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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.
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.
Background. Nephrotic syndrome (NS) is associated with a high risk of thrombotic complications. In this group of patients, routine local tests for assessing hemostasis do not accurately reflect hypercoagulable state. Global functional tests for assessing hemostasis, including thrombodynamics (TD), are considered promising for assessing disorders in the blood coagulation system of these patients. Aim. To compare the rate of hypercoagulability according to routine hemostatic tests and TD and to evaluate the factors associated with increased risk of thrombotic complications in patients with chronic glomerulonephritis (CGN). Materials and methods. The study included 94 patients with active CGN who were not receiving anticoagulant therapy; 63 (80.3%) patients had NS, and 31 (19.7%) had active CGN without NS. Hemostasis parameters were assessed using local coagulation tests and TD test. Using logistic regression analysis, factors associated with the risk of thrombosis were assessed. Results. Of the 94 patients with active CGN in 63 without preventive anticoagulant therapy, hypercoagulability according to routine tests was detected in 6 (9.5%) patients with NS and in 3 (9.7%) patients without NS (p0.05). Hypercoagulability according to the TD test was detected in 24 (53.9%) patients with NS and in 5 (32.2%) without NS (p0.05). The formation of spontaneous clots was observed in 29 (30.9%) of patients with CGN, most of them 24 (83%) with NS. 10.6% of patients in our cohort experienced thromboembolic events. The risk of thromboembolic events according to the univariate regression analysis was associated with older age, higher lipid levels, use of glucocorticosteroids and detection of spontaneous clots by the TD test. No association of thromboembolic events with abnormalities in routine hemostasis tests was obtained. Conclusion. In patients with CGN with nephrotic syndrome, hypercoagulability is detected in 9.5% of cases with routine coagulation tests and in 53.9% of cases with TD test. Detection of spontaneous clots by TD test is associated with a risk of thromboembolic events.
Aim. To study the indices of standard coagulogram and thrombodynamics test in native plasma and in the test with phospholipids in relation to the activity of rheumatoid arthritis (RA) and the ongoing therapy.Material and methods. We examined 28 patients with rheumatoid arthritis and eight age- and sex-matched healthy controls: 11 patients with high rheumatoid arthritis activity (DAS28>5.2) (Group 1), nine patients with low and moderate rheumatoid arthritis activity (DAS28<5.2) (Group 2) and eight rheumatoid arthritis patients receiving anticoagulants (Group 3). Results. Elevated fibrinogen was more common in the RA patient groups: 5/11(45%) in group 1, 3/9(33%) in group 2 and 3/8(38%) in group 3. In the control group, fibrinogen was normal, p><0.05. Increased SFMC was found in all patients in all three groups (100%) and only in 2 of the controls (25%), with p><0.05. Mean clot density was significantly higher in RA groups than in controls: 26811, 25437 and 24740 versus 20631 c.u. in groups 1, 2, 3 and control, respectively, p><0,01. In patients with anticoagulants, lag time (1.4 minutes) was longer than without anticoagulants (1.1-1.2 minutes), with p><0.05 in all cases. Spontaneous clots were detected only in patients: 3 in groups 1 and 1 each in groups 2 and 3. Hypocoagulation was detected only in group 3 in 1/8(12%) patients, and thrombotic readiness status was detected in groups 1 and 2: in 2/11(18%) and 1/9(11%) patients, respectively. The frequency of normal- and hypercoagulation did not differ between the patient and control groups. Conclusion. According to the thrombodynamics test, hypercoagulability is present in RA patients. Thrombodynamics test can be used to identify the risk of thrombosis and to individualize therapy in RA patients. Keywords: prothrombotic state, hypercoagulation, rheumatoid arthritis, thrombodynamics>˂ 5.2) (Group 2) and eight rheumatoid arthritis patients receiving anticoagulants (Group 3).Results. Elevated fibrinogen was more common in the RA patient groups: 5/11(45%) in group 1, 3/9(33%) in group 2 and 3/8(38%) in group 3. In the control group, fibrinogen was normal, p˂ 0.05. Increased SFMC was found in all patients in all three groups (100%) and only in 2 of the controls (25%), with p˂ 0.05. Mean clot density was significantly higher in RA groups than in controls: 26811, 25437 and 24740 versus 20631 c.u. in groups 1, 2, 3 and control, respectively, p˂ 0,01. In patients with anticoagulants, lag time (1.4 minutes) was longer than without anticoagulants (1.1-1.2 minutes), with p˂ 0.05 in all cases. Spontaneous clots were detected only in patients: 3 in groups 1 and 1 each in groups 2 and 3. Hypocoagulation was detected only in group 3 in 1/8(12%) patients, and thrombotic readiness status was detected in groups 1 and 2: in 2/11(18%) and 1/9(11%) patients, respectively. The frequency of normal- and hypercoagulation did not differ between the patient and control groups.Conclusion. According to the thrombodynamics test, hypercoagulability is present in RA patients. Thrombodynamics test can be used to identify the risk of thrombosis and to individualize therapy in RA patients.
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