Materiały źródłowe

• #1 Deep vein thrombosis: pathogenesis, diagnosis, and medical management

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5778510/

  Deep vein thrombosis (DVT) is a major preventable cause of morbidity and mortality worldwide. […] Normal blood physiology hinges on a delicate balance between pro- and anti-coagulant factors. Virchows Triad distills the multitude of risk factors for DVT into three basic elements favoring thrombus formation: venous stasis, vascular injury, and hypercoagulability. […] Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg. […] The hypercoagulable micro-environment that ensues may downregulate certain antithrombotic proteins that are preferentially expressed on venous valves including thrombomodulin and endothelial protein C receptor (EPCR). […] Debate remains regarding the precise location of tissue factor in this process, whether expressed on the endothelium or by cells within the extravascular tissue, but there is general agreement that tissue factor serves as the primary nidus for thrombus formation.

• #1 Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1911303-overview

  In the 19th century, Rudolf Virchow described three factors that are critically important in the development of venous thrombosis (DVT): (1) venous stasis, (2) activation of blood coagulation, and (3) venous endothelial (intimal) damage. These factors have come to be known as the Virchow triad. […] Venous stasis occurs as a result of anything that slows or obstructs the flow of venous blood. This results in increased blood viscosity and the formation of microthrombi, which are not washed away by fluid movement; the thrombus that forms may then grow and propagate. Endothelial damage in the blood vessel may be intrinsic or secondary to external trauma. It may result from accidental injury or surgical insult. A hypercoagulable state can occur due to a biochemical imbalance between circulating factors. This may result from an increase in circulating tissue activation factor, combined with a decrease in circulating plasma antithrombin and fibrinolysins.

• #1 Deep vein thrombosis: pathogenesis, diagnosis, and medical management – Stone – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/16872/html

  Virchows Triad, first described in 1856, implicates three contributing factors in the formation of thrombosis: venous stasis, vascular injury, and hypercoagulability. Venous stasis is the most consequential of the three factors, but stasis alone appears to be insufficient to cause thrombus formation. However, the concurrent presence of venous stasis and vascular injury or hypercoagulability greatly increases the risk for clot formation. The clinical conditions most closely associated with DVT are fundamentally related to the elements of Virchows Triad; these include surgery or trauma, malignancy, prolonged immobility, pregnancy, congestive heart failure, varicose veins, obesity, advancing age, and a history of DVT. […] Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg. While valves help to promote blood flow through the venous circulation, they are also potential locations for venous stasis and hypoxia. Multiple postmortem studies have demonstrated the propensity for venous thrombi to form in the sinuses adjacent to venous valves. As blood flow slows, oxygen tension declines with a coincident increase in hematocrit. The hypercoagulable micro-environment that ensues may downregulate certain antithrombotic proteins that are preferentially expressed on venous valves including thrombomodulin and endothelial protein C receptor (EPCR). In addition to reducing important anticoagulant proteins, hypoxia drives the expression of certain procoagulants. Among these is P-selectin, an adhesion molecule which attracts immunologic cells containing tissue factor to the endothelium. Debate remains regarding the precise location of tissue factor in this process, whether expressed on the endothelium or by cells within the extravascular tissue, but there is general agreement that tissue factor serves as the primary nidus for thrombus formation. Thrombus formation appears to require both tissue factor and P-selectin.

• #2 Deep Vein Thrombosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK507708/

  Deep vein thrombosis (DVT) is an obstructive disease with a hindering venous reflux mechanism. DVT usually involves the lower limb venous system, with clot formation originating in a deep calf vein and propagating proximally. […] According to the Virchow triad, the following are the main pathophysiological mechanisms involved in DVT: Damage to the vessel wall, Blood flow turbulence, Hypercoagulability. […] The triggers of venous thrombosis are frequently multifactorial, with the different parts of the triad of Virchow contributing in varying degrees in each patient, but all result in early thrombus interaction with the endothelium. This stimulates local cytokine production and causes leukocyte adhesion to the endothelium, promoting venous thrombosis. Depending on the relative balance between the coagulation and thrombolytic pathways, thrombus propagation occurs. DVT is commonest in the lower limb below the knee and starts at low-flow sites, such as the soleal sinuses, behind venous valve pockets. […] A potential correlation between DVT and atherosclerosis (AS) has been proposed. The endothelial dysfunction involved in the pathophysiological mechanism of DVT would potentially result in AS. Accordingly, a greater risk of subsequent AS in patients with DVT is predicted.

