Risk Of Developing Thrombosis Research Articles

Odds and associated factors for thrombosis development among Lebanese COVID-19 patients: a case-control retrospective study.

Thromboembolism is reported to be up to 27% in COVID-19 patients due to SARS-CoV-2 infection. Dysregulated systemic inflammation and various patient traits play a vital role in thrombosis progression. To assess odds and associated factors for thrombosis development among Lebanese COVID-19 patients. This was a case-control retrospective study conducted in January-May 2021. Patients infected with COVID-19 and developed thrombosis were classified as cases and patients who were thrombosis-free identified as control. A questionnaire assessed socio-demographics, clinical parameters, and WHO COVID-19 disease severity. Among 267 patients, 26 (9.7%) developed thrombosis and the majority of thrombosis 34.6% was myocardial infarction, and the least (3.8%) was for catheter-related thrombosis. Results showed that the risk of thrombosis development is higher in patients with previous thromboembolic event (OR = 9.160) and previous intake of anti-hypertensive medications at home (OR = 3.116). However, females (OR = 0.330; CI: 0.118-0.925), intake of anticoagulants during hospital admission (OR = 0.126; CI: 0.053-0.300) and non-severe COVID-19 were at lower thrombosis risk (OR = 0.273). Patients who developed thromboembolic events had longer hospital stay (OR = 0.077). Patients with COVID-19 and thromboembolism were at higher risk of mortality as compared to patients with COVID-19 but without thromboembolism. The use of anticoagulants significantly reduced the risk for thromboembolism.

312.6: Model for Virtual Vascular Reconstruction in Liver Transplantation Using Computational Fluid Dynamics

Introduction: Computational anatomy is a modern research method that has become available using computer technology and computational fluid dynamics. It is promising to use it for perioperative planning and modeling, including organ transplantation. Aim of study is to prepare investigational model of blood flow in liver during liver transplantation. Matherials and methods: Contrast research was done among 53 men who were patients in surgery departments at Krasnoyarsk regional hospital #1, Russia (KRH). Estimations were made using 3D models of portal system (working stations GE Advantage Workstation, Siemens singo.via), based on multi-slices computed tomography of abdominal cavity with bolus contrasting with help of medication “Ultravist-370”. The volume of the used contrasting stuff made 100 ml, the speed of infiltration was 4 ml per second, and the average radial strain was 11,3 m3v. DICOM data segmentation was performed using Dragonfly software (Object Research Systems, Canada) at the Innovation Technology Management Resources of the Reaviz University. Using series with arterial and vein contrast, we performed the segmentation of contrasting vessels, and obtained three-dimensional data topology in.obj format. Then we processed the obtained models using scripts prepared for the pythonOCC framework. We built the central lines of the vessels and formed the branching tree. Methods of computational hemodynamics were implemented using the Visual-CFD application for OpenFOAM environment (ESI, France). Mesh example of portal vein shown in figure 1.Results: With the use of created three-dimensional computer model, the blood flow in the portal vein and liver arteries at various variants of its structure was simulated. It was obtained that, in the presence of the main type of structure with predominance of blood flow along the splenic vein, the blood flow turbulence and risk of thrombosis development are higher. At the same time, with virtual thrombosis of the portal vein trunk, the pressure gradient is 1.4 times higher than with the bulk type, which is more favorable for the proposed reconstruction. Thus, these data can be used for preoperative planning in surgical treatment of portal vein thrombosis in liver transplantation. Conclusion: The proposed model of blood flow is promising and allows you to create an interactive tool for calculating the hemodynamic situation in various reconstructions during liver transplantation.

Atypical antipsychotic clozapine binds fibrinogen and affects fibrin formation

Clozapine is an atypical antipsychotic used for the treatment of schizophrenia. The prescribed target daily doses may reach 900 mg. Literature studies report a connection between clozapine usage and thrombosis development. Our in vitro study aimed to provide insight into molecular bases of this observation, investigating clozapine binding to fibrinogen, the main plasma protein involved in hemostasis. Fibrinogen/clozapine interaction was confirmed by protein fluorescence quenching, with an affinity constant of 1.7 × 105 M−1. Direct interactions did not affect the structure of fibrinogen, nor fibrinogen melting temperature. Clozapine binding affected fibrin formation by reducing coagulation speed and thickness of fibrin fibers suggesting that in the presence of clozapine, fibrinogen may acquire thrombogenic characteristics. Although no difference in fibrin gel porosity was detected, other factors present in the blood may act synergistically with altered fibrin formation to modify fibrin clot, thus increasing the risk for development of thrombosis in patients on clozapine treatment. ORAC and HORAC assays showed that clozapine reduced free radical-induced oxidation of fibrinogen. All observed effects of clozapine on fibrinogen are dose-dependent, with the effect on fibrin formation being more pronounced.

