myocarditis, which was complicated by a rupture of the myocardium, and pericardial gemotamponade. The difficulties of differential diagnosis of myocarditis and acute coronary syndrome and the features of treatment tactics in elderly patients with thyrotoxicosis are discussed.

© 2018 GEOTAR Media. All rights reserved. Aim: to value the significance of various predictors of sudden cardiac death (SCD) and clarify the selection criteria for implantation of cardioverter-defibrillators in patients with cardiomyopathies [dilated (DCM), arrhythmogenic right ventricular (ARVC), left ventricular noncompaction (LVNC)]. Material and methods. 220 patients with DCM syndrome were observed, 151 men, average age 47.5±12.5 years [mean left ventricular end-diastolic dimension (LV EDD) 6.5 [6.0, 7.1] cm, LV EF 30.3±10.1%], 50 patients with ARVC (definite diagnosis in 26 patients, probable in 13, possible in 11), 20 men, average age 38.1±14.6 years and 108 patients with a definite diagnosis of LVNC, 63 men, average age 45.4±14.8 years [mean LV ejection fraction (LF EV) 38.4±14.4%, LV EDD 5.9±0.8 cm]. The average follow-up periods were 16 [6, 37], 13.5 [4, 34] and 14 [3, 5, 36.0] months accordingly. The decision to implant the ICD / CRT-D was taken individually. The endpoints of the study were overall mortality, SCD, death + transplantation, appropriate defibrillators shocks and the "shocks + SCD". Results. The overall mortality in DCM, ARVC, and LVNC was 19.1%, 14.0% and 14.8%. It was mainly determined by terminal heart failure; SCD was recorded in 2.7%, 4.0% and 2.8%. Cardioverter-defibrillators were implanted in 66 (30%) patients with DCM (37 ICD, 29 CRT-D, 93.9% as the primary prevention of SCD), in 13 (26%) patients with ARVC (only ICD, primary prevention in 32,1%) and in 33 (30,6%) patients with LVNC (24 ICD, 9 CRTD, primary prevention in 88,1%). The frequency of appropriate shocks was 18.2% (15.0% in the primary prevention group and 50.0% in the secondary group) in patients with DCM syndrome, 69.2% (33.3% and 80.0% %) in ARVC, and 27.2% in LVNC (22.2% and 50.0%). The primary (genetic) nature of DCM (RR 1.58, OR 10.93), stable VT (RR 18, OR 26.5), and unstable VT (RR 1.43), a low QRS voltage (RR 1.75, OR 1.98), absence of LV hypertrophy signs on the ECG (RR 1.37, OR 2.56) were identified as criteria for selection for the implantation of a defibrillators in patients with DCM syndrome. In the patients with ARVC, these were a stable VT/VF and syncope (RR 4.75, OR 19), male sex (RR 1.25, OR 2), the low QRS voltage (RR 2.2, OR 10.5), chronic heart failure (OR 2.4, OR 8.0), the size of RV 2.85 cm (RR 1.55, OR 3.5), LV EDD> 5.5 cm (RR 2.1, OR 16, 7). In patients with LVNC the criteria were a stable VT/ VF, the presence of myocarditis (RR 3.3, OR 6.3), more than 500 PVBs per day (RR 3.3, OR 4.9), the low QRS voltage (RR 1,1, ОR 1,1), the follow up more than one year (RR 1,5, ОR 1,8). EF is not a statistically significant predictor of appropriate defibrillators shocks. Conclusions. In patients with various cardiomyopathies, which are accompanied by a high risk of SCD, the implantation of a cardioverter-defibrillators is an effective method of preventing SCD, including primary prevention. Due to adequate use of cardioverter-defibrillators in patients with DCM, ARVC and LVNC implanted in view of conventional and additional indications established in the study, mortality is determined primarily not by SCD, but terminal heart failure. Isolated myocarditis as the cause of DCM syndrome is not accompanied by a high risk of SCD, but its adherence to genetic cardiomyopathy determines the high risk of SCD.