• #2 Deep vein thrombosis: pathogenesis, diagnosis, and medical management – Stone – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/16872/html

  Virchows Triad, first described in 1856, implicates three contributing factors in the formation of thrombosis: venous stasis, vascular injury, and hypercoagulability. Venous stasis is the most consequential of the three factors, but stasis alone appears to be insufficient to cause thrombus formation. However, the concurrent presence of venous stasis and vascular injury or hypercoagulability greatly increases the risk for clot formation. The clinical conditions most closely associated with DVT are fundamentally related to the elements of Virchows Triad; these include surgery or trauma, malignancy, prolonged immobility, pregnancy, congestive heart failure, varicose veins, obesity, advancing age, and a history of DVT. […] Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg. While valves help to promote blood flow through the venous circulation, they are also potential locations for venous stasis and hypoxia. Multiple postmortem studies have demonstrated the propensity for venous thrombi to form in the sinuses adjacent to venous valves. As blood flow slows, oxygen tension declines with a coincident increase in hematocrit. The hypercoagulable micro-environment that ensues may downregulate certain antithrombotic proteins that are preferentially expressed on venous valves including thrombomodulin and endothelial protein C receptor (EPCR). In addition to reducing important anticoagulant proteins, hypoxia drives the expression of certain procoagulants. Among these is P-selectin, an adhesion molecule which attracts immunologic cells containing tissue factor to the endothelium. Debate remains regarding the precise location of tissue factor in this process, whether expressed on the endothelium or by cells within the extravascular tissue, but there is general agreement that tissue factor serves as the primary nidus for thrombus formation. Thrombus formation appears to require both tissue factor and P-selectin.

• #2 Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1911303-overview

  In the 19th century, Rudolf Virchow described three factors that are critically important in the development of venous thrombosis (DVT): (1) venous stasis, (2) activation of blood coagulation, and (3) venous endothelial (intimal) damage. These factors have come to be known as the Virchow triad. […] Venous stasis occurs as a result of anything that slows or obstructs the flow of venous blood. This results in increased blood viscosity and the formation of microthrombi, which are not washed away by fluid movement; the thrombus that forms may then grow and propagate. Endothelial damage in the blood vessel may be intrinsic or secondary to external trauma. It may result from accidental injury or surgical insult. A hypercoagulable state can occur due to a biochemical imbalance between circulating factors. This may result from an increase in circulating tissue activation factor, combined with a decrease in circulating plasma antithrombin and fibrinolysins.

• #3 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  Studies in animal models have improved our understanding of the pathophysiology of thrombosis. […] The events on a molecular level during venous stasis have been investigated. […] Situations when venous stasis is implicated in the generation of thrombosis include deep vein thrombosis (DVT) in the lower extremity during immobilization. […] On a molecular level, there are a few possible mechanisms: hypoxemia, activated coagulation factors, and inflammatory reaction. […] In a dog model, as well as in patients, it has been shown that the blood within the pocket of the venous valves, also called valve sinus, became rapidly hypoxic during stasis, and thrombus formation on the valve cusp could be demonstrated after 2 h of non-pulsatile flow. […] The transcription factor early growth response-1 (Egr-1) seems to be an important modulator of the TF expression because in homozygous-Egr-1-null mice, there was no increase in TF antigen and no fibrin deposition during hypoxia.

• #4 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  Another pathway is via the hypoxia-inducible factor-1α (HIF-1α), which normally is hydroxylated and degraded, but under hypoxic conditions, it becomes stabilized and able to mediate transcriptional activation of various genes, including those involved in angiogenesis, apoptosis, and metastases, and this is mediated by TF. […] The main hypoxia-induced pathways leading to increased thrombus formation are summarized in Figure 1. […] It can then be hypothesized that, during venous stasis, there is a change in the balance towards hypercoagulability. […] When the venous circulation is impaired, it is quite possible that these coagulation factors, activated platelets and leukocytes fail to clear and instead promote thrombin generation locally. […] In a study with whole-exome sequencing, followed by gene-based collapsing analysis, 400 patients with VTE were compared with a large, general population cohort, and rare variants associated with VTE were identified.