The Effect of Complex Treatment on Platelet Aggregation Activity in Patients with Grade 3 Arterial Hypertension with Metabolic Syndrome

The combination of arterial hypertension and metabolic syndrome causes a whole complex of disorders in the patients' body, contributing to the risk of developing thrombosis in them. In this regard, it is very important to develop a comprehensive therapy for this patient population, which positively influences the activity of platelets, which is an important factor in the formation of thrombophilia in them. The aim of the work is to establish the intensity of the dynamics of platelet aggregation ability and the state of functional capabilities, the individual mechanisms of their determining in patients with arterial hypertension of the third degree in the metabolic syndrome. 24 patients with arterial hypertension of the 3rd degree, risk 4, including 10 men and 14 women of mature age, were under observation. The control group consisted of 25 clinically healthy people of similar age. The surplus platelet activity observed in the in vitro and in vivo patients is based on an increase in the adhesive and aggregation activity of platelets with a weakening of their ability to disaggregate, largely due to an imbalance in their blood pressure and anti-aggregational compounds. The complex therapy, including amlodipine, valsartan, pioglitazone, hypocaloric diet and dose physical exercise, provided patients with arterial hypertension 3 degrees with metabolic syndrome after 4 months. Stable normalization of initially high platelet activity, significantly reducing their risk of developing thrombosis, despite the non-strict compliance with the non-drug component of treatment after 16 weeks of treatment.

Elevated coagulation FIX and risk of thrombosis development

Elevated coagulation FIX and risk of thrombosis development

Elevated Coagulation Factor IX and Risk of Thrombosis Development

Coagulation involves the regulated sequence of proteolytic activation of a series of zymogens to achieve an appropriate and timely hemostasis in an injured vessel in an environment that favors an anticoagulant state. Alteration of hemostatic balance between the prothrombotic and antithrombotic factors can result in insufficient inhibition of coagulation ‘thrombosis’ or bleeding due to excessive antithrombotic treatment. Fibrin is the key component of thrombi and anticoagulant drugs that reduce thrombin formation are effective in both prevention and treatment of thrombosis. Therefore, an increased circulating level of coagulation factor is a must for treatment mechanisms of both venous and arterial thrombosis. The existing anticoagulants may have only limited effects due to their modest therapeutic benefits, increased bleeding risks, narrow clinical applications, and drug-induced thrombophilia. However, some new oral anticoagulants, when administered optimally, are associated with significant anti-ischemic benefits and lower bleeding risk when compared with heparin and vitamin K antagonists. Since factor IX (FIX) plays a key role in tissue factor-mediated thrombin production, it may represent a promising target for drug development. This review aims to summarize the current data for FIX and its role in the development of thrombosis (although thrombosis is a platelet-centric process and FIX may not have any direct and specific effect on platelets).

POLİSİTEMİA VERA: PATOGENEZ, TEŞHİS VE TEDAVİDE GÜNCEL BİLGİLER

Polycythemia vera (PV) is a myeloproliferative neoplasm characterized by increased red blood cell mass and usually overproduction of granulocytes and platelets and increased spleen size. JAK2V617F mutation is present in more than 95% of PV patients. Bone marrow examination reveals excessive proliferation of erythroid, myeloid, and megakaryocytic elements. The prognosis of PV depends on the severity of the complications occurring during the clinical course. Thrombotic complications are the main cause of morbidity and mortality in PV. Survival is affected whether appropriate therapy is applied during the erythrocytotic phase of the disease. Uncontrolled erythrocytosis poses very high risk for development of thrombosis. Some studies suggest that PV patients have a normal or near-normal lifeexpectancy. Most studies, however, report excess mortality caused by thrombotic complications and acute leukemia transformation during course of PV. This review aims to highlight the pathogenesis, diagnosis and current management in PV

EComment. Is the maintenance of haemostasis possible without fibrinogen?