to investigate the myocardial expression of some structural proteins and markers of cellular proliferation and innate immunity for assessing their possible diagnostic and prognostic role in patients with chronic myocarditis. Subjects and methods. The investigation enrolled 23 patients (16 men; mean age, 52.0±12.4 years (range, 27 to 73) with various forms of noncoronarogenic myocardial injury who underwent right ventricular endomyocardial biopsy (n=4), intraoperative left ventricular biopsy (n=17) or autopsy (n=2). Prior to their morphological examination, the patients were divided into two groups: 1) 10 patients with dilated cardiomyopathy and presumptive myocarditis; 2) 13 patients with valvular heart disease, hypertrophic cardiomyopathy, myxoma, and chronic pulmonary thromboembolism, presumptively without myocarditis. Along with myocardial histological and immunohistochemical (IHC) examinations, the expression of vimentin, desmin, c-kit, Ki-67, and Toll-like receptors (TLR) 2 and 9 was determined. Polymerase chain reaction was used to identify whether herpes viruses of and parvovirus B19 genomes were present in the blood and myocardial samples; indirect ELISA was applied to estimate the blood level of antibodies against various cardiac antigens. Results. According to the histological findings, active/borderline lymphocytic myocarditis was diagnosed in all the patients (Group 1) and in 6 patients (Group 2) in conjunction with the underlying disease (only in 9 and 7 patients, respectively), viral genome was detected in the myocardium of 15 patients, including in 5 without morphological signs of myocarditis (parvovirus B19 (n=11), herpesvirus 6 (n=4), herpes simplex virus types 1 and 2 (n=1), Epstein-Barr virus (n=2), and cytomegalovirus (n=1)), and in the blood (n=4). A marked correlation was found between TLR2 and TLR9 expressions and the morphological pattern of active myocarditis in the absence of this correlation with the expression level of other studied markers. The expression level of TLR2 in patients with and without borderline myocarditis was 0 [0; 0,75] and in those with active myocarditis was 1.5 [1; 1,5] points; that of TLR9 was 2 [2; 2] and 4 [3; 4] points, respectively (p0.001). The expression of TLR2 and TLR9 in patients with borderline myocarditis was lower than in those without myocarditis (0 [0; 0] versus 0 [0; 1] and 2 [1,5; 2] versus 2 [2; 3] points), which can reflect cardiomyocyte destruction/depletion at later stages of the disease. There was also a close correlation between the expression level of TLR2 and that of TLR9 (r=0.824; p0.001) and with Ki-67 levels (r=-0.531 and r=-0.702; p0.01). There was also a correlation of the expression of the studied markers with viral persistence (desmin), the degree of myocardial dysfunction and cardiosclerosis (c-kit), which calls for further investigations. Conclusion. Determination of the myocardial expression level of TLR2 and TLR9 may serve as an immunohistochemical marker for myocarditis and preservation of its activity, which is especially valuable in patients with borderline forms. The marked expression of these markers for innate immunity may reflect both one of the mechanisms of genetic predisposition to myocarditis and its severe course and their secondary activation in the pathogenesis of the disease and is a potential target of therapy.

© 2018, Silicea-Poligraf. All rights reserved. Aim. To study the efficacy of plasmapheresis as the main type of pathogenic treatment or in combination with immunosuppressive therapy in patients with dilated cardiomyopathy (DCMP) and arrhythmias of immune-inflammatory nature. Material and methods. The main group included 20 patients with arrhythmic myocarditis (with premature supraventricular / ventricular contraction >3000/day, n=3/8, atrial fibrillation (AF) n=9) and 14 patients with DCMP syndrome (enddiastolic volume (EDV) left ventricle (LV) 6,3±0,6 cm, ejection fraction (EF) 33,5±8,1%). The inclusion criterion was an increase of at least 2 types of anti-cardiac antibodies titers ≥ twice. Myocarditis is diagnosed using myocardial biopsy, magnetic resonance imaging, multispiral computed tomography, scintigraphy, coronary angiography. We used a course of discrete plasmapheresis. The comparison group included 26 patients with an arrhythmic myocarditis and 19 with DCMP syndrome (EDV 6,6±0,8 cm, EF 32,6±7,3%), which plasmapheresis was not used. Dynamics was assessed at 6 and 12 months. Results. In groups of patients with arrhythmias and DCMP, a significant decrease in anti-cardiac antibodies titers was observed immediately after plasmapheresis and in control studies (p<0,05). In patients with arrhythmias, a health-promoting effect (a decrease in the number of premature contraction and a frequency of atrial fibrillation ≥75%) was observed in 65% of the main group and 58% of the comparison group. Predictor of plasmapheresis efficiency was a titer of specific antinuclear factor ≥1: 40 (sensitivity — 92,3%, specificity — 71,4%, AUC — 0,813, p<0,05). Methylprednisolone was prescribed to 45% of patients in the main group and 73% to patients in the comparison group (p>0,05) at a dose of 8 [4; 16] and 16 [10; 24] mg per day, respectively, p>0,05. In patients with DCMP in the main group, a significant increase in EF (p<0,05) (up to 41,4±8,2% and 46,3±12,7% vs 39,1±13,7% and 37,2±10,7% in the comparison group) and the distance of 6-minute walking test was obtained. A good effect (increase in EF by 10% or more) was noted in 50% of the main group and 32% of the comparison group. The predictor of plasmapheresis efficacy was systolic pressure in the pulmonary artery ≥28,5 mm Hg. (sensitivity — 100%, specificity — 71,4%, AUC — 0,893, p<0,05). In the main group, methylprednisolone was assigned to 43% of patients, in the comparison group — 89%, p<0,05. The average doses of methylprednisolone in the main group were significantly lower than in the comparison group (8 [8; 17,25] vs 16 [13; 28] mg per day, p<0,05). Conclusion. Positive clinical response to plasmapheresis was noted in 65% of patients with arrhythmias and in 50% of patients with DCMP of immune-inflammatory nature. In patients with different types of myocarditis, plasmapheresis increases the efficacy of antiarrhythmic and immunosuppressive therapy.

© 2018, Silicea-Poligraf. All rights reserved. Aim. To evaluate the exact efficacy of the implantable cardioverter-defibrillators (ICD) and combination devices (CRT-D), and to evaluate their influence on the rate of sudden death and overall mortality in patients with the dilation cardiomyopathy syndrome (DCMP), and to clarify the selection criteria for implantation. Material and methods. Totally, 220 DCMP patients investigated: 66 (30%) of them (mean age 48,5±12,8 y. o., 47 males) underwent implantation of ICD (n=37) and CRT-D (n=29), 154 (70%) patients were in comparison group (mean age 47,1±12,4 y. o., 104 males). In 60 patients (93,9%) the devices were implanted for primary prevention of sudden cardiac death (SCD). Follow-up lasted for 16 [6; 37] months. As primary endpoints, the following parameters were used: “death+transplantation”, mortality, SCD, “SCD+shock” and “death+transplantation+proper shocks of the defibrillators”. Results. Mortality in all DCMP patients was 19,1%, “death+transplantation” — 21,4%, SCD — 2,7%. There were no significant differences by these values in patients with both devices (19,7%; 22,7% and 1,5%), ICD (21,6%; 24,3% and 2,7%), CRT-D (17,2%; 20,7; and 0) and patients with no devices (18,8%; 20,8% and 3,2%). Significantly higher rates by “SCD+shocks” (18,2% v 3,2%, p<0,001) and “death+transplantation+shocks” (36,4% vs 20,8%, p<0,05) in patients with the implanted devices witness for real impact of the defibrillators in equality of overall mortality and SCD parameters. Among the patients with implanted devices, the genetic and mixed (genetic and inflammatory) nature of DCMP predominated (62,1 v 35,7%, p<0,001), there was significantly lower EF (26,3±9,2 v 30,7±10,3%, p<0,01), its end value (31,1±11,0 v 39,2±13,5%, p<0,01), significantly higher end diastolic size of the left ventricle (EDS, LV, 6,8±0,8 v 6,5±0,8 cm, p<0,05) and the grade of mitral regurgitation. In patients with the devices, rate of proper shocks was 18,2%. In isolated myocarditis there were no shocks (35,3±9,1% v 26,8±9,3%, p<0,05), EDS significantly lower (6,2±0,6 cm v 6,9±0,9 cm, p<0,01), ECG signs of LV hypertrophy were more rare (16,7% v 56,3%, p<0,05), but more commonly — the low voltage of QRS (33,3% v 10,6%, p=0,53); there were no differences in the rates of cardiotropic drugs prescription. Main predictors of the shocks were genetic origin of DCMP (isolated or with myocarditis, 25/75%, comparing with 20/33% in patients with no shocks, p<0,01, HR 1,58, OR 10,93, sensitivity 94,1%, negative predictive value 99,2%), and sustained (HR 18,0, sensitivity 98,1%) and non-sustained ventricular tachycardia (HR 1,43, sensitivity and negative predictive value 100%), decrease of QRS voltage and absence of the signs of LV hypertrophy on ECG (negative predictive value 92,8% and 95,6%). Conclusion. In DCMP patients, implanting of ICD/CRT-D was performed with acknowledged additional criteria (genetic or mixed DCMP etiology, lower EF and worse response to treatment); due to more effective ICD therapy, the values of mortality, “death+transplantation” and SCD were not higher than in less severe patients with no such devices. Proper shocks developed in patients with significantly higher EF. As an independent SCD risk factor and a criteria for patients selection to defibrillator implantation, genetic origin of DCMP should be used, especially if comorbid with myocarditis. As the predictors for benign outcome — absence of non-sustained ventricular tachycardia, lower QRS voltage, signs of LV hypertrophy on ECG. An algorithm proposed of DCMP patients selection for ICD treatment.