• #5 Deep vein thrombosis: pathogenesis, diagnosis, and medical management

  https://pmc.ncbi.nlm.nih.gov/articles/PMC5778510/

  A venous thrombus has essentially two components, an inner platelet rich white thrombus forming the so-called lines of Zahn surrounded by an outer red cell dense fibrin clot. […] As the ratio of procoagulants to anticoagulants increases, so does the risk of thrombus formation. […] In humans, less is known regarding the role of tissue factor inhibitor pathway. […] Taken together, thrombosis formation is a dynamic, multicausal process that hinges on a fine balance of physical and biochemical factors.

• #6 Deep vein thrombosis: pathogenesis, diagnosis, and medical management – Stone – Cardiovascular Diagnosis and Therapy

  https://cdt.amegroups.org/article/view/16872/html

  A venous thrombus has essentially two components, an inner platelet rich white thrombus forming the so-called lines of Zahn surrounded by an outer red cell dense fibrin clot. Fibrin and extracellular DNA complexed with histone proteins forms the outer scaffold, which may be important in determining thrombus susceptibility to tissue plasminogen activator (TPA) and thrombolysis. As the ratio of procoagulants to anticoagulants increases, so does the risk of thrombus formation. The proportion of proteins is in part determined by the ratio of endothelial cell surface to blood volume. A decreased cell surface to blood volume ratio (i.e., large vessels) favors procoagulants. Factor VIII, von Willebrand factor, factor VII and prothrombin seem to be particularly influential in tipping the scale towards coagulation. In addition to promoting thrombin generation, prothrombin inhibits the anticoagulant properties of activated protein C, thereby dampening a natural anticoagulant pathway. There are three such pathways: the protein C anticoagulant pathway (protein C, protein S, thrombomodulin, and perhaps EPCR), heparin-antithrombin pathway, and tissue factor inhibitor pathway. Defects in these pathways are associated with an increased risk for thrombus formation. In humans, less is known regarding the role of tissue factor inhibitor pathway. There are also a number of familial variants that predispose to thrombus formation by increasing the levels of factor VII, VIII, IX, von Willebrand factor, and prothrombin. In factor V Leiden, which affects up to 5% of Caucasians and increases the risk of thrombosis 7-fold, activated factor Va is resistant to the inhibitory influence of protein C. Other risk factors for clot formation include cancer, oral contraceptives, obesity, and advancing age. Malignancy can exert a compressive effect on veins contributing to stasis. It also leads to shedding of procoagulants such as tissue factor on membrane particles that promotes thrombosis. Obesity and oral contraceptive use are independent risk factors for thrombosis. Together, they increase thrombosis risk synergistically. Finally, advancing age is associated with an increased risk for thrombosis. While the cause for this remains unsettled, several factors related to aging have been observed: greater prevalence of obesity, increased frequency of illness and periods of prolonged immobility, comorbid medical conditions, and an increase in the level of procoagulants without a commensurate increase in anticoagulants such as protein C. Taken together, thrombosis formation is a dynamic, multicausal process that hinges on a fine balance of physical and biochemical factors.

• #7 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  Deep vein thrombosis (DVT) is a type of venous thrombosis involving the formation of a blood clot in a deep vein, most commonly in the legs or pelvis. The mechanism behind DVT formation typically involves some combination of decreased blood flow, increased tendency to clot, changes to the blood vessel wall, and inflammation. Risk factors include recent surgery, older age, active cancer, obesity, infection, inflammatory diseases, antiphospholipid syndrome, personal history and family history of VTE, trauma, injuries, lack of movement, hormonal birth control, pregnancy, and the period following birth. VTE has a strong genetic component, accounting for approximately 50 to 60% of the variability in VTE rates. […] The beginning of venous thrombosis is thought to arise from „activation of endothelial cells, platelets, and leukocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system” via tissue factor. Vein wall inflammation is likely the inciting event.

