scholarly journals Quantitative and qualitative changes in blood cells associated with COVID-19

2021 ◽  
Vol 102 (2) ◽  
pp. 141-155
Author(s):  
N G Evtugina ◽  
S S Sannikova ◽  
A D Peshkova ◽  
S I Safiullina ◽  
I A Andrianova ◽  
...  
Keyword(s):  
Blood Cells ◽  
Heart Diseases ◽  
Blood Clot ◽  
Immunosuppressive Drugs ◽  
Coronary Heart Diseases ◽  
Hematological Disorders ◽  
Cell Counts ◽  
Blood Clots ◽  
Clot Contraction ◽  
Qualitative Changes

Aim. To establish the relationship of hematological disorders with the pathogenesis, course and outcomes of COVID-19. Methods. We examined 235 hospitalized patients with moderate and severe forms of acute COVID-19 receiving anticoagulants and immunosuppressive drugs. We studied the full blood cell counts and morphology along with the platelet function by flow cytometry in comparison with the clinical features and synthesis of inflammatory markers. To assess platelet contractility, blood clot contraction (retraction) kinetics was used in combination with scanning electron microscopy of platelets and blood clots. Results. Hemolytic anemia, neutrophilia and lymphopenia were associated with immature erythrocytes and leukocytes, indicating activation of hematopoiesis. Contraction of blood clots in COVID-19 was impaired, especially in severe and lethal cases, as well as in the presence of comorbidities, including myeloproliferative and coronary heart diseases and acute cerebrovascular disease. In male patients, the changes in clot contraction were more pronounced. Suppression of clot contraction correlated directly with anemia and coagulopathy, including a high D-dimer level, which confirms the pathogenetic significance of blood clot contraction in COVID-19. A decrease in platelet contractility was due to moderate thrombocytopenia in combination with chronic platelet activation and secondary platelet dysfunction. The structure and cellular composition of blood clots depended on the extent of contraction; clots with impaired contraction were porous, had a low content of deformed polyhedral erythrocytes (polyhedrocytes) and an even distribution of fibrin. Conclusion. Blood cells undergoing both quantitative and qualitative changes are involved in the pathogenesis of COVID-19; the suppressed platelet-driven contraction of intravital blood clots may be a part of the prothrombotic mechanisms.

scholarly journals Impaired contraction of blood clots precedes and predicts postoperative venous thromboembolism

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Natalia G. Evtugina ◽  
Alina D. Peshkova ◽  
Arseniy A. Pichugin ◽  
John W. Weisel ◽  
Rustem I. Litvinov
Keyword(s):  
Brain Tumors ◽  
Blood Clot ◽  
Surgical Interventions ◽  
Hematologic Tests ◽  
Vein Thrombosis ◽  
Blood Clots ◽  
Postoperative Thrombosis ◽  
Clot Contraction ◽  
Deep Vein ◽  
Contraction Assay

Abstract Deep vein thrombosis (DVT) is a common but unpredictable complication of surgical interventions. To reveal an association between the blood clot contraction (retraction) and the incidence of postoperative venous thrombosis, 78 patients with brain tumors that were operated on were studied, of which 23 (29%) were diagnosed with postoperative DVT. A clot contraction assay, along with other hemostatic and hematologic tests, was performed 1–3 days before the surgery and on the 1st day and 5–7th days after the surgery. On the 1st postoperative day, clot contraction was significantly suppressed in patients who subsequently developed DVT, compared to the patients without DVT. Importantly, this difference was observed at least 5 days before DVT had developed. The weakening of contraction on the 1st postoperative day was more pronounced in the DVT patients with malignant versus benign brain tumors, atherosclerosis, hypertension, as well as in patients receiving steroids before and during the operation. These results indicate that impaired clot contraction in the postoperative period is associated with imminent DVT, suggesting that it is a prothrombotic risk factor and promotional mechanism. The clot contraction assay has a predictive value in assessing the threat of postoperative thrombosis in patients with benign and malignant brain tumors.

