ОСОБЕННОСТИ ТЕЧЕНИЯ ФИБРИЛЛЯЦИИ ПРЕДСЕРДИЙ У ПАЦИЕНТОВ С КОМОРБИДНОСТЬЮ В ЗАВИСИМОСТИ ОТ ПРОВОДИМОЙ ТЕРАПИИ

Aim. To study the clinical course of atrial fibrillation in patients with arterial hypertension and extracardiac comorbid pathology depending on the administered therapy.Methods. 207 men aged 45–65 years with atrial fibrillation (paroxysmal and persistent) and arterial hypertension in combination with diabetes mellitus (n = 40), abdominal obesity (n = 64) and chronic obstructive pulmonary disease (n = 47) were recruited to a observational cohort study. 56 patients with atrial fibrillation and arterial hypertension but without any extracardiac diseases were included in the comparison group. Clinical and anthropometric parameters were assessed in all patients. Adherence to therapy was estimated with the Morisky-Green test. All patients underwent ECG; electrocardiographic holter monitoring, 24-hour blood pressure monitoring with the Daily Monitoring Systems SCHILLER (Schiller, Switzerland), 2D and M-mode echocardiography using a Vivid 7 device (General Electric, USA). The statistical analysis was performed in the Rstudio software (version 0.99.879, RStudio, Inc., MA, USA).Results. 66% of patients with atrial fibrillation and arterial hypertension had concomitant extracardiac comorbid pathology, of them 20% of had diabetes mellitus, 22% with chronic obstructive pulmonary disease, and 24% with abdominal obesity. The clinical groups were comparable in electro impulse and drug therapy. Patients who received medical treatment were frequently admitted to hospitals for atrial fibrillation recurrence (p<0.001), compared with those who underwent electro impulse therapy. Adherence to antiarrhythmic therapy was low in the entire cohort of patients. There were no significant differences found between the clinical groups.Conclusion. Early diagnosis of the factors contributing to the progression of AF, the prescription of additional therapy for the secondary prevention of arrhythmia and the choice of its optimal treatment strategy may slow the progression of arrhythmia and the development of CHF, which will improve not only the clinical status of patients, but also their prognosis.Цель. Изучить особенности течения фибрилляции предсердий (ФП) у больных артериальной гипертонией (АГ) и экстракардиальной коморбидной патологией в зависимости от проводимой терапии, а также оценить приверженность к антиаритмической терапии.Материалы и методы. В обсервационном когортном исследовании наблюдалось 207 мужчин 45–65 лет с ФП (пароксизмальная и персистирующая форма) и АГ в сочетании с сахарным диабетом (СД) (n = 40), абдоминальным ожирением (АО) (n = 64) и хронической обструктивной болезнью легких (ХОБЛ) (n = 47). Группу сравнения составили 56 больных с ФП и АГ, без экстракардиальных заболеваний. В работе оценивались клинические, антропометрические показатели, тест для оценки приверженности Мориски-Грина, результаты инструментальной диагностики: электрокардиография (ЭКГ); холтеровское мониторирование электрокардиограммы (ХМ ЭКГ), суточное мониторирование артериального давления (СМАД) – системы суточного мониторирования SCHILLER (Шиллер, Швейцария), Эхокардиография – в М и 2D режимах на аппарате Vivid 7 (General Electric, USA). Все статистические расчёты проводили в программе Rstudio (version 0.99.879, RStudio, Inc., MA, USA).Результаты. Среди больных с ФП и АГ было выявлено 66% с сопутствующей экстракардиальной коморбидной патологией, из них с СД 20% больных; ХОБЛ выявлена у 22% пациентов, а АО отмечалось у 44% пациентов. По частоте электроимпульсной терапии (ЭИТ) и медикаментозной терапии (МТ) клинические группы были сопоставимы. Доказано, что пациенты, которым была проведена МТ, госпитализировались по поводу повторных приступов ФП достоверно чаще (р<0,001) по сравнению с группой пациентов, которым проводилась ЭИТ. Приверженность к антиаритмической терапии низкая у всей когорты обследованных, а при сравнительном анализе между клиническими группами не было выявлено достоверных различий.Заключение. Ранняя диагностика факторов прогрессирования ФП, назначение дополнительной терапии для вторичной профилактики аритмии и выбор правильной стратегии ее лечения могут замедлить прогрессирование аритмии и развитие хронической сердечной недостаточности, что улучшает не только клинический статус пациентов, но и их прогноз