• #8 Deep vein thrombosis – Wikipedia

  https://en.wikipedia.org/wiki/Deep_vein_thrombosis

  The process of fibrinolysis, where DVT clots can be dissolved back into the blood, acts to temper the process of thrombus growth. This is the preferred process. Aside from the potentially deadly process of embolization, a clot can resolve through organization, which can damage the valves of veins, cause vein fibrosis, and result in non-compliant veins. […] The activated endothelium of veins interacts with circulating white blood cells (leukocytes). While leukocytes normally help prevent blood from clotting (as does normal endothelium), upon stimulation, leukocytes facilitate clotting. Neutrophils are recruited early in the process of venous thrombi formation. They release pro-coagulant granules and neutrophil extracellular traps (NETs) or their components, which play a role in venous thrombi formation. NET components are pro-thrombotic through both the intrinsic and extrinsic coagulation pathways.

• #9 Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1911303-overview

  The origin of venous thrombosis is frequently multifactorial, with components of the Virchow triad assuming variable importance in individual patients, but the end result is early thrombus interaction with the endothelium. This interaction stimulates local cytokine production and facilitates leukocyte adhesion to the endothelium, both of which promote venous thrombosis. Depending on the relative balance between activated coagulation and thrombolysis, thrombus propagation occurs. […] Thrombosis is the homeostatic mechanism whereby blood coagulates or clots, a process crucial to the establishment of hemostasis after a wound. It may be initiated via several pathways, usually consisting of cascading activation of enzymes that magnify the effect of an initial trigger event. A similar complex of events results in fibrinolysis, or the dissolution of thrombi. Microscopic thrombus formation and thrombolysis (dissolution) are continuous events, but with increased stasis, procoagulant factors, or endothelial injury, the coagulation-fibrinolysis balance may favor the pathologic formation of an obstructive thrombus. Clinically relevant deep venous thrombosis is the persistent formation of macroscopic thrombus in the deep proximal veins.

• #10 Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1911303-overview

  The extrinsic system operates as the result of activation by tissue lipoprotein, usually released as the result of some mechanical injury or trauma. The intrinsic system usually involves circulating plasma factors. Both of these pathways come together at the level of factor X, which is activated to form factor Xa. This in turn promotes the conversion of prothrombin to thrombin (factor II). This is the key step in clot formation, for active thrombin is necessary for the transformation of fibrinogen to a fibrin clot. […] Once a fibrin clot is formed and has performed its function of hemostasis, mechanisms exist in the body to restore the normal blood flow by lysing the fibrin deposit. Circulating plasmin performs this function by digesting fibrin and deactivating clotting factors V and VIII and fibrinogen.

• #11 Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1911303-overview

  Three naturally occurring anticoagulant mechanisms exist to prevent inadvertent activation of the clotting process. These include the heparin-antithrombin III (ATIII), protein C and thrombomodulin protein S, and the tissue factor inhibition pathways. When trauma occurs, or when surgery is performed, circulating ATIII is decreased. This has the effect of potentiating the coagulation process. Studies have demonstrated that levels of circulating ATIII are decreased, and stay reduced longer, after total hip replacement (THR) than after general surgical cases. […] Under normal circumstances, a physiologic balance is present between factors that promote and hinder coagulation. A disturbance in this equilibrium may result in the coagulation process occurring at an inopportune time or location, or in an excessive manner. Alternatively, failure of the normal coagulation mechanisms may lead to hemorrhage.

• #12 Deep Venous Thrombosis (DVT): Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1911303-overview

  ThrombI usually form behind valve cusps or at venous branch points, most of which begin in the calf. Venodilation or turbulent flow in these areas may disrupt the endothelial cell barrier and expose the subendothelium. Platelets adhere to the subendothelial surface by means of von Willebrand factor or fibrinogen in the vessel wall. Neutrophils also adhere to the basement membrane and migrate into the subendothelium. Activation of both neutrophils and platelets then leads to the release of procoagulant and inflammatory mediators, forming complexes on the surface of platelets and increasing the rate of thrombin generation and fibrin formation. Stimulated leukocytes irreversibly bind to endothelial receptors and extravasate into the vein wall by means of mural chemotaxis. Because mature thrombus composed of platelets, leukocytes and fibrin develops, and an active thrombotic and inflammatory process occurs at the inner surface of the vein, an active inflammatory response occurs in the wall of the vein.

