scholarly journals The Prothrombotic Predominance in Metabolic Syndrome: A Complex Pathomechanism

2021 ◽  
Vol 2 (4) ◽  
pp. 4-9
Author(s):  
Fahmy Rusnanta ◽  
Mohammad Saifur Rohman
Keyword(s):  
Metabolic Syndrome ◽  
Platelet Activation ◽  
Fibrinolytic Activity ◽  
Preventive Measures ◽  
Blood Clot ◽  
Coagulation Factors ◽  
Cardiovascular Complications ◽  
Clot Formation ◽  
Premature Atherosclerosis ◽  
Clot Structure

Patients with metabolic syndrome (MS) have many cardiovascular complications related to atherothrombotic complications. MS contributes premature atherosclerosis, increases platelet activation, promotes coagulation factors, and reduces fibrinolytic activity. The last step in the atherothrombotic cascade is blood clot formation, and altered clot structure is a key role to determine cardiovascular complications. The MS, caused in part by an excess of atherosclerosis and in part by fibrinolytic dysfunction, is profoundly related to an excess of CVD. These combinations of factors involved in MS parameters contribute the increased propensity of people with MS to develop atherothrombosis and fibrinolysis. Awareness and preventive measures are important to improve outcomes in patients with MS.

scholarly journals Role of Endothelial Cells in Acute and Chronic Thrombosis

2019 ◽  
Vol 39 (02) ◽  
pp. 128-139 ◽  
Author(s):  
Magdalena L. Bochenek ◽  
Katrin Schäfer
Keyword(s):  
Endothelial Cells ◽  
Platelet Activation ◽  
Thrombus Formation ◽  
Blood Clot ◽  
Vascular Occlusion ◽  
Coagulation Factors ◽  
Activated Platelets ◽  
Endothelial Cell Response ◽  
Von Willebrand

AbstractHaemostasis encompasses a set of strictly regulated actions, such as vasoconstriction, platelet activation and blood coagulation. Endothelial cells play a crucial role in all of these processes and are an integral part of the vascular response to injury resulting in thrombus formation. Healthy endothelium expresses mediators to prevent platelet activation, including prostacyclin and nitric oxide, and to inhibit coagulation, such as thrombomodulin or RNase1. Upon activation, endothelial cells expose von Willebrand factor, integrins and other receptors to interact with activated platelets, erythrocytes and coagulation factors, respectively, resulting in blood clot formation. The endothelial cell response to cytokines and growth factors released from activated platelets and immune cells abundantly present in arterial and venous thrombi also plays an important role for thrombus resolution, whereas failure to completely resolve thrombi may initiate fibrotic remodelling and chronic vascular occlusion both in the arterial and venous tree. Therefore, endothelial cells are increasingly recognized as potential target to prevent thrombotic events and to accelerate thrombus resolution. Here, we discuss recent publications from our group in the context of other studies on the role of the endothelium during acute and chronic thrombotic events.

Changes with age in Fibrinolytic Activity, Coagulation Factors and Lipids in an Industrial Population

1975 ◽  
Author(s):  
R. Chakrabarti ◽  
M. Brozovic ◽  
T. W. Meade ◽  
W. R. S. North ◽  
Y. Stirling
Keyword(s):  
Fibrinolytic Activity ◽  
Blood Clot ◽  
Coagulation Factors ◽  
Blood Cholesterol ◽  
Factor Vii ◽  
Clot Lysis ◽  
Factor V ◽  
Cholesterol Levels ◽  
Lysis Time ◽  
Similar Factor

Fibrinolytic activity, coagulation factors I, V, VII and VIII, blood cholesterol and triglyceride levels have been measured in a randomyl selected group of 650 men aged 17–64 and 350 women aged 17–59 working in an industrial population. Fibrinolytic activity (the reciprocal of the dilute blood clot lysis time in hours) decreases significantly (0.003 per annum) with advancing age in men; there is no significant change in women. Factors I and V increase significantly with age in both men and women at about the same rate (1.0% per annum for factor I and 0.6% for factor V), their mean levels in each group being very similar. Factor VIII also increases significantly with age in both sexes up to the age of about 50 years, after which levels continue to rise in men, but fall in women. Factor VII and blood cholesterol levels are lower in young women than in young men; they rise in both sexes, but significantly faster in women than in men (1.1% and 0.4%, respectively for factor VII, for example), so that in older women they are substantially higher than in older men. Triglyceride levels rise with age in both sexes, levels in men being hig er than those in women.

