In order to prevent complications of coronavirus disease COVID-19 (impaired platelet hemostasis, endothelial function, heart rate variability and QT interval, which increase the risk of thromboembolic complications and cardiovascular mortality), it is promising to study the relationship between heart rate variability and platelet hemostasis in patients with coronary artery disease in combination with COVID-19. The aim of the study was to investigate the effect of COVID-19 on the interdependence of changes in platelet hemostasis and heart rate variability in patients with CHD. The clinical and instrumental results of 102 patients were analyzed, who were divided into 3 groups: group 1 - coronary heart disease (CHD) without COVID-19 (n = 32); group 2 - CHD in combination with COVID-19 (n = 35); group 3 - COVID-19 without CHD (n = 35). The control group included 30 conditionally healthy individuals. In the group of CHD + COVID-19, changes in platelet hemostasis were determined by laser aggregometry by the turbidimetric method according to Born and analysis of light transmission fluctuations (to assess the average size of aggregates) with an assessment of spontaneous and induced aggregation: adenosine diphosphate (ADP), arachidonic acid (AA), epinephrine, collagen, ristomycin. Aggregation parameters were recorded on a BIOLA LA230-2 analyzer using the AGGR program. According to the results of the study, an aggregogram was obtained with the following parameters: according to the curve. In patients with coronary heart disease with concomitant COVID-19, a wide range of disorders of the functional state of platelet hemostasis was observed, in particular, an increase in the degree, rate and time of spontaneous platelet aggregation, as well as a decrease in the degree, rate and time of platelet aggregation induced by epinephrine. At the same time, the profile of the course of CHD in combination with COVID-19, in contrast to the “isolated” course of both conditions, was characterized by a predominance of a decrease in the rate of aggregation during induction with arachidonic acid and ADP in patients of group 2. The degree of aggregation was greater in group 2 when using collagen and ristomycin. The aggregation time was shorter when using an adrenaline inducer in group 2. Patients with chronic coronary artery disease, in particular in its combination with COVID-19, showed signs of autonomic nervous system dysfunction, namely a decrease in overall HRV (by SDNN, SDАNN and SDNNi) and a decrease in the activity of the parasympathetic nervous system (by rMSSD, pNN50 and HF). The detected changes in the autonomic regulation of the heart were most pronounced among patients with associated coronary artery disease and COVID-19 in terms of HRV parameters such as SDNN and pNN50. Increases in QT interval duration and variability recorded in patients with chronic coronary artery disease and COVID-19 were most pronounced in the combination of the two nosologies and the collagen-induced aggregation time had a direct correlation with HF. There are inverse relationships between the rate of spontaneous aggregation induced by adrenaline and collagen on the one hand and the indicators characterizing the sympathetic link of the ANS on the other. A direct correlation was observed between the degree of spontaneous aggregation and ADP-induced aggregation and between the rate of spontaneous aggregation induced by adrenaline and collagen and the parasympathetic part of the ANS. The aggregation time induced by epinephrine was directly related to the integral indices of the ANS and PNS. Inverse relationships with the ANS were observed with the time of platelet aggregation induced by ristomycin. Regarding the variability of the QT interval, inverse relationships with neurogenic, myogenic and respiratory fluxmotions were observed. The standard deviation and coefficient of variation of QT were inversely related to the degree of aggregation induced by ristomycin and directly to epinephrine. The time of spontaneous aggregation, as well as that induced by ADP and collagen, was directly correlated with the QT mode and mean QT. The standard deviation and coefficient of variation of the QT interval inversely affected the time of spontaneous aggregation induced by collagen, AK and ristomycin. The rate of aggregation did not affect the variability of the QT interval. Given the established relationships of HRV parameters and QT interval variability with indicators of the functional state of platelet hemostasis, additional consideration of the characteristics of autonomic dysfunction, as well as prolongation of the QT interval with increased variability, is appropriate in the system of management of patients with coronary artery disease and concomitant coronavirus disease. There is a need for widespread use of noninvasive methods of assessing the state of the microcirculatory system and assessing platelet hemostasis in the management of patients with coronary artery disease suffering from COVID-19. Patients with chronic coronary artery disease and concomitant COVID-19, along with platelet hemostasis dysfunction, showed signs of autonomic dysregulation and increased QT interval duration and variability. Additional consideration of the characteristics of platelet hemostasis function, heart rate variability and QT interval is advisable in the management of such patients.