• #13 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  The main protein of plasminogen-plasminase system, plasminogen activator inhibitor-1 (PAI-1), is a significant inhibitor of tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (U-PA). […] Inflammation stimulates endothelial cells to release tPA and PAI-1 locally. […] The role of inflammation and inflammation-related biomarkers in cerebrovascular thrombotic disease is a subject of ongoing debate. […] The dysregulation of miRNAs has also been reported in venous thrombosis, suggesting the involvement of miRNAs in the progression of venous thrombosis. […] In addition, it has been showed that one of the ways that neutrophils promote venous thrombosis is the formation of neutrophil extracellular traps (NETs). […] The risk of venous thrombosis increases with age, but the mechanisms underlying the increased risk of thrombosis with age are not well understood.

• #14 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  Therefore, it is believed that one of ways in which neutrophils encourage venous thrombosis is by forming NETs. […] The elevated levels of Fn-EDA in plasma may be an important mechanism for promoting DVT in the context of diet-induced obesity. […] Over the past few years, growing research suggest that the production of venous thrombosis also involves the immune system. […] The immune cells support the related molecules and produce specific intravascular scaffolds that promote pathogen recognition, containment, and destruction. […] The previous study showed IL-6, IL-8, and monocyte chemoattractant protein (MCP-1) were the independent predictors of accelerated VTE development and they concluded that systemic inflammation is a key driver of VTE risk after major trauma. […] The more clearly the mechanisms of venous thrombosis are understood, the greater therapeutic and diagnostic targets for venous thrombosis are identified.

• #15 The Basic Principles of Pathophysiology of Venous Thrombosis

  https://www.mdpi.com/1422-0067/25/21/11447

  The corresponding protein is Stabilin-2, which is a scavenger receptor on the endothelial surface. […] The initiation of thrombus formation happens when factor VIIa, together with TF, expressed on monocytes, activates factor X to Xa, which, in turn, with factor Va as cofactor on a phospholipid bilayer (monocyte or endothelium), activates factor II (prothrombin) to IIa (thrombin). […] This review will focus on the roles of interleukins, neutrophil extracellular traps, the complement system, and a possible genetic risk factor. […] These prothrombotic responses are collectively termed thromboinflammation (sometimes interchangeably with immunothrombosis), which implies a pathophysiologic condition with injured vascular endothelium, impaired anti-inflammatory and antithrombotic functions.

• #16 Mechanism of Deep Vein Thrombosis and its Complications

  https://www.walshmedicalmedia.com/open-access/mechanism-of-deep-vein-thrombosis-and-its-complications-114774.html

  Deep Vein Thrombosis (DVT) is a type of Venous Thrombosis (VT) in which a blood clot forms in a deep vein, usually in the legs or pelvis. DVTs can cause pain, swelling, redness, and enhanced veins in the affected region, but some deep vein thrombosis have no symptoms. […] Deep vein thrombosis formation is usually caused by a combination of decreased blood flow, increased clotting tendency, changes to the blood vessel wall, and inflammatory processes. […] Major injury, older age, effective disease, obesity, infection, inflammatory diseases, antiphospholipid syndrome, personal and family origins of venous thrombo-embolism, trauma, injuries, lack of flexibility, reproductive hormones pregnancy prevention, childbirth, and the period following delivery are all risk factors of venous thrombo-embolism. […] VTE has a strong genetic component that provides evidence for 50 to 60% of the variance in VTE percentages.

• #17 The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE)

  https://www.ebmconsult.com/articles/oral-contraceptive-clotting-factors-thrombosis-dvt-pe

  The estimated incidence of venous thromboembolism (VTE) in women of child bearing age who are not taking oral contraceptives is 1 in 10,000 per year. This is increased 3-5 fold when women of child bearing age use estrogen containing oral contraceptives. […] Estrogen containing oral contraceptives increase the plasma concentration of clotting factors II, VII, X, XII, factor VIII, and fibrinogen. […] Estrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, estrogen increases plasma concentrations of these clotting factors by increasing gene transcription. […] Higher doses of estrogen appear to confer a greater risk of venous thrombus formation. This can be explained by a greater degree of nuclear receptor binding and overall activation of gene transcription for these clotting factors.

