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Introduction: Over the years, heart failure remains one of the most common and prognostically unfavorable conditions. The aim of our study was to determine the frequency of complications in patients with CHF depending on the body weight and intoxication syndrome of varying degrees of severity. Materials and methods: A complete clinical examination was performed in 58 patients (41 (70.6%) men and 17 (29.4%) women) with CHF. In addition to the standard examination in accordance with the protocol, the level of endogenous intoxication was determined by the level of medium-weight molecules (MWM254) and leptin. The patients were randomized into 4 groups depending on their body mass index and the degree of endogenous intoxication. Statistical processing of the results was carried out using the methods of variation statistics “Statistica 6.0”. Results: It was revealed that the worst survival rate is observed in patients with normal body mass against the background of the expressed endogenous intoxication syndrome, the best survival rate is observed provided that there are a normal body mass and endogenous intoxication of a minimum degree. An inverse correlation between the body mass index and the endogenous intoxication indicator (blood MWM) was detected. Patients with CHF should have their leptin level evaluated. An increase in its level was associated with arterial hypertension, an increase in blood glucose levels and lipid metabolism disorders. Conclusions: Increased level of blood MWM worsens the forecast of CHF. The unfavorable outcome was observed in patients with the combination of hypoleptinemia with severe endogenous intoxication.

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Важную роль в патогенезе хронической сердечной недостаточности (ХСН) занимает синдром эндогенной интоксикации (СЭИ) [1][2][3][4][5], который характеризуется ме-таболическими, морфологическими, функциональ-ными нарушениями различных органов и систем и воз-никает в ответ на совокупность факторов внешней и внут-ренней среды. В результате в тканях и биологических жидкостях происходит накопление продуктов нор-мального и нарушенного обмена веществ или факто-ров клеточного ответа [6], которые обладают токсиче-ским действием. При ХСН, кроме непрерывного воз-действия продуктов асептического воспаления, воз-никают гипоксия кишечника (что приводит к мальаб-сорбции), нарушения тканевого метаболизма, сниже-ние детоксикационной функции печени. Все это спо-собствует появлению в крови молекул средней массы (МСМ), фенола, мочевины и т.п., что усиливает эндо-токсикоз. Прямое и косвенное токсическое действие на ткани ухудшает микроциркуляцию и еще больше углуб-ляет органную патологию [7]. Экспериментальные ис-следования показали, что в условиях хронической эн-дотоксемии в сердечной мышце происходят тканевые преобразования -дисметаболическая кардиомиопа-тия [8]. Установлена связь между проявлениями мета-болической интоксикации и степенью снижения со-кратительной способности миокарда, поскольку пока-зано, что МСМ обладают отрицательным инотроп-ным действием [9]. Однако этот вопрос в литературе освещен недостаточно.В связи с этим целью работы стало установление из-менений структурно-функциональных показателей сердца у больных с ХСН в зависимости от уровня мо-лекул средней массы. Материалы и методыПроведено полное клиническое обследование 110 пациентов с ХСН, вызванной хроническими формами ишемической болезни сердца (ИБС) и артериальной ги- Цель. Изучить особенности структурно-функциональных параметров сердца у больных хронической сердечной недостаточностью (ХСН) в зависимости от степени выраженно-сти синдрома эндогенной интоксикации, который определяли по уровню молекул средней массы (МСМ) в периферической крови. Материал и методы. У 110 больных ХСН кроме стандартных клинических, лабораторных и инструментальных (эхокардиография) обследований определяли уровень МСМ, по которому пациенты были разделены на группы с минимальной, умеренной и выраженной эндогенной интоксикацией. Результаты. 41,8% больных имели минимальную выраженность эндогенной интоксикации, средняя степень была у 39,1%, высокая степень -у 19,1%. Больные с максималь-ными показателями МСМ характеризировались низкой фракцией выброса левого желудочка (р<0,05), наибольшим размером правого желудочка, минимальной частотой ди-агностики сохраненной функции левого желудочка и высокой частотой обнаружения увеличенных размеров левого предсердия, межжелудочковой перегородки и правого же-лудочка. Заключение. Уровень МСМ может служить критерием прогноза ХСН. Худший прогноз имеют пациенты с высоким содержанием МСМ крови. Ключевые слова: хроническая сердечная недостаточность, молекулы средней массы, эндогенная интоксикация, структурно-функциональные параметры сердца. РФК 2013;9(1):40-43S...