Clopidogrel Bisulfate (Plavix)

Top Drugs ◽  
2015 ◽  
Author(s):  
Jie Jack Li
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Coronary Thrombosis ◽  
Blood Clot ◽  
White Blood Cells ◽  
Blood Protein ◽  
Heart Attacks ◽  
Blood Clots ◽  
Hospital Patients ◽  
Blood Transport

Three types of blood cells exist in the human body: red blood cells, white blood cells, and platelets. Red blood cells, 45% of the blood, transport oxygen from the lungs to other body parts. White cells, less than 1% of the blood, defend us against bacterial and viral invasions. Platelets, also less than 1% of the blood (55% of the remaining blood is plasma), are small cell fragments that are involved in helping the blood clot, a process known as blood coagulation. Coagulation takes place when the enzyme thrombin elicits platelets and fibrin, a blood protein. Without platelets, coagulation at the site of an injury does not occur and uncontrolled bleeding ensues. Individuals with no ability to clot have a genetic condition called hemophilia. These individuals must periodically administer a clotting factor to their blood to prevent constant bleeding. Conversely, thrombosis, the formation of blood clots inside blood vessels, can block coronary arteries and constrict vital oxygen supplies, resulting in a heart attack or stroke. Coronary thrombosis is a life-threatening blood clot in the artery. Deep-vein thrombosis (DVT) is commonly associated with long-distance air travel, when passengers are confined to cramped spaces for many hours. In contrast with thrombosis, in which the clot is stationary, embolus is when an object such as a clot migrates from one part of the body through blood circulation and causes blockage. A pulmonary embolism occurs when emboli travel to the lungs. Approximately 90% of heart attacks and 80% of strokes are caused by blood clots, which kill some 200,000 hospital patients in the US each year. Anticoagulants (blood thinners) are the drugs of choice to prevent and treat both thrombosis and embolism. To date, heparin, warfarin, and aspirin have all been widely used as blood thinners to prevent blood clots from forming. Heparin is one of the oldest medicines still in widespread clinical use. Heparin was extracted in 1916 by Jay McLean from dog’s liver in the laboratories of William Howell at the Johns Hopkins University.

Effects of Platelets and Erythrocytes on the Dynamic Size and Mechanical Properties of Blood Clots during Contraction

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4225-4225
Author(s):  
Valerie Tutwiler ◽  
Rustem I. Litvinov ◽  
Tatiana Lebedeva ◽  
Fazoil I. Ataullakhanov ◽  
Douglas B. Cines ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Viscoelastic Properties ◽  
Blood Clot ◽  
Final Size ◽  
Fibrin Network ◽  
Blood Clots ◽  
Platelet Concentration ◽  
Clot Contraction ◽  
Contractile Forces ◽  
Kinetics Of

Abstract Clot contraction is a final step of blood clotting and plays a key role in hemostasis and restoring blood flow past obstructive thrombi. The volume shrinkage of clots is driven by the contractile forces generated by activated platelets and propagated by the platelet-attached viscoelastic fibrin fibers throughout the entire clot. We have recently shown that blood clot contraction results in the formation of compressed. tightly packed, polyhedral erythrocytes (polyhedrocytes) and in the redistribution of platelets and fibrin to the surface of the contracted clot as a result of the complex interplay between platelets, fibrin, and erythrocytes. This study further investigates the role of these major blood cells in the dynamic mechanical (or viscoelastic) properties of the clot and the kinetics of clot contraction. Platelet and erythrocyte levels were varied through the use of partially reconstituted blood. Samples of platelet-containing plasma with or without added erythrocytes were recalcified and activated with thrombin. The viscoelastic properties and the force of contraction of the resultant clot were determined using high precision rheology. The kinetics of contraction was analyzed using a Thromboimager (HemaCore, Moscow, Russia), which allows continuous tracking and quantitative characterization of dynamic clot size by sensing changes in the light scattering of the clot over time. As predicted, the rate and degree of clot contraction depended linearly on the platelet count over a broad range (R2=0.9881). Increased platelet concentration of greater than 500 k/μl resulted in a more than 30% increase (p<0.001) in the percentage of clot contraction at 30 minutes when compared to the lowest platelet concentration (<75 k/μl). There was a significant increase in the rate and a ~15% increase (p<0.001) in the percentage of clot contraction seen in samples with 250-300k/μl, however, and no difference in samples with 125-150k/μl when compared to the lowest platelet concentration. It was observed that increasing the hematocrit level also affected the degree of contraction with a 30% decrease (p<0.001) in the percentage of contraction seen as the erythrocyte level was increased to hematocrit >40% when compared to <10% hematocrit. There was a 10-15% decrease in the percentage of contraction seen at intermediate hematocrit levels (p<0.05). In addition to decreasing the degree of contraction, changing the cellular composition also affected the rate of contraction. Increasing the concentration of either erythrocytes or platelets resulted in a relative increase in the viscous (or plastic) properties when compared to elastic (or stiffness) properties of the clot (p<0.01), showing a complex dependence of the viscoelastic behavior of the contracting clot as a result of the addition of cells. The presence of erythrocytes resulted in a 63% increase (p<0.05) in the contractile forces that were generated by the platelet-fibrin network when compared to platelets alone. We interpret these results as a profound effect of erythrocytes on the course of clot contraction and on the final size and mechanical properties of contracted blood clots. These results reveal that the concentration of cellular components critically affects the ability of the platelet-fibrin network on the outside of the clot to generate forces needed to reduce the clot size and to compact the erythrocytes, resulting in the formation of a stiff, dense hemostatic plug with low permeability. Disclosures Ataullakhanov: HemaCore LLC: Employment, Membership on an entity's Board of Directors or advisory committees.

