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.