The aim: To evaluate the structural changes of the brain in relation to the formation of cognitive disorders (CD) in patients with arrhythmias Materials and methods: 147 patients with different clinical forms arrhythmias against the background of ischemic heart disease were examine. At the first stage, all patients with arrhythmias assessed cognitive functions. At the second stage, patients were distributed divided into two groups: the main group patients with CD, control – patients without CD. These groups underwent computed tomography examination of the brain. Results: CD were established in 83% patients with arrhythmias. Mild CD were more often diagnosed in patients with persistent form of atrial fibrillation (AF), severe CD – in patients with permanent form of AF and atrioventricular blockade ІI-III degrees. Neuroimaging changes were found in 73.8% patients with CD and in 36% patients without CD. They were manifested by atrophic changes of the cortex, internal hydrocephalus, a decrease in the density of the brain sub¬stance of the periventricular area. In patients with CD, compared to patients without CD, showed lacunar foci with predominant localization in the parietal and frontal lobes of the brain, periventricular and subcortical leukoaraiosis. Multiple correlations were established between CD and structural changes of the brain. Conclusions: The increase in the severity of CD in patients with arrhythmias is associated with atrophic changes at the cortical-subcortical level, accompanied by the phenomena of internal hydrocephalus, periventricular and subcortical LA, lacunar foci, with a predominant localization in the frontal-temporal-occipital lobes, in the visual hump and basal ganglia of both cerebral hemispheres.

The aim was to highlight the leading links of pathogenesis of chronic obstructive pulmonary disease (COPD) using published data and the results of own research. Material and methods. The publications of the last 5 years have been picked up for review from Pubmed library. Own research has been based on retrospective analysis of medical records from 470 patients with COPD (246 men and 224 women, median age 62 years). Results. According to literature data chronic persistent inflammation, manifesting by activation of multiple cells with excessive production of number of biologically active substances, is a leading link of COPD pathogenesis. Second important link of COPD pathogenesis is energydependent hypoxia with signalling pathway change and super expression of hypoxia-inducible factor. An important role plays chronic disease anaemia, occurring due to effect of pro-inflammatory cytokines and hypoxia-inducible factor which, in turn, preserves inflammation and hypoxia. According to own data a decrease of blood oxygenation and decline in lung function also testify to existing relationship between inflammation and hypoxia. Active inflammation correlated with decreased bronchial patency. Anaemic syndrome in COPD patients was associated with higher levels of neutrophils, ESR, C-reactive protein, total fibrinogen, seromucoids and integral haematological indices, as well as low blood oxygenation and decrease of velocity parameters of lung function. Conclusion. Inflammation, hypoxia and anaemia are three connected links of pathogenesis of COPD, which create vicious circle and possibly determine disease progression. Key words: chronic obstructive pulmonary disease, pathogenesis, inflammation, hypoxia, hypoxia-inducible factor, anaemia.

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Patients with chronic obstructive pulmonary disease (COPD) in combination with anemia of chronic disease (ACD), are of particular interest to both scientific and practical health care. The purpose of the work - to study the activity of systemic inflammation.Material and methods. The results of the examination of 475 patients with exacerbation of COPD were analyzed, which were divided into two groups: group I - 155 people (61,3% men and 38,7% women) with ACD; group II - 320 patients (46,9% of men and 53,1% of women) without the anemic syndrome. Determination of the activity of the inflammatory process was performed by hemocytogram, serum markers of inflammation and integrated hematological indices. The results of the study. It was found that COPD in combination with ACD was accompanied by activation of the inflammatory process (erythrocyte sedimentation rate, segmented neutrophils content) and suppression of lymphocyte-monocyte inflammation, significantly higher integral hematological indices (leukocyte shift index; ratio of leukocytes, non-segmented neutrophils and all neutrophils to the erythrocyte sedimentation rate; the ratio of neutrophils to lymphocytes and the integrated index of inflammation), which increased with the deepening of the anemic syndrome, increasing patients age and was more pronounced in women. Activation of inflammation was associated with deterioration of bronchial patency according velocity parameters (Tiffno index, mean and peak volumetric velocities, maximal volumetric velocities by 25% and 75% of the forced ungs vital capacity). Anemic syndrome was also associated with higher levels of C-reactive protein (p>0,05), general fibrinogen (p<0,05) and seromucoids (p>0,05), the content of which varied in parallel with the leukocyte shift index. Conclusion. Anemic syndrome, as a manifestation of persistent systemic inflammation, worsens the course of a chronic obstructive pulmonary disease through affecting the respiratory function and the inflammatory process activation.