Role fibrosis markers to stratify risk of atrial fibrillation in patients with arterial hypertension and ekstakardialnoy pathology

The aim of the study was to study the role of fibrosis markers (galectin — 3 and NT-proBNP) in stratification of atrial fibrillation risk in patients with arterial hypertension in combination with extracardial diseases. Materials and methods. In a prospective cohort study, 140 men aged 35-65 years with hypertension and AF (paroxysmal and persistent form), 57 – AH, AF and chronic obstructive pulmonary disease (COPD) and 83 patients with hypertension, AF without comorbidity (control) were observed. Serum galectin-3 and NT-proBNP levels were assessed by enzyme immunoassay. Anthropometry, lipid spectrum and Echocardiography studies were performed for all examined patients. Results. The level of galectin-3 in blood serum of patients with AF and COPD was higher-36.02 ng / ml. than in the control group-19.23 ng / ml, p=0.001. The average level of NT-proBNP in all the study group was significantly higher and amounted to 123.8 PG/ml , p<0.001, compared with the control group 67.99 PG / ml. Conclusion. Markers of fibrosis galectin-3 and NT-proBNP in serum of patients with atrial fibrillation and arterial hypertension in combination with chronic obstructive pulmonary disease are higher than in patients with atrial fibrillation and arterial hypertensionЦель исследования — изучить роль маркеров фиброза (галектина-3 и NT-proBNP) в стратификации риска фибрилляции предсердий у больных с артериальной гипертонией в сочетании с экстракардиальными заболеваниями. (ФП). Материалы и методы. В проспективном когортном исследовании наблюдались 140 мужчин 35-65 лет с АГ и ФП (пароксизмальная и персистирующая форма), из них 57пациентов с АГ, ФП и хроническим обструктивным заболеванием легких (ХоБЛ) и 83 пациента с АГ, ФП без сопутствующей патологии (контроль). Всем обследованным выполнены антропометрия, исследования липидного спектра, ЭхоКГ. Уровни галектина-3 и NT-proBNP в сыворотке крови оценивались методом иммуноферментного анализа. результаты. Уровень галектина-3 в сыворотке крови у больных АГ с ФП и ХОБЛ был выше - 36.02 нг/мл, чем в группе контроля - 19.23 нг/мл, р=0.001. Средний уровень NT-proBNP во всех исследуемой группе оказался достоверно выше и составил 123,8 пг/мл, р<0.001, по сравнению с группой контроля 67.99 пг/мл. Заключение. Маркеры фиброза галектин-3 и NT-proBNP в сыворотке крови у больных с фибрилляцией предсердий и артериальной гипертонией в сочетании с хроническим обструктивным заболеванием легких выше, чем у пациентов с фибрилляцией предсердий и артериальной гипертони

INFLAMMATORY REACTIONS IN EXPERIMENTAL MYOCARDIAL DAMAGE

Aim. To study the role of hormonal and metabolic changes specific to myocardial infarction in the development of inflammatory reactions in the experimental non-coronarogenic myocardial damage. Material and methods. Wistar male rats weighing 180–220 g (n=80) were used in the study. Metabolic myocardial infarction in intact rats and rats with alloxan diabetes was induced by epinephrine injected subcutaneously as single dose or daily (7 days). Myocardial infarction was verified by ECG analysis, and by histological control. Nitroblue tetrazolium test (NBT-test) both spontaneous and zymosan induced NBT-test was used to determine the oxygen-dependent functional activity of neutrophils and their biocidal reserve. Determination of cationic proteins in neutrophils of peripheral blood was performed using lysosomal-cationic test. Results. Increase in oxygen-dependent neutrophil biocidal activity was found as well as reduction in biocidal reserves. Indicators of zymosan induced NBT-test raised according to aggravation of hormonal changes much slower: alloxan increased them by 10% only , epinephrine single dose — by 35%, long-term epinephrine administration simultaneously with alloxan — by 54%. At the same time oxygen-independent neutrophil activity determined by intra-neutrophil cationic proteins level was significantly reduced. Blood levels of pro-inflammatory cytokines raised according to progression of the changes in myocardium: tumor necrosis factor-α (from 5.5±0.03 to 12.6±1.23 pg/ml) and interleukin-1β (from 6.0±0.18 to 11.1±0.78 pg/ml). Conclusion. Experimental model of hormonal changes specific to myocardial infarction detected a relationship between inflammatory reactions accompanying myocardial damage and increased catecholamine production

