Articles
| Open Access |
https://doi.org/10.37547/ijmscr/Volume05Issue11-32
Mechanism Of The Virchow’s Triad In The Development Of Thrombosis
Abstract
Thrombosis is a complex pathological process characterized by the formation of a blood clot within the vascular system, which is one of the most dangerous conditions for human health [1]. In explaining this process, the concept of Virchow's triad — endothelial damage, impaired blood flow (stasis), and hyperhomocoagulation — is accepted as the main pathophysiological mechanism [2]. In the last decade, molecular and clinical studies of each component of this triad have revealed many new aspects of the development of thrombosis [3]. For example, endothelial dysfunction occurs as a result of atherosclerosis, hypertension, chronic inflammation, and oxidative stress, which leads to the loss of anticoagulant properties of the vascular wall and creates conditions for thrombus formation [4]. Stasis of blood flow is observed in the venous system, especially in conditions such as heart failure, varicose veins, or prolonged immobilization, and it increases erythrocyte aggregation and platelet adhesion to the wall [5]. Hyperhemocoagulation can be associated with genetic mutations (e.g., F5 Leiden or Prothrombin G20210A) or develop secondarily as a result of pregnancy, cancer, or autoimmune diseases [6].
Studies from 2020–2025 have shown that these three factors are interconnected and synergistically increase the risk of thrombosis [7]. Also, using RNA-seq and proteomics technologies, the expression of endothelial inflammatory markers (e.g., ICAM-1, VCAM-1, IL-6) has been found to increase the susceptibility to thrombosis [8]. At the same time, thrombotic events associated with cardiovascular diseases, COVID-19 infection, and hormonal therapy are also explained on the basis of Virchow's triad [9].
This article analyzes the role of each component of Virchow's triad in the formation of thrombosis and their modern molecular mechanisms. The results of the study provide an important theoretical and practical basis for individualizing the prevention and treatment of thrombosis [10].
Keywords
Virchow's triad, thrombosis, endothelial damage, blood flow stasis
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