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1.
Ter Arkh ; 93(11): 1255-1263, 2021 Nov 15.
Article in Russian | MEDLINE | ID: mdl-36286646

ABSTRACT

AIM: To study the relationship of hemostatic disorders with inflammation and estimate their role in the course and outcomes of COVID-19. MATERIALS AND METHODS: We examined 215 consecutive patients with moderate and severe forms of acute COVID-19. The patients were on anticoagulants and immunosuppressive drugs. Hemostasis was assessed using the thrombodynamics assay, thromboelastography, fibrinogen and D-dimer levels, prothrombin time, and soluble fibrin-monomer complexes (ethanol gelation test). The hemostatic parameters were correlated with hematological and biochemical tests, including markers of inflammation (C-reactive protein, interleukins 6 and 8), as well as with the disease severity and outcomes. RESULTS: Laboratory signs of coagulopathy were revealed in the vast majority of the cases. Despite the use of low-molecular-weight heparins in the prophylactic and therapeutic doses, coagulopathy in COVID-19 manifested predominantly as hypercoagulability that correlated directly with the systemic inflammation and metabolic changes due to liver and kidney dysfunction. A direct relationship was found between the grade of coagulopathy and the severity of COVID-19, including comorbidities and the mortality. The chronometric hypocoagulability observed in about 1/4 cases was associated with a high level of C-reactive protein, which may decelerate coagulation in vitro and thereby mask the true inflammatory thrombophilia. Persistent hyperfibrinogenemia and high D-dimer in the absence of consumption coagulopathy suggest the predominance of local and/or regional microthrombosis over disseminated intravascular coagulation. CONCLUSION: The results obtained substantiate the need for laboratory monitoring of hemostasis and active prophylaxis and treatment of thrombotic complications in COVID-19.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Disseminated Intravascular Coagulation , Hemostatics , Thrombophilia , Thrombosis , Humans , COVID-19/complications , SARS-CoV-2 , C-Reactive Protein , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/complications , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/drug therapy , Heparin, Low-Molecular-Weight/therapeutic use , Thrombophilia/complications , Anticoagulants/therapeutic use , Fibrinogen , Inflammation , Interleukins , Ethanol
2.
Angiol Sosud Khir ; 24(1): 21-28, 2018.
Article in Russian | MEDLINE | ID: mdl-29688191

ABSTRACT

Haemostatic disorders play an important role in the pathogenesis of acute venous thrombosis. One of the least studied reactions of blood coagulation and thrombogenesis is spontaneous contraction of blood clots, which takes place at the expense of the contractility apparatus of activated blood platelets adhered to fibrin fibres. The work was aimed at studying the parameters of contraction of blood clots, formed in vitro, in blood of 41 patients with acute venous thromboses as compared with the same parameters in apparently healthy donors. We used a new instrumental method making it possible to determine the time from initiation to the beginning of contraction, as well as the degree and velocity of clot contraction. It was revealed that in patients with venous thrombosis the ability of clots to shrink was significantly reduced as compared with the control. We detected a statistically significant retardation of and decrease in of blood clot concentration in patients with venous thrombosis complicated by pulmonary artery thromboembolism as compared with contraction in patients with isolated deep vein thrombosis, witch may be important for early diagnosis and determination of the risk of thromboembolism. Besides, we revealed a statistically significant retardation of contraction in patients with proximal thrombosis as compared with contraction in patients with distal thrombosis, with similar values of the degree of contraction. Contraction was statistically significantly reduced in acute thrombosis (less than 21 days), whereas in subacute thrombosis (more than 21 days) the parameters of contraction were closer to normal values. The obtained findings suggest that reduction of blood clot contraction may be a new, hitherto unstudied pathogenetic mechanism deteriorating the course and outcome of venous thrombosis. The clinical significance of contraction and its impairments, as well as the diagnostic and prognostic value of the laboratory test for blood clot contraction would merit further study.


Subject(s)
Platelet Activation/physiology , Pulmonary Embolism , Thrombosis , Venous Thrombosis , Aged , Blood Coagulation Tests/methods , Female , Fibrin Clot Lysis Time/methods , Humans , Male , Middle Aged , Patient Acuity , Predictive Value of Tests , Prognosis , Pulmonary Embolism/diagnosis , Pulmonary Embolism/physiopathology , Thrombosis/diagnosis , Thrombosis/physiopathology , Time Factors , Venous Thrombosis/diagnosis , Venous Thrombosis/physiopathology
3.
Zh Nevrol Psikhiatr Im S S Korsakova ; 116(3 Pt 2): 9-17, 2016.
Article in Russian | MEDLINE | ID: mdl-27296795

ABSTRACT

AIM: To study a possible pathogenetic role of the blood clot contraction and its disturbances in the acute stage of ischemic stroke (IS). MATERIAL AND METHODS: Using a new instrumental technique to study the dynamics of clot contraction in vitro, the authors have determined quantitative parameters of clot contraction (the extent and rate of contraction, duration of the lag-period) in the blood of 85 patients with acute IS. RESULTS AND CONCLUSION: The contractile activity of blood clots was substantially reduced compared to the blood of healthy subjects. Correlations between hemostatic and contractile parameters suggest that the reduced clot contraction in stroke is due to the lower platelet count and impaired platelet functionality, higher levels of fibrinogen and antithrombin III as well as higher hematocrit and hemoglobin contents, leukocytosis, and changes in the biochemical blood composition. The results show that the reduced ability of clots may be a novel pathogenic mechanism that aggravates the course and outcomes of IS.


Subject(s)
Brain Ischemia/physiopathology , Stroke/physiopathology , Thrombosis , Blood Platelets/physiology , Fibrinogen , Hemostasis , Humans
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