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The aim of the review is to highlight the main mechanisms of thrombotic readiness state (TRS) formation in patients with cardiovascular pathology (CHD, atherosclerosis, arterial hypertension) and aggravated oncoanamnesis. A keyword search in the text databases Scopus, Web of Science, and PubMed was conducted on literature sources on factors associated with the development of hypercoagulability in cardiovascular pathology and cancer history. Pathological STH is characterised by disturbances not only in the haemostasis system, but also in the microcirculatory channel, in the vascular endothelium. In ischaemic heart disease (IHD), the following mechanisms that increase the procoagulant potential of blood are identified: endothelial damage, blood stasis under conditions of decreased cardiac output, and slowing of fibrinolysis. Two main mechanisms of haemocoagulation activation in the presence of oncoprocess have been studied: direct activation of haemocoagulation and platelets due to cancer cell factors (tissue factor, podoplanin, platelet agonists, phosphatidylserine, cancer procoagulant, plasminogen activation inhibitor-1) and indirect activation resulting in the release of neutrophil extracellular traps. Data on the joint influence of CHD and cancer history on haemostasis are rather limited. Current methods of diagnosing this condition, including dilated coagulogram, thromboelastometry, thrombin generation test, and thrombodynamics test were analysed. The introduction of global tests (thromboelastometry, thrombin generation test, thrombodynamics test) for the diagnosis of STH is an important step in understanding the mechanisms underlying this condition.
Keywords:cardiovascular pathology, thrombotic readiness state, thrombodynamics test, methods of haemostasis system research, aggravated oncoanamnesis.
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