Although fibrinogen is a key factor in thrombosis, its role in the pathogenesis of haemostatic disturbances after cardiac surgery is often underestimated. Therefore we were glad to read the article by Gielen et al. [1]. Apparently during the postoperative period, decrease in fibrinogen often coincides with the deficiency of other clotting factors and platelet dysfunction, and the level of postoperative blood loss does not depend only on the fibrinogen concentration. Thus, there are no linear connections between blood loss and the level of fibrinogen. However, we cannot underestimate the contribution of this clotting factor in the mechanical stability of clots, which also depends on platelets, coagulation factor XIII and von Willebrand factor. The deficiency of those factors, primarily fibrinogen, leads to the decrease in the fibrin monomer and its polymerization, which further results in delayed thrombus formation along with increase of fibrinolysis sensitivity and blood loss. Based on thromboelastography data, a feedback loop exists between the fibrinogen level and maximum lysis [2]. Therefore, the fibrinogen level serves as an integral value of the formation and stabilization of the clot. It is necessary to note that the velocity of fibrin formation may be affected by the absolute quantity of fibrinogen and its concentration, therefore hypofibrinogenaemia may be the result either of fibrinogen loss or haemodilution. The main target of haemodilution is the formation and stability of the clot, but not the thrombin formation [3]. We tested the connection between pre- and postoperative coagulation values and the level of blood loss after cardiac surgical procedures in children. For patients with congenital heart disease, we consider a threshold fibrinogen concentration of 2.5 g/l to be necessary for prevention of bleeding. In cases with lower concentrations of fibrinogen, we observed postoperative blood losses of 0.75 ml/kg/h to 1.27 ml/kg/h [4]. Hypofibrinogenaemia in children may be caused by hypotrophy due to social (early artificial feeding) and medical factors, impaired hepatic protein synthesis, and a decrease in terminal elimination half-life in cyanotic patients. A postoperative level of fibrinogen less than 2 g/l led to blood loss of 0.61 to 0.85 ml/kg/h [2]. Indeed, there is insufficient evidence to prove that the use of fibrinogen concentrate after cardiac surgery is successful. However, a controlled replacement therapy of blood loss via the use of fibrinogen concentrate in hypofibrinogenaemia is efficient and abolishes the deficiency of other haemostasis components without the risk of thrombosis development. On the other hand, based on stoichiometry, a possible way to circumvent a low level of fibrinogen concentration may be the optimization of the circulating blood volume via the application of ultrafiltration. Conflict of interest: none declared

Risk Factors for Venous Thromboses Development in Knee Joint Arthroplasty

Retrospective analysis of case histories of 125 patients (36-77 years) after total knee arthroplasty for III-IV stage of gonarthrosis was performed. On 4-5 day after operation deep vein thrombosis was diagnosed in 30 (23.6%) patients. It was stated that additional factors which trustworthily influenced the risk factors of thromboembolic complications development were the following: application of tourniquet to the femur for more than 1 hour; application of tourniquet to the patients with initial venous pathology (varicosis of vena saphena magna and vena saphena parva, consequences of thrombophlebitis); obesity of II-III degree in women. No reliable influence of various methods of anesthesia and infusion therapy upon the risk of thrombosis development was detected. Obtained data confirm the necessity to perform compulsory examination of lower extremities veins in patients prior to knee joint arthroplasty and take additional measures on thrombosis prevention in high risk groups. Observance of the proposed antithrombotic protocol in the postoperative period prevents vein thrombosis progression, thrombus fragmentation and floating as well as promotes accelerated recanalization of thrombotic veins.

Venous thromboembolism and oral contraception

Because of their safety and efficacy oral contraceptives are available without prescription in many countries. Monophasic combined oral contraceptives are a combination of estrogen and progestin taken in constant amounts. Combined oral contraceptives slightly increase the risk of venous thromboemolism, but this event is very rare among non-pregnant women of reproductive age. The absolute risk rises with age, obesity, recent surgery and certain forms of thrombophilia. The estrogen component of combined oral contraceptives increases the synthesis of several coagulation factors in a dose-dependent manner. Changes of most of these parameters are very small and there is no evidence that they have any effect upon the clinical risk of developing venous thrombosis. If a woman has an inherited coagulation disorder that increases her risk of developing thrombosis, the risk is increased several fold if she ingests estrogen containing oral contraception. The increased risk of venous thromboembolism associated with combined oral contraceptives should have little impact on healthy women, but may have substantial impact on women with a history of thromboembolism. Combined oral contraceptive use increases the risk of venous thromboembolosm in a dose-dependent manner. The absolute risk of venous thromboembolism rises with age, obesity, recent surgery and certain forms of thrombophilia, as well.

Clinical features of thrombophilia in families with gene defects in protein C or protein S combined with factor V Leiden.

Twenty-nine clinically well-characterized, symptomatic index patients, 15 with protein C and 14 with protein S deficiency, in whom the genetic defect had been identified, were investigated for the presence of factor V Leiden. In six of 15 (40%) propositi with protein C and four of 14 (29%) with protein S deficiency, factor V Leiden was present. The age at first thrombosis was significantly lower (P < 0.001) in the ten propositi with a combined genetic defect (mean age 18.4 +/- 6.6 years) than in those with a single defect (mean age 32.6 +/- 10.4 years). Spontaneous occurrence, recurrence and site of thrombosis were similar in propositi with the single and the combined defect. Family studies led to the identification of a combined defect in 18 individuals from 11 families (11 propositi and 29 relatives), seven subjects had no abnormality, and in 15 a single defect was found. In individuals with a combined defect, thrombosis-free survival time was significantly shorter than in individuals with a single defect, even after exclusion of index patients. None of the seven individuals without genetic abnormality had experienced thrombosis. Our findings indicate a higher risk for development of thrombosis in individuals with a combined defect compared with those with a single defect.