scholarly journals Reduced Contraction of Blood Clots in Venous Thromboembolism Is a Potential Thrombogenic and Embologenic Mechanism

TH Open ◽  
2018 ◽  
Vol 02 (01) ◽  
pp. e104-e115 ◽  
Author(s):  
Alina Peshkova ◽  
Dmitry Malyasyov ◽  
Roman Bredikhin ◽  
Giang Le Minh ◽  
Izabella Andrianova ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Ex Vivo ◽  
Blood Clot ◽  
Chemical Activation ◽  
Healthy Controls ◽  
Activation Markers ◽  
Fold Reduction ◽  
Blood Clots ◽  
Clot Contraction

AbstractContraction (retraction) of the blood clot is a part of the clotting process driven by activated platelets attached to fibrin that can potentially modulate the obstructiveness and integrity of thrombi. The aim of this work was to reveal the pathogenic importance of contraction of clots and thrombi in venous thromboembolism (VTE). We investigated the kinetics of clot contraction in the blood of 55 patients with VTE. In addition, we studied the ultrastructure of ex vivo venous thrombi as well as the morphology and functionality of isolated platelets. Thrombi from VTE patients contained compressed polyhedral erythrocytes, a marker for clot contraction in vivo. The extent and rate of contraction were reduced by twofold in clots from the blood of VTE patients compared with healthy controls. The contraction of clots from the blood of patients with pulmonary embolism was significantly impaired compared with that of those with isolated venous thrombosis, suggesting that less compacted thrombi are prone to embolization. The reduced ability of clots to contract correlated with continuous platelet activation followed by their partial refractoriness. Morphologically, 75% of platelets from VTE patients were spontaneously activated (with filopodia) compared with only 21% from healthy controls. At the same time, platelets from VTE patients showed a 1.4-fold reduction in activation markers expressed in response to chemical activation when compared with healthy individuals. The results obtained suggest that the impaired contraction of thrombi is an underappreciated pathogenic mechanism in VTE that may regulate the obstructiveness and embologenicity of venous thrombi.

scholarly journals Effects of Hyperhomocysteinemia on the Platelet-Driven Contraction of Blood Clots

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 354
Author(s):  
Rustem I. Litvinov ◽  
Alina D. Peshkova ◽  
Giang Le Minh ◽  
Nail N. Khaertdinov ◽  
Natalia G. Evtugina ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Platelet Activation ◽  
Rat Model ◽  
Binding Capacity ◽  
Blood Clot ◽  
Fibrinogen Binding ◽  
Blood Clots ◽  
Clot Contraction ◽  
Dose Dependent