© 2018, Silicea-Poligraf. All rights reserved. Aim. To classify established clinical types of the right ventricle arrhythmogenic dysplasia (RVAD) taken a variety of genetic and inflammatory mechanisms, and to analyze the specifics of differential diagnostics and management of the respective types. Material and methods. Main group consisted of 50 patients with evident (n=26), probable (n=13) and possible (n=11) RVAD diagnosis, mean age 38,1±14,6 y. o., males — 20 (40%), follow up time 13,5 [4; 34] months. Comparison group consisted of 58 patients with some of the RVAD criteria insufficient for evident diagnosis. All patients underwent ECG, Holter ECG 24 hours, EchoCG; in the main group additionally — DNA-diagnostics (n=46), cardiac MRI (n=44), high definition ECG (n=16), endomyocardial biopsy of the RV (n=2), autopsy (n=2). In comparison group, MRI was done in 32 patients, biopsy to 7, and in 1 case — autopsy. Results. Based upon the clinical data and specifics of the disease course, 4 types of established clinical RVAD were selected, that do not tend to overlap: latent arrhythmic (50% patients), manifest arrhythmic (20%), RVAD with predominant biventricular chronic heart failure (CHF, 16%), and RVAD with non-compaction left ventricle myocardium (14%). The development of one or another type is based on genetic factors, as on comorbid myocarditis (in percent in the following, respectively). In diagnostics of the latent arrhythmic type (frequent right ventricle extrasystoly, VE and/or non-sustained right ventricular tachicardia, VT) the key role played female sex, syncopes in anamnesis (16%), family history of sudden death (12%), ECG-criteria and positive results of DNA diagnostics (24%). For manifest arrhythmic type (sustained VT) — sudden death family anamnesis (in 20%), MRI-criteria (enlarged RV with lower EF), ECG-criteria and positive DNA tests (50%). For RVAD with progressing CHF — sustained VT (50%), syncopes (37,5%), predominance of RV failure with its severely reduced EF (25,7±15,0%), major MRI-and ECG-criteria, decreased QRS-voltage and positive DNA test (38%). Comorbidity of RVAD and non-compaction myocardium differ by frequent VE, aggressive VT (57,1%), syncope (42,9%) and CHF with significantly lower than in DCMP EF LV. Mortality rate in I-IV types was, respectively, 0%, 10%, 25%, 14,3%, and relevant shocks in 8 of 13 (61,5%) patients with ICD. Conclusion. It is worthy to use the proposed RVAD classification in clinical practice to define the spectrum of diagnostical and management events and assess the individual patient prognosis.

© 2018 Bentham Science Publishers. The burden of cardiovascular and metabolic diseases is increasing with every year. Although the management of these conditions has improved greatly over the years, it is still far from perfect. With all of this in mind, there is a need for new methods of prophylaxis and treatment. Coenzyme Q10 (CoQ10) is an essential compound of the human body. There is growing evidence that CoQ10 is tightly linked to cardiometabolic disorders. Its supplementation can be useful in a variety of chronic and acute disorders. This review analyses the role of CoQ10 in hypertension, ischemic heart disease, myocardial infarction, heart failure, viral myocarditis, cardiomyopathies, cardiac toxicity, dyslipidemia, obesity, type 2 diabetes mellitus, metabolic syndrome, cardiac procedures and resuscitation.

