Попонина Татьяна Михайловна -д-р мед. наук, профессор, профессор кафедры кардиологии ФПК и ППС СибГМУ (г. Томск).Гундерина Ксения Ивановна () -аспирант кафедры кардиологии ФПК и ППС СибГМУ (г. Томск).Попонина Юлия Сергеевна -канд. мед.наук, доцент кафедры кардиологии ФПК и ППС СибГМУ, врач-кардиолог отделения неотложной кардиологии НИИ кардиологии СО РАМН (г. Томск).Марков Валентин Алексеевич -д-р мед. наук, профессор, зав. кафедрой кардиологии ФПК и ППС СибГМУ, руководитель отделения неотложной кардиологии НИИ кардиологии СО РАМН (г. Томск).

Aim: to study the changes in heart rate variability (HRV) in patients with anxiety and depressive disorders who suffered acute coronary syndrome (ACS) and to determine the effects of antidepressant agomelatine on HRV and sleep quality during six-month follow up.Material and Methods. The study included 54 people with ACS, anxiety, and depressive disorders. Patients were randomly assigned to two groups. Antidepressant agomelatine 25 mg/day was administered to patients of group 1 in addition to standard therapy for ACS; group 2 received placebo. Twenty four-hour Holter ECG monitoring, HRV study, mental status monitoring, and sleep quality assessment were performed during hospitalization and at six-month follow up.Results. Patients of both groups had clinically significant anxiety, subclinical depression, and insomnia of varying severity. According to Holter monitoring data, all patients had decline in HRV parameters. After six months, anxiety and depression significantly improved in patients administered with agomelatine; these patients had sleep normalization and improved HRV. The comparison group did not have similar changes.Conclusion. Additional administration of agomelatine 25 mg/day to patients with anxiety and depressive disorders after ACS resulted in improvement of mental status, heart rate variability, and sleep quality. Due to the absence of pro-arrhythmogenic effects, administration of agomelatine allows to correct anxiety-depressive disorders in patients with ACS.

Funding Acknowledgements Type of funding sources: None. Background In clinical medicine, there is still a need for a highly sensitive laboratory marker that reflects brain damage. In some cases, myocardial infarction proceeds with aggravation of cerebral ischemia, stroke, psychosomatic disorders. One of the candidates for laboratory diagnosis of brain damage is the S 100B protein. Aim of the study to analyze the level of brain-specific protein S 100B in blood plasma in patients with acute coronary syndrome associated with anxiety-depressive disorders. Methods and Results All patients were diagnosed with clinically severe anxiety of 55.2 [40; 64] points and depression of an average degree of 24.5 [19; 28] points. In the hospital, blood samples were taken for S 100B protein. The intragroup analysis of the S 100B protein level revealed that in 3 patients (5%) the S 100B protein level was below the normal limit 42.56 [32.6; 52.6] ng/L, in 13 patients (24%) the S 100B was within the normal range of 84.1 [75.27; 86.57] ng/L. In 38 patients (70%), the concentration of S100B protein was increased to 129.65 [110; 144] ng/L. The analysis of the group with a high concentration of S 100B protein found that the highest indicators of the S 100B protein level were in patients suffering from carbohydrate metabolism disorders, with a long history of hypertension, high levels of anxiety and depression. When studying the mental status of patients, a positive correlation was found between the concentration of the S100B protein and the level of anxiety (p = 0.00065). In 5 patients (9%), the maximum increase in the level of protein S 100 B 184.6 [166.26; 209.34] ng/L was revealed. These patients aged 60 to 70 years, had stroke in the past, had a long history of ischemic heart disease, type 2 diabetes, the course of AMI proceeded with a decrease in left ventricular ejection fraction to 34-40%. Patients with a protein level of 84.1 [75.27; 86.57] ng/L were younger, age 50-60 years, without a history of diabetes, with preserved left ventricular ejection fraction. Conclusion An increase in the S 100B protein level was observed in polymorbid patients, with a history of possible impairment of the blood-brain barrier permeability, which could have formed due to the toxic effect of the S 100B protein. This group of patients has more pronounced anxiety-depressive symptoms. Thus, the S 100B protein can be considered as a potential therapeutic target.