Malignant Hematologic Disorders

2016 ◽  
pp. 427-438
Author(s):  
Carrie A. Thompson
Keyword(s):  
Platelet Activation ◽  
Vascular Injury ◽  
Coagulation Factors ◽  
Fibrin Clot ◽  
Clot Formation ◽  
Coagulation System ◽  
Hematologic Disorders ◽  
Blood Clots ◽  
Anticoagulant System ◽  
Plug Formation

The 2 essential functions of the coagulation system (maintaining hemostasis and preventing and limiting thrombosis) are served by the procoagulant and anticoagulant components. Vascular injury results in activation of the phases of hemostasis, including vasospasm, platelet plug formation (platelet activation, adhesion, and aggregation), and fibrin clot formation (by activation of coagulation factors in the procoagulant system). The anticoagulant system controls excessive clot formation, while the fibrinolytic system breaks down and remodels blood clots.

Effect of Tranexamic Acid on Coagulation and Fibrin Clot Properties in Children Undergoing Craniofacial Surgery

2020 ◽  
Vol 120 (03) ◽  
pp. 392-399 ◽  
Author(s):  
Christian Fenger-Eriksen ◽  
Alexander D'Amore Lindholm ◽  
Lisbeth Krogh ◽  
Tobias Hell ◽  
Martin Berger ◽  
...  
Keyword(s):  
Data Analysis ◽  
Blood Loss ◽  
Tranexamic Acid ◽  
Thrombin Generation ◽  
Blood Clot ◽  
Fibrin Clot ◽  
Clot Formation ◽  
Clot Lysis ◽  
Clot Strength ◽  
Clot Structure

Abstract Objective Craniosynostosis surgery in small children is very often associated with a high blood loss. Tranexamic acid (TXA) reduces blood loss during this procedure, although the potential underlying coagulopathy in these children is not known in detail. Objective was to determine the nature of any coagulopathy found during and after craniosynostosis surgery and to characterize the effect of TXA on fibrin clot formation, clot strength, and fibrinolysis. Materials and Methods Thirty children received either TXA (bolus dose of 10 mg/kg followed by 8 hours continuous infusion of 3 mg/kg/h) or placebo. Dynamic whole blood clot formation assessed by thromboelastometry, platelet count, dynamic thrombin generation/thrombin-antithrombin, clot lysis assay, and fibrinogen/factor XIII (FXIII) levels were measured. Additionally, clot structure was investigated by real-time live confocal microscopy and topical data analysis. Results Increased ability of thrombin generation was observed together with a tendency toward shortened activated partial thromboplastin time and clotting time. Postoperative maximum clot firmness was higher among children receiving TXA. FXIII decreased significantly during surgery in both groups.Resistance toward tissue plasminogen activator-induced fibrinolysis was higher in children that received TXA, as evidenced by topical data analysis and by a significant longer lysis time. Fibrinogen levels were higher in the TXA group at 24 hours. Conclusion A significant coagulopathy mainly characterized by changes in clot stability and not parameters of thrombin generation was reported. Tranexamic acid improved clot strength and reduced fibrinolysis, thereby avoiding reduction in fibrinogen levels.

Influence of sulfated polysaccharides from Ulva lactuca L. upon Xa and IIa coagulation factors and on venous blood clot formation

2020 ◽  
Vol 45 ◽  
pp. 101750 ◽  
Author(s):  
Samara E. Reis ◽  
Rogeria Gabriela C. Andrade ◽  
Camila M. Accardo ◽  
Lenize F. Maia ◽  
Luiz F.C. Oliveira ◽  
...  
Keyword(s):  
Blood Clot ◽  
Venous Blood ◽  
Coagulation Factors ◽  
Ulva Lactuca ◽  
Clot Formation ◽  
Sulfated Polysaccharides

scholarly journals Factors Affecting the Formation and Treatment of Thrombosis by Natural and Synthetic Compounds

2020 ◽  
Vol 21 (21) ◽  
pp. 7975
Author(s):  
Anna Lichota ◽  
Eligia M. Szewczyk ◽  
Krzysztof Gwozdzinski
Keyword(s):  
Cell Activation ◽  
Blood Clot ◽  
White Blood Cells ◽  
Coagulation Factors ◽  
The Body ◽  
Clot Formation ◽  
Factors Affecting ◽  
Vein Thrombosis ◽  
Deep Vein ◽  
The Impact