Hyperhomocysteinemia (HHcy) is associated with thrombosis, but the mechanistic links between them are not understood. We studied effects of homocysteine (Hcy) on clot contraction in vitro and in a rat model of HHcy. Incubation of blood with exogenous Hcy for 1 min enhanced clot contraction, while 15-min incubation led to a dose-dependent suppression of contraction. These effects were likely due to direct Hcy-induced platelet activation followed by exhaustion, as revealed by an increase in fibrinogen-binding capacity and P-selectin expression determined by flow cytometry. In the blood of rats with HHcy, clot contraction was enhanced at moderately elevated Hcy levels (10–50 μM), while at higher Hcy levels (>50 μM), the onset of clot contraction was delayed. HHcy was associated with thrombocytosis combined with a reduced erythrocyte count and hypofibrinogenemia. These data suggest that in HHcy, platelets get activated directly and indirectly, leading to enhanced clot contraction that is facilitated by the reduced content and resilience of fibrin and erythrocytes in the clot. The excessive platelet activation can lead to exhaustion and impaired contractility, which makes clots larger and more obstructive. In conclusion, HHcy modulates blood clot contraction, which may comprise an underappreciated pro- or antithrombotic mechanism.

Blood Thinners: From Heparin to Plavix

2014 ◽  
Author(s):  
Jie Jack Li
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Blood Clot ◽  
White Blood Cells ◽  
Clotting Factor ◽  
Blood Protein ◽  
Body Parts ◽  
Heart Attacks ◽  
Blood Clots ◽  
Clot Blood

Three types of blood cells exist in the human body: red blood cells, white blood cells, and platelets, in addition to plasma, which takes up 55 percent of the blood’s volume. Red blood cells take up approximately 45 percent of the blood’s volume. They transport oxygen from the lungs to other body parts. White cells defend us against bacterial and viral invasions. Platelets (less than 1 percent of the blood), the third type of blood cells, are sticky little cell fragments that are involved in helping the blood clot, a process known as coagulation. Without platelets (even though they constitute less than 1 percent of blood), our blood would not be able to clot, and we would have uncontrolled bleeding. However, formation of blood clots is a double-edged sword. Clots are beneficial because they heal cuts and wounds; blood clots in the bloodstream are harmful because they block coronary arteries, constrict vital oxygen supplies, and cause heart attacks and strokes, more and more frequent modern maladies as the baby boomers get older. Whenever the body is cut or injured and blood comes into contact with cells outside the bloodstream, a tissue factor on these cells encounters a particular protein within the blood, which triggers the clotting process. In the same vein, a series of other blood factors then come into action and amplify one another to quickly form a jelly-like blood clot. Blood clots form when an enzyme called thrombin marshals fibrin (a blood protein) and platelets (tiny cells that circulate in the blood) to coagulate at the site of an injury. Individuals with no ability to clot have a genetic condition called hemophilia; such people are also known as “bleeders.” Queen Victoria was hemophilic, and she passed on her genes to her many heirs who ruled Europe for over a century. This is why hemophilia is sometimes known as the royal disease. Symptoms of hemophilia manifest only in male offspring. People with hemophilia must periodically administer a clotting factor to their blood to prevent constant bleeding.

Erythrocyte Rigidity Affects Blood Clot Contraction and Formation of Polyhedrocytes

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 3814-3814
Author(s):  
Valerie Tutwiler ◽  
Rustem I. Litvinov ◽  
Chandrasekaran Nagaswami ◽  
J. Eric Russell ◽  
Don L. Siegel ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Healthy Subjects ◽  
Blood Clot ◽  
Human Erythrocytes ◽  
Osmotic Resistance ◽  
Centrifugal Forces ◽  
Deformability Of Erythrocytes ◽  
Blood Clots ◽  
Clot Contraction ◽  
Erythrocyte Rigidity