© Team of authors, 2018. The article describes the clinical case of subacute myocarditis in a child with an outcome in dilated cardiomyopathy, complicated with congestive heart failure. Difficulties in diagnosing the disease that manifested with cardiac arrhythmia are discussed. The main signs suggesting postmiocardic cardiomyopathy included a reduced deflection voltage and frequent ventricular extrasystoles with episodes of the ventricular tachycardia in the onset of the disease, left ventricular dilatation, a significant decrease in ejection fraction, increased activity of natriuretic peptide, findings of perfusion scintigraphy and magnetic resonance imaging. Medical therapy and implantation of a cardioverter defibrillator were ineffective. The child repeatedly suffered from syncopal conditions with circulatory arrest, which required resuscitation. Due to the ineffectiveness of drug therapy conducted in the leading federal centres, considering cardiac transplantation abroad was recommended.

© 2018, Silicea-Poligraf. All rights reserved. Aim. To evaluate the prevalence of myocarditis in adult patients with non-compaction myocardium (NCM) of the left ventricle (LV), and its influence on the disease course, results of treatment and outcomes. Material and methods. To the study, 103 adult patients included, with NCM, 61 males, mean age 45,6±14,9 y. o. (from 18 to 78). Mean end diastolic LV size was 6,0±0,8 сm, EF LV 38,8±14,5%. Diagnosis of NCM had been done by echocardiography, multispiral computed tomography (n=81) and magnetic resonance tomography (n=39). DNA-diagnostics was performed by NGS method with further Senger sequencing. Pathogenic mutations were found in 9% of patients in the genes MYH7, MyBPC3, LAMP2, DES, DSP, TTN. The investigation also included anticardiac antibodies, genome of cardiotropic viruses by PCR, coronary arteriography (n=26), scintigraphy (n=25). Morphological assessment of the myocardium was done in 19 patients (12 endomyocardial biopsies), 1 intraoperation biopsy, 3 explanted hearts, incl. 2 after biopsy, and 5 autopsies. Mean follow-up 12 [2; 32] months. Results. Myocarditis was found in 53,4%, incl. virus-positive in 32,7% of those, with morphology done for 19 patients (active myocarditis in 10, borderline in 6; with minimal signs of activeness in 3). Viral genome in myocardium found in 8 patients (42,1%). The prevalence of myocarditis 44,4% in an arrhythmic variant of NCM, 12,5% in chronic ischemic, 57,5% in dilation cardiomyopathy, 50,0% in NCM patients with other cardiomyopathies. Special cases were acute/subacute myocarditis in NCM (10,7% of all), acute necrosis (infarction) in 4,9%. Comorbidity with myocarditis in NCM led to significantly more severe LV dysfunction (CHF FC 2 [1; 3] v 1,75 [0; 2], p<0,01, EF 33,8±13,5 v 44,7±13,6%, p<0,001), more prevalent non-sustained ventricular tachycardia (67,3% v 29,3%, p<0,01), proper shocks (38,9% v 0, p<0,05), deaths (16,4 and 4,2%, OR 5,75, 95% CI 1,21-27,43, p<0,05) and transplantation (7,3% v 2,1%, p>0,05). Only in myocarditis patients, as a result of basis (antiviral, immune suppression) and cardiotropic therapy there was significant increase of EF (in acute myocarditis from 25,4±7,9 to 38,6±9,5%, p<0,01), decrease of LV size and pulmonary systolic pressure. Conclusion. Myocarditis is typical phenomenon developing in patients with the primary, i. e. genetically verified NCM. The nature of myocarditis in NCM varies (primary infectious-autoimmune, secondary as a response on genetic/ischemic damage of cardiomyocytes), however regardless of this, it leads to significant worsening of structural and functional parameters, increase of the life-threatening arrhythmias rate, and outcomes (death + transplantation, proper shocks), demanding for active basic therapy.