Venous thromboembolism (VTE) refers to deep vein thrombosis (DVT), whose consequence may be a pulmonary embolism (PE). Thrombosis is associated with significant morbidity and mortality and is the third most common cardiovascular disease after myocardial infarction and stroke. DVT is associated with the formation of a blood clot in a deep vein in the body. Thrombosis promotes slowed blood flow, hypoxia, cell activation, and the associated release of many active substances involved in blood clot formation. All thrombi which adhere to endothelium consist of fibrin, platelets, and trapped red and white blood cells. In this review, we summarise the impact of various factors affecting haemostatic disorders leading to blood clot formation. The paper discusses the causes of thrombosis, the mechanism of blood clot formation, and factors such as hypoxia, the involvement of endothelial cells (ECs), and the activation of platelets and neutrophils along with the effects of bacteria and reactive oxygen species (ROS). Mechanisms related to the action of anticoagulants affecting coagulation factors including antiplatelet drugs have also been discussed. However, many aspects related to the pathogenesis of thrombosis still need to be clarified. A review of the drugs used to treat and prevent thrombosis and natural anticoagulants that occur in the plant world and are traditionally used in Far Eastern medicine has also been carried out.

Laboratory hemostasis: from biology to the bench

2018 ◽  
Vol 56 (7) ◽  
pp. 1035-1045 ◽  
Author(s):  
Giuseppe Lippi ◽  
Emmanuel J. Favaloro
Keyword(s):  
Blood Vessels ◽  
Blood Clot ◽  
Clinical Signs ◽  
Clinical Information ◽  
Signs And Symptoms ◽  
Coagulation Factors ◽  
Clot Formation ◽  
Screening Tests ◽  
Coagulation Cascade ◽  
Excessive Bleeding

AbstractPhysiological hemostasis is an intricate biological system, where procoagulant and anticoagulant forces interplay and preserves blood fluidity when blood vessels are intact, or trigger clot formation to prevent excessive bleeding when blood vessels are injured. The modern model of hemostasis is divided into two principal phases. The first, defined as primary hemostasis, involves the platelet-vessel interplay, whilst the second, defined as secondary hemostasis, mainly involves coagulation factors, damaged cells and platelet surfaces, where the so-called coagulation cascade rapidly develops. The activation and amplification of the coagulation cascade is finely modulated by the activity of several physiological inhibitors. Once bleeding has been efficiently stopped by blood clot formation, dissolution of the thrombus is essential to restore vessel permeability. This process, known as fibrinolysis, also develops through coordinate action of a vast array of proteins and enzymes. An accurate diagnosis of hemostasis disturbance entails a multifaceted approach, encompassing family and personal history of hemostatic disorders, accurate collection of clinical signs and symptoms, integrated with laboratory hemostasis testing. Regarding laboratory testing, a reasonable approach entails classifying hemostasis testing according to cost, complexity and available clinical information. Laboratory workout may hence initiate with some rapid and inexpensive “screening” tests, characterized by high negative predictive value, then followed by second- or third-line analyses, specifically aimed to clarify the nature and severity of bleeding or thrombotic phenotype. This article aims to provide a general overview of the hemostatic process, and to provide some general suggestions to optimally facilitate laboratory hemostasis testing.

On The Mechanism Of Heparin-Induced Potentiation Of Platelet Aggregation

1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Coagulation Factors ◽  
Marked Enhancement ◽  
Matrix Bound ◽  
Induced Aggregation ◽  
Aggregation Of Platelets ◽  
Plasma Heparin

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.

Cardiovascular Complications in Patients with Klinefelter’s Syndrome

2020 ◽  
Vol 26 (43) ◽  
pp. 5556-5563
Author(s):  
Franz Sesti ◽  
Riccardo Pofi ◽  
Carlotta Pozza ◽  
Marianna Minnetti ◽  
Daniele Gianfrilli ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Klinefelter Syndrome ◽  
Subclinical Atherosclerosis ◽  
Cardiovascular Complications ◽  
High Risk Population ◽  
Metabolic Disturbances ◽  
Future Studies ◽  
Increased Risk ◽  
Chromosome Disorder

More than 70 years have passed since the first description of Klinefelter Syndrome (KS), the most frequent chromosome disorder causing male infertility and hypogonadism. KS is associated with increased cardiovascular (CV) mortality due to several comorbidities, including hypogonadism, as well as metabolic syndrome and type 2 diabetes, which are highly prevalent in these patients. Aside from metabolic disturbances, patients with KS suffer from both acquired and congenital CV abnormalities, cerebrovascular thromboembolic disease, subclinical atherosclerosis and endothelial dysfunction, which may all contribute to increased CV mortality. The mechanisms involved in this increased risk of CV morbidity and mortality are not entirely understood. More research is needed to better characterise the CV manifestations, elucidate the pathophysiological mechanisms and define the contribution of testosterone replacement to restoring CV health in KS patients. This review explores the complex association between KS, metabolic syndrome and CV risk in order to plan future studies and improve strategies to reduce mortality in this high-risk population.

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