Abstract Blood clot contraction or retraction has been implicated to play a significant role in hemostasis, reduction of thrombus volume, and wound healing. Clot contraction is driven by forces that are generated by platelets and transmitted by fibrin and results in volume shrinkage followed by the compaction of erythrocytes into the core of the blood clot, resulting in their mechanical deformation towards a polyhedral shape, giving rise to the term polyhedrocytes. Despite the fact that erythrocytes are a major component of blood clots, relatively little is known about the influence of the mechanical properties or deformability of erythrocytes on the process of clot contraction. Increased hematocrit reduces extent of clot contraction due to mechanical resilience of erythrocytes and it is likely that in addition to a volume fraction the stiffness of erythrocytes can also affect the extent and rate of clot contraction. Here we tested this assumption by using artificially or naturally stiffened erythrocytes that have pathophysiological implications. The reduced deformability of erythrocytes is associated with a number of pathological conditions, such as hypertension, diabetes mellitus, atherosclerosis and smoking, but perhaps one of the most well-known diseases associated with increased erythrocyte rigidity is sickle cell disease (SCD). Another example of naturally stiff erythrocyte membrane is that of llama or camel that have red blood cells with increased osmotic resistance. To assess the extent of clot contraction, we used an optical tracking methodology that allows for the quantitative tracking for clot size. To assess the influence of erythrocyte rigidity on clot contraction we also used scanning electron microscopy to evaluate deformations of the erythrocytes, including the presence of polyhedrocytes. Centrifugation of citrated blood can be used to mimic the contractile forces generated by platelets and has been shown to cause polyhedrocyte formation. Increasing the erythrocyte rigidity through their treatment with a low concentration of glutaraldehyde resulted in a decrease in polyhedrocyte formation and the requirement of larger centrifugal forces to observe erythrocyte deformation, suggesting that the mechanical properties of erythrocytes could influence the process of clot contraction. As residual glutaraldehyde may have unwanted effects on platelets, clot contraction experiments were completed using naturally stiffer erythrocytes from SCD patients and llama ovalocytes, which are stiffer than human erythrocytes due to the increased amount of the membrane cytoskeletal protein spectrin. SCD patients were only included in this study if they had Sickle Trait, SCD Hb SS, SCD Hb SC and have not received recent transfusions. The blood samples of SCD patients were examined and on average had a 53% decrease (p<0.0001) in the extent of clot contraction compared to healthy subjects. Likewise, addition of llama ovalocytes to human platelet rich plasma resulted in a 28% decrease in extent of clot contraction compared to human erythrocytes and larger centrifugal forces were needed to see red cell deformation. SCD patients contracted 2.4X slower (p<0.001) during linear contraction (Phase 2) and 2.7X slower (p<0.05) during mechanical stabilization (Phase 3) when compared to healthy subjects. Clot contraction was impaired also by erythrocytes treated with antibodies that bind to the Wright b epitope on the erythrocytes and exert a rigidifying effect on the cells. The binding of the antibody to erythrocytes was determined by flow cytometry and the KD was ~50 nM. Increased red blood cell rigidity following exposure to antibodies was confirmed through mechanical and osmotic resistance and compared to unaltered erythrocytes. Collectively, these results demonstrate that erythrocyte mechanical properties can influence the process of clot contraction so that stiffer cells reduce the rate and extent of clot contraction. A better understanding of the role of erythrocyte deformability in the process of clot contraction has the potential to inform the development of more targeted treatments for limiting bleeding and thrombosis in patients who are prone to having altered erythrocyte content and mechanical properties of these highly abundant cells embedded into blood clots and thrombi. Disclosures Weisel: Bayer: Research Funding.

scholarly journals Prevalence of Coronary Heart Diseases Risk Factors among Healthcare Male Students in KSAU-HS Riyadh, Saudi Arabia

2021 ◽  
pp. 237-243
Author(s):  
Awadelkarim Abdulla Elneama ◽  
Aamir Omair ◽  
Abdullah Abdulhadi Alharbi ◽  
Alhommedi Shaker Alhabbad ◽  
Raed Awadh Alshehri ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Fast Food ◽  
Heart Diseases ◽  
Blood Clot ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Coronary Heart Diseases ◽  
Physical Measurements

Background: Coronary heart disease (CHD) is a condition in which plaque builds up on the inner walls of coronary arteries and can lead to blood clot formation. It is the leading cause of death worldwide. Developing coronary heart disease takes long period and its risk factors can be found in young people. Objectives: Study of risk factors that contribute to the pathogenesis of coronary artery disease. Methods: A cross-sectional study was done at King Saud bin Abdul-Aziz University in Riyadh. Non-probability convenience sampling was used to select 151 health care students. The data was collected through questionnaire and physical measurements. The data was entered and analyzed by SPSS. Results: More than half of the students eat fruits one or less time per week which accounts for 53.6%. Moreover, 28.5% of them eat vegetables one time or less per week. Regarding healthy food containing healthy fat such as fish, 76.2% of the students include healthy fat food in their diet more than two times per week. The percentage of those who eat fast food and consume soft drinks is 80.8% and 70.2% more than two times per week respectively. Furthermore, the percentage of the students who are smokers, either currently or occasionally is 49%. Concerning physical activity, 31.3% of the students exercise more than two times weekly, and only 7.3% of the students watch TV more than four hours per day. On the other hand, the majority which accounts for 54.3% of the students use computer, laptop, or tablet more than four hours per day. Regarding premature CAD, 3.3% of the students reported positive and 16.2% of them reported positive for CHD family history. Finally, 1.3% of the found to have DM.

