Abstract
Thrombosis becomes the cause and complication of many cardiovascular diseases, and their prevalence remains a leader in the structure of morbidity and mortality in Russia and throughout the world. Modern fundamental and clinical research has significantly supplemented traditional ideas about the mechanisms of thrombus formation. First of all, Virchow's triad has been rethought, in which, according to new data, the leading role is assigned to vascular damage, and slowing down blood flow plays a primary role in the formation of only venous, but not arterial, blood clots. In recent years, the mechanisms of endothelial dysfunction underlying thrombosis associated with inflammatory (immunothrombosis) and atherosclerotic (atherothrombosis) damage to the vascular wall have been studied in detail. The cellular and molecular mechanisms of acquired hypercoagulability and hereditary thrombophilia have been deciphered. The traditional concept of dividing blood clots into “red” (venous, consisting of fibrin and red blood cells) and “white” (arterial, platelet) is being revised. It has been shown that red blood cells can occupy most of the volume of not only venous, but also arterial thrombi, and play an important role in thrombus formation reactions. The process of compression (contraction, retraction) of blood clots, caused by contraction of activated platelets, changing the structure of the blood clot and affecting the course and outcome of thrombosis, is being actively studied. A deep understanding of the pathogenesis of thrombosis, taking into account modern concepts, is necessary for effective prevention, early diagnosis and treatment of thrombotic conditions.