INFLAMMATORY REACTIONS IN EXPERIMENTAL MYOCARDIAL DAMAGE

Aim. To study the role of hormonal and metabolic changes specific to myocardial infarction in the development of inflammatory reactions in the experimental non-coronarogenic myocardial damage. Material and methods. Wistar male rats weighing 180–220 g (n=80) were used in the study. Metabolic myocardial infarction in intact rats and rats with alloxan diabetes was induced by epinephrine injected subcutaneously as single dose or daily (7 days). Myocardial infarction was verified by ECG analysis, and by histological control. Nitroblue tetrazolium test (NBT-test) both spontaneous and zymosan induced NBT-test was used to determine the oxygen-dependent functional activity of neutrophils and their biocidal reserve. Determination of cationic proteins in neutrophils of peripheral blood was performed using lysosomal-cationic test. Results. Increase in oxygen-dependent neutrophil biocidal activity was found as well as reduction in biocidal reserves. Indicators of zymosan induced NBT-test raised according to aggravation of hormonal changes much slower: alloxan increased them by 10% only , epinephrine single dose — by 35%, long-term epinephrine administration simultaneously with alloxan — by 54%. At the same time oxygen-independent neutrophil activity determined by intra-neutrophil cationic proteins level was significantly reduced. Blood levels of pro-inflammatory cytokines raised according to progression of the changes in myocardium: tumor necrosis factor-α (from 5.5±0.03 to 12.6±1.23 pg/ml) and interleukin-1β (from 6.0±0.18 to 11.1±0.78 pg/ml). Conclusion. Experimental model of hormonal changes specific to myocardial infarction detected a relationship between inflammatory reactions accompanying myocardial damage and increased catecholamine production.</p

The impact of chronic obstructive pulmonary disease and hypertension on the development and progression of atrial fibrillation

The article presents a review of the literature, reflecting ideas about the effect of chronic obstructive pulmonary disease on the development and progression of atrial fibrillation. Modern concepts regarding the substrate and triggers of paroxysms of atrial fibrillation have recently changed significantly. The role of concomitant diseases, in particular arterial hypertension and chronic obstructive pulmonary disease, formed the basis for changes in the electrophysiological properties of the myocardium

Inflammatory reaction in experimental non-coronary metabolic myocardial infarction

Aim. To study inflammatory reaction specifics in Vistar rats with non-coronary metabolic myocardial infarction (MMI). Material and methods. Electrocardiographical and histological verification of MMI. Measurement of neutrophil biocide activity, antioxidant system activity, the levels of lipid peroxidation (LP) products and pro-inflammatory cytokines, and plasma lipoprotein (LP) profile assessment. Results. In MMI rats, neutrophil biocide activity was increased, the balance between pro- and antioxidant systems was disturbed, plasma LP profile was affected, with increased pro-inflammatory LP levels, and pro-inflammatory cytokine concentrations were elevated. Conclusion. The observed inflammatory reaction specifics determined the clinical course of MMI

Features of Atrial Fibrillation in Patients with Arterial Hypertension and Extracardial Disorders

Aim. To study the features of the progression of atrial fibrillation (AF) in patients with arterial hypertension (HT) and comorbid extracardiac diseases.Material and methods. In the observational cohort study 308 men 45-65 years old with AF and HT were observed Most patients also had the following comorbid extracardiac diseases: diabetes mellitus (DM; n=40), diffuse toxic goiter (DTG; n=42); hypothyroidism (HTH; n=59), abdominal obesity (AO; n=64), and chronic obstructive pulmonary disease (COPD; n=47). The comparison group consisted of 56 patients with AF and HT only. Clinical, anthropometric, laboratory parameters, levels of NT-proBNP and galectin-3, results of ECG, daily monitoring of ECG and blood pressure wereassessed initially and after 12 months.Results. Persistent AF (29.6-65.2%) and long-term persistent AF (16-31.3%) were more common in groups with extracardiac diseases compared with the AF+HT group (20.4% and 14.2%, respectively). Permanent form of AF was statistically significantly more common in the DM (11.1%), AO (14.8%) and HTH (6.2%) groups compared with the AF+HT group (0.6%). A comparative assessment of risk factors (smoking and alcohol) did not show significant differences in prevalence in the groups (22-44%). An assessment of the levels of fibrosis and remodeling markers found a statistically significant increase in the level of galectin-3 in groups of patients with concomitant extracardiac diseases and an increase in the NT-proBNP level, relative to reference values in all groups except DTG.Conclusion. Patients with AF in combination with HT and comorbid extracardiac diseases have a more rapid AF progression