scholarly journals Accelerated Spatial Fibrin Growth and Impaired Contraction of Blood Clots in Patients with Rheumatoid Arthritis

2020 ◽  
Vol 21 (24) ◽  
pp. 9434
Author(s):  
Alina D. Peshkova ◽  
Tatiana A. Evdokimova ◽  
Timur B. Sibgatullin ◽  
Fazoil I. Ataullakhanov ◽  
Rustem I. Litvinov ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Binding Capacity ◽  
Blood Clot ◽  
Clinical Manifestations ◽  
Fibrin Clot ◽  
Control Group ◽  
Plasma Clot ◽  
Blood Clots ◽  
Clot Contraction ◽  
Hemostatic Disorders

Rheumatoid arthritis (RA) is an autoimmune disease associated with thrombotic complications. To elucidate pathogenic mechanisms, hemostatic disorders in RA were correlated with other laboratory and clinical manifestations. Hemostasis was assessed using relatively new complementary tests, the spatial growth of a plasma clot (Thrombodynamics assay), and contraction of whole blood clots. Platelet functionality was assessed with flow cytometry that quantified the expression of P-selectin and the fibrinogen-binding capacity of platelets before and after activation with a thrombin receptor-activating peptide. Parameters of fibrin clot growth and the kinetics of contraction of blood clots were significantly altered in patients with RA compared to the control group. In Thrombodynamics measurements, an increase in the clot growth rate, size, and optical density of plasma clots altogether indicated chronic hypercoagulability. The rate and extent of blood clot contraction in patients with RA was significantly reduced and associated with platelet dysfunction revealed by an impaired response to activation. Changes in the parameters of clot growth and contraction correlated with the laboratory signs of systemic inflammation, including hyperfibrinogenemia. These results confirm the pathogenic role of hemostatic disorders in RA and support the validity of fibrin clot growth and the blood clot contraction assay as indicators of a (pro)thrombotic state.

scholarly journals Altered platelet and coagulation function in moderate-to-severe COVID-19

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rustem I. Litvinov ◽  
Natalia G. Evtugina ◽  
Alina D. Peshkova ◽  
Svetlana I. Safiullina ◽  
Izabella A. Andrianova ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Blood Clot ◽  
Immunosuppressive Drugs ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Blood Clots ◽  
Thrombotic Complications ◽  
Hemostatic Disorders ◽  
Kinetics Of

AbstractTo reveal if coagulopathies relate to the course of COVID-19, we examined 255 patients with moderate and severe COVID-19, receiving anticoagulants and immunosuppressive drugs. Coagulopathy manifested predominantly as hypercoagulability that correlated directly with systemic inflammation, disease severity, comorbidities, and mortality risk. The prolonged clotting tests in about ¼ of cases were associated with high levels of C-reactive protein and antiphospholipid antibodies, which impeded coagulation in vitro. Contraction of blood clots was hindered in about ½ of patients, especially in severe and fatal cases, and correlated directly with prothrombotic parameters. A decrease in platelet contractility was due to moderate thrombocytopenia in combination with platelet dysfunction. Clots with impaired contraction were porous, had a low content of compressed polyhedral erythrocytes (polyhedrocytes) and an even distribution of fibrin, suggesting that the uncompacted intravital clots are more obstructive but patients could also be prone to bleeding. The absence of consumption coagulopathy suggests the predominance of local and/or regional microthrombosis rather than disseminated intravascular coagulation. The results obtained (i) confirm the importance of hemostatic disorders in COVID-19 and their relation to systemic inflammation; (ii) justify monitoring of hemostasis, including the kinetics of blood clot contraction; (iii) substantiate the active prophylaxis of thrombotic complications in COVID-19.

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