• #18 The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE)

  https://www.ebmconsult.com/articles/oral-contraceptive-clotting-factors-thrombosis-dvt-pe

  Estrogen containing oral contraceptives increase the plasma concentrations of clotting factors II, VII, X, XII, factor VIII, fibrinogen, and thrombin activatable fibrinolysis inhibitor (TAFI). […] Estrogen, like many lipophilic hormones, affects the gene transcription of various proteins. Thus, estrogen increases plasma concentrations of these clotting factors by increasing gene transcription. […] The degree of influence that estrogen has on gene transcription is unfortunately more complex and not limited to nuclear receptor binding to DNA. Estrogen bound to nuclear receptors (estrogen receptors) also regulates gene expression through protein-protein interaction with other transcription factors. […] Higher doses of estrogen appear to confer a greater risk of venous thrombus formation. This can be explained by a greater degree of nuclear receptor binding and overall activation of gene transcription for these clotting factors.

• #19 Molecular mechanisms of venous thrombosis | JIR

  https://www.dovepress.com/recent-advances-on-the-molecular-mechanism-and-clinical-trials-of-veno-peer-reviewed-fulltext-article-JIR

  Venous thromboembolism is a condition that includes deep vein thrombosis and pulmonary embolism. […] Over the past few years, growing research suggests that venous thrombosis is also related to the immune system and inflammatory factors have been confirmed to be involved in venous thrombosis. […] DVT is a consequence of a complicated interaction between enzymes and cellular processes, in which the endothelium, platelets, and leukocytes coordinate a pro-inflammatory state that ultimately leads to the clot formation with higher mortality rate for acute DVT. […] Therefore, exploring the mechanism is essential for effective treatment of venous thrombosis. Recently, there has been a lot of discussion on the mechanisms of venous thrombosis, including inflammatory, immunological, and neutrophil extracellular trap formation aspects, other factors under investigation include age, p-selection, MicroRNA(miRNA), PAI-1-induced venous thrombosis and extracellular vesicles (EVs).

• #20 The role of valve stiffness in the insurgence of deep vein thrombosis | Communications Materials

  https://www.nature.com/articles/s43246-020-00066-2

  Deep vein thrombosis is a life-threatening development of blood clots in deep veins. Immobility and blood flow stagnancy are typical risk factors indicating that fluid dynamics play an important role in the initiation of venous clots. […] The significance of reduction in flow as a risk factor implies that local characteristics of flow play a leading role in DVT pathogenesis. […] Blood flow stagnation up to stasis is considered one of the major factors triggering DVT. […] Two counter-rotating vortices are formed in the valve space contributing to the prolonged residence of blood in the area. […] The vortex encourages circulation of the cellular and humoral prothrombotic factors facilitating their interaction. […] An important feature of our model is the use of pulsatile flow, which mimics the effect of the muscle pump, accelerating blood flow in the veins. Thus, we demonstrate herein that changes in valve stiffness may affect thrombus formation.

• #21 The role of valve stiffness in the insurgence of deep vein thrombosis | Communications Materials

  https://www.nature.com/articles/s43246-020-00066-2

  This approach may be useful for future studies of the physical parameters predisposing to DVT initiation. […] The asymmetry altered the flow patterns around the valve flaps forcing particles to get trapped in the recirculation zone behind the valve. […] Our results are consistent with findings that the risk of DVT increases with old age as valves become stiffer, and also suggest that circumstances where valve symmetries are not maintained might increase the risk of DVT. […] This parameter has not been investigated so far and it could be a potential indication of a higher DVT risk.

• #22 Deep vein thrombosis (DVT) – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/symptoms-causes/syc-20352557

  Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in the body, usually in the legs. […] You can get deep vein thrombosis (DVT) if you have certain medical conditions that affect how the blood clots. A blood clot in the legs can also develop if you don’t move for a long time. […] Deep vein thrombosis can be serious because blood clots in the veins can break loose. The clots can then travel through the bloodstream and get stuck in the lungs, blocking blood flow (pulmonary embolism). When DVT and pulmonary embolism occur together, it’s called venous thromboembolism (VTE). […] Anything that prevents the blood from flowing or properly clotting can cause a blood clot. […] The main causes of deep vein thrombosis (DVT) are damage to a vein from surgery or inflammation and damage due to infection or injury.

• #23 Deep vein thrombosis (DVT) – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/symptoms-causes/syc-20352557

  Many things can increase the risk of developing deep vein thrombosis (DVT). The more risk factors you have, the greater your risk of DVT. […] Sometimes, a blood clot in a vein can occur with no identifiable risk factor. This is called an unprovoked venous thromboembolism (VTE). […] Complications of DVT can include: […] PE is a potentially life-threatening complication associated with DVT. It occurs when a blood clot (thrombus) in a leg or other body area breaks free and gets stuck in a blood vessel in a lung.

