Вплив Антитромбоцитарного Лікування На Агрегаційну Здатність Тромбоцитів У Хворих На Ішемічну Хворобу Серця Та У Поєднанні З Цукровим Діабетом 2-Го Типу

Abstract

The number of diabetes mellitus (DM) is steadily increasing and such a rapid increase will lead to an increase in cardiovascular events, mainly due to coronary heart disease (CHD), in which coronary atherosclerosis and its progression is one of the causes of mortality. The course of atherosclerosis is closely related to the state of the hemostasis system. The basis for the development of atherosclerosis is arterial thrombosis, with the activation of platelets playing a leading role in the disruption of hemostasis in coronary heart disease, increasing the risk of thrombotic complications. At present, data on the relationship of different hemostasis units in coronary heart disease in combination with diabetes are mixed, complicating the prognosis of adverse effects taking into account the status of platelet hemostasis. Given the relevance of the topic, the purpose of this study was to evaluate the spontaneous and induced platelet aggregation in patients with various forms of acute coronary heart disease (ACHD) and to identify features of platelet aggregation activity in the combination of ACHD and DM.Adequate reduction of platelet functional activity in patients with coronary heart disease receiving antiplatelet treatment is the basis for effective prevention of thrombus formation in the coronary vessels and the development of adverse cardiovascular events. However, according to the data obtained, the highest activation of platelet hemostasis was observed in the group of patients with ACHD in combination with DM, which showed a significant (relative to the control group) increase in the level of spontaneous platelet aggregation by 4.6 times. At the same time, the percentage of patients who had increased the above indicators was significantly lower in the group of patients with ACHD without disorders of carbohydrate metabolism. In patients with ACHD in combination with DM, activation of the spontaneous aggregation rate was also observed, which accelerated the formation of aggregates by 30% compared with the isolated ACHD group (p <0.05). In the study of induced platelet aggregation, it was taken into account that patients in both groups received dual antiplatelet therapy, which had a significant effect on their activity. However, the expected inhibition of aggregation potential was revealed only by the action of arachidonic acid (AA). Thus, the degree of platelet aggregation in response to AA in group I was 1.9 times significantly lower than the control values ​​of 18.8% [12,1; 26,4], in group II - 1,5 times and made 24,38% [21,5; 32.9] (p <0.001 for both cases). According to ADP-induced platelet aggregation, the effect of antiplatelet drugs was less effective. Thus, a moderate decrease in the degree of ADP-aggregation was observed only in the group of isolated ACHD, whose indicators were 1.42 times lower than in the control group (p <0.01). Thus, dual antiplatelet therapy was accompanied by an effective reduction in platelet function only in the group of patients with isolated ACHD.