The study of pathogenetic predictors of the development of anxiety-depressive disorders in myocardial infarction will make it possible to develop ways of their correction, thereby reducing the frequency of complications of the postinfarction period. Clinical studies were based on the examination of 58 patients with MI (mean age 59.2 ± 4.7 years) who were admitted to the cardiological hospital for treatment, and the observation data for them at the stage of rehabilitation. On the basis of the presence of anxiety-depressive symptoms, the patients were divided into 2 groups. The first control group consisted of 14 patients with MI without depressive disorders. The second group included 44 age-matched patients who underwent MI with symptoms of anxiety and depression without comorbid cardiovascular pathology. The diagnosis of myocardial infarction was based on the results of clinical examination, ECG changes, laboratory parameters, and echocardiographic data. In order to assess the mental status of the subjects, subjective methods were used: the hospital anxiety and depression scale (HADS) for patients in a somatic hospital and recommended for use in patients with post-infarction period. Markers of endothelial dysfunction in blood plasma were determined by enzyme immunoassay using appropriate test systems. Since fibrinogen is one of the key factors in the blood coagulation process, disorders of which with a tendency to thrombotic changes are one of the central links in the pathogenesis of MI, the level of oxidized fibrinogen with parameters of the functional state of endothelial cells was studied. In the early stages after myocardial infarction, the level of oxidized fibrinogen was 1.7 times higher in the study group compared to the control, although, in general, the level of fibrinogen in the study group was within normal values. In the subsequent periods of the study, the level of oxidized fibrinogen was in high values and, on average, exceeded the control values by 1.64 times. Since one of the key roles in the development of dysfunction and endothelial destruction is assigned to the factors of oxidative stress, a correlation analysis of the relationship between the oxidative modification of fibrinogen and the parameters of endothelial function was carried out. A direct correlation was shown between the level of oxidized fibrinogen and the level of Endothelin-1 (r = 0.78, p <0.01), and a direct correlation with the level of von Willebrand factor (r = 0.365, p <0.01). Linear regression analysis confirmed the associations of oxidized fibrinogen with the indicated parameters of endothelial dysfunction. Based on the results obtained, it can be emphasized that with MI, in patients with developed DS, along with increased oxidative changes in lipids and plasma proteins, there is also a significant oxidative modification of fibrinogen, which does not depend on the concentration of fibrinogen. Oxidized fibrinogen potentiates potentially prothrombogenic changes in the vascular-platelet link of hemostasis, in particular, the acceleration of leukocyte-platelet aggregation. The revealed signs of thrombotic and hypercoagulant hemostasis disorders in patients with MI with depressive disorders, such as signs of endothelial dysfunction, elevated von Willebrand factor levels, are associated with oxidative changes in plasma fibrinogen in patients with MI with the development of DS, have a high diagnostic value.
The article shows the strengthening of the Soviet power in Turkestan, the military-political processes in the country based on the materials of the "Gornist" newspaper. Also, the structural structure of the newspaper, the topics covered in it, its place in ideological and ideological politics, etc., are explained based on information from a number of sources.
Слизистая оболочка полости рта и пародонта заселена множеством микроорганизмов. При ослаблении иммунитета равновесие между местной бактериальной флорой и защитными силами организма нарушается, что способствует развитию инфекционного процесса в слизистой оболочке полости рта и пародонта. Поэтому лечебные мероприятия у таких больных должны быть направлены не только на ликвидацию клинических симптомов воспаления, но и на усиление факторов местной и общей иммунной защиты
A study of 341 patients with an established diagnosis of acute myocardial infarction was carried out. The patients are divided into 2 groups. The first, main, included 233 patients with acute myocardial infarction, who subsequently developed depressive disorders, confirmed clinically and using diagnostic scales; the second group consisted of 108 patients who also had acute myocardial infarction, but did not subsequently suffer from symptoms of depression. Clinical and dynamic observation of patients in the postinfarction period was carried out with control of the condition in a month, three months, six months, 12 months after myocardial infarction. Clinical observation was used to detect the presence of symptoms of depression. Among patients with MI with DS in the first days after MI, more than half (51.1%) reported a permanent decrease in mood more often than other symptoms, i.e. these patients showed an affective component of depression, while the ideator component of depression, which manifested itself in thinking retardation to one degree or another, was in 27.5% of patients, motor retardation (motor component) was detected in 21.5% of those observed. In patients with almost the same frequency, the anxious and melancholic type of affect was noted (47.0% and 41.2%, respectively), the dysphoric type of affect was found in 11.8% of cases, which is 4 times less than anxious and 3.5 times less than the melancholic type. In cases of prolonged depression, the severity of affective disorders more often directly correlated with the severity of the physical condition. If not so long-term depressive episodes were largely due to "their own vision of the disease", the severity of their symptoms depended on the conversation with the doctor and the information received from him, the degree of awareness of his diagnosis, possible complications, and not very much depended on the general somatic status itself. then the course of prolonged depression in patients worsened with the aggravation of the cardiological and general somatic condition of patients. Psychosomatic parallelism in the majority of protracted depressions was manifested by the generalization of asthenic symptom complexes (increased general weakness, intolerance to exertion, lethargy, adynamia, severe daytime sleepiness in combination with early insomnia) with deterioration of the somatic state. At the same time, it was noted that with prolonged depression, there were always more or less pronounced cognitive disorders (reduced memory for past events, limited ability to comprehend what was happening around, remember new information, impaired concentration). Postinfarction depressive episodes lasting up to six months can be attributed to nosogenies; depressive episodes of postinfarction genesis with a protracted course, probably with a high degree of confidence can be attributed to somatogenias.