Оцінка вихідного стану системи гемостазу у хворих на облітеруючий атеросклероз судин нижніх кінцівок

Abstract

Метою даного дослідження є оцінка вихідного стану системи гемостазу у хворих на облітеруючий атеросклероз нижніх кінцівок, вивчення функціонального стану судинно-тромбоцитарної, коагуляційної ланок і фібринолізу системи гемостазу та їх розладів за допомогою низькочастотної вібраційної п’єзоелектричної тромбоеластографії (НПТЕГ).

Relevance. The problem of treatment of obliterative atherosclerosis (OA) of the vessels of the lower extremities is currently very relevant. The reasons are, on the one hand, progressive type of disease, leading to severe ischemia and trophic changes in 5–15 years, and, on the other hand, ambiguous results of traditional methods of operative and conservative treatment. Objective of the study. The purpose of this study is to evaluate the initial state of the hemostasis system in patients with obliterating atherosclerosis of the lower extremities, the study of the functional state of the vascular – platelet, coagulation and fibrinolysis of the hemostasis system and their disorders with low – frequency vibration piezoelectric thromboelastography. Materials and methods. The initial state of the hemostasis system was studied in 90 patients undergoing treatment for obliterating atherosclerosis of the lower limbs in the Odessa Regional Clinical Hospital. Results. The results of the studies represent a group of OA patients as a model in which are pronounced disorders of the aggregate state of the blood, where hypercoagulation dominates the anticoagulant potential. Inadequately enhanced activation of one or both coagulation units, even with the normal functioning of the anticoagulant system, can lead to generalized thrombus formation. Therefore, it is necessary to take into account the prevalence of thrombogenesis processes over fibrinolysis processes in this patient population and to consider the activation of platelet aggregation as an additional factor that participates in providing mechanisms for hypercoagulability.