• #24 Pulmonary Embolism: DVT to PE | Ausmed

  https://www.ausmed.com/learn/articles/pulmonary-embolism

  Pulmonary embolism (PE) is a natural consequence of a cascade of unfortunate events that begin with a thrombus formation, typically in a deep vein of the legs, thighs or pelvis. […] The presence of these risk factors places patients at a significantly elevated risk of the venous event turning into a much bigger pulmonary problem. […] Over 50% of patients with deep venous thrombi will eventually end up with a diagnosis of PE. […] Risk factors for DVT (and thus for PE) include many events that tend to lead to injuries to the venous structures of the leg, thigh, hip or pelvis. […] Fractures, surgery and significant muscle tears are all conditions that create the potential for DVT formation. […] Individuals with slow blood flow have an elevated risk; this flow problem can be due to prolonged sitting from long car rides or aeroplane flights, bed rest, or paralysis.

• #25 DVT during Pregnancy Symptoms, Causes, Treatment & Risks

  https://www.medicinenet.com/dvt_deep_vein_thrombosis_and_pregnancy/article.htm

  Treatment and management guidelines for deep vein thrombosis (DVT) during pregnancy may include: Anticoagulation therapy is the treatment for DVT diagnosed during pregnancy. Low-molecular-weight heparins (LMWHs) usually are the first-line medications. Anticoagulant therapy may need to be continued into the postpartum period when the risk of DVT/VTE increases. […] Complications of deep vein thrombosis (DVT) during pregnancy may include: If a blood clot in the legs breaks off and travels to the lungs, this can result in a pulmonary embolism (PE), which can be fatal. PE is the seventh leading cause of maternal death (mortality), accounting for 9% of maternal deaths.

• #26 Deep Vein Thrombosis (DVT)

  https://my.clevelandclinic.org/health/diseases/16911-deep-vein-thrombosis-dvt

  Deep vein thrombosis (DVT, also called venous thrombosis) occurs when a thrombus (blood clot) develops in veins deep in your body because your veins are injured or the blood flowing through them is too sluggish. The blood clots may partially or completely block blood flow through your vein. […] Even though DVT itself is not life-threatening, the blood clots have the potential to break free and travel through your bloodstream. […] As many as half of those who get a DVT in their legs develop symptoms of intermittent leg pain and swelling that may last months to years. These symptoms are called post-thrombotic syndrome and can happen because of damage to the valves and inner lining of your veins leading to blood pooling more than it should. […] These conditions can increase your risk of a deep vein thrombosis: Having an inherited (genetic) condition increases your risk of blood clots.

• #27 Deep Vein Thrombosis (DVT) – Venous Thromboembolism (VTE) – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicine

  https://empendium.com/mcmtextbook/chapter/B31.II.2.33.1.

  Long-term complications of DVT include postthrombotic syndrome (chronic venous insufficiency) as well as pulmonary hypertension as a complication of PE. In approximately two-thirds of patients treated for DVT, the thrombus undergoes organization and the affected vein is partially recanalized (a total dissolution of the thrombus occurs only in a third of patients). This leads to chronic venous insufficiency and postthrombotic syndrome: organization of the thrombus results in damage to the venous valves, retrograde flow of venous blood, and eventually in venous hypertension.

• #28 Pulmonary Embolism: DVT to PE | Ausmed

  https://www.ausmed.com/learn/articles/pulmonary-embolism

  Pregnancy, hormone replacement therapy and contraceptive medicines are also major culprits due to a common theme: they cause an increase in oestrogen to be delivered to the body. […] Chronic thromboembolic pulmonary hypertension (CTEPH) is associated with a high risk of death. Its estimated to occur in up to 5% of post-PE patients but may be underdiagnosed due to initial nonspecific symptoms.

• #29 Deep Venous Thrombosis (DVT) – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/peripheral-venous-disorders/deep-venous-thrombosis-dvt

  In phlegmasia cerulea dolens, massive iliofemoral venous thrombosis causes near-total venous occlusion; the leg becomes ischemic, extremely painful, and cyanotic. Pathophysiology may involve complete stasis of venous and arterial blood flow in the lower extremity because venous return is occluded or massive edema cuts off arterial blood flow.

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