Thrombosis and embolism after injury.

Sevitt, S.

doi:10.1136/jcp.s3-4.1.86

Cited by 21 publications

(11 citation statements)

References 44 publications

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“…Multiple direct histologic studies of thrombi by Sevitt, [31][32][33][34][35] however, have shown no pathologic or structural differences associated with thrombus location. Hence, if a thrombus is detected, the mechanical properties of thigh, popliteal, and calf vein thrombi should be identical.…”

Section: Discussionmentioning

confidence: 99%

Sonographic Elasticity Imaging of Acute and Chronic Deep Venous Thrombosis in Humans

Rubin

Xie

Kim

et al. 2006

Journal of Ultrasound in Medicine

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Section: Discussionmentioning

confidence: 99%

Sonographic Elasticity Imaging of Acute and Chronic Deep Venous Thrombosis in Humans

Rubin

Xie

Kim

et al. 2006

Journal of Ultrasound in Medicine

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“…Evidence suggest that platelets also play a role in VTE, although less important than in arterial thrombosis. However, the involvement of platelets in the formation of venous thrombi appears at a later stage, since the initial core is plateletfree, while subsequent layers contain some platelets (65). Indeed, activated platelets may catalyse both extrinsic and intrinsic thrombin generation (62).…”

Section: The Role Of Inflammation In the Pathophysiology Of Arterial mentioning

confidence: 99%

Epidemiology and pathophysiology of venous thromboembolism: similarities with atherothrombosis and the role of inflammation

Riva¹,

Donadini²,

Ageno³

2015

Thromb Haemost

109

114

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Venous thromboembolism (VTE) is a multifactorial disease. Major provoking factors (e. g. surgery, cancer, major trauma, and immobilisation) are identified in 50-60 % of patients, while the remaining cases are classified as unprovoked. However, minor predisposing conditions may be detectable in these patients, possibly concurring to the pathophysiology of the disease, especially when co-existing. In recent years, the role of chronic inflammatory disorders, infectious diseases and traditional cardiovascular risk factors has been extensively investigated. Inflammation, with its underlying prothrombotic state, could be the potential link between these risk factors, as well as the explanation for the reported association between arterial and venous thromboembolic events.

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“…First, the older work shows that as the formation of the thrombus propagates, the successive layers do contain platelets. 24 Second, (activated) platelets are important catalysts of both intrinsic and extrinsic thrombin generation and thus fibrin production. 25 Third, the platelet collagen receptor glycoprotein 6 was recently identified in a genome-wide association study that searched for novel risk factors for VTE.…”

Section: Plateletsmentioning

confidence: 99%

“…Older work also suggests that primary venous thrombi are platelet free, confirming the notion that platelets are not involved in the formation of the original nidus. 24 Based on these structural characteristics, platelets have historically been ignored in studies of VTE. Several lines of research indicate though that platelets play a determining role.…”

Section: Plateletsmentioning

confidence: 99%

Mechanistic View of Risk Factors for Venous Thromboembolism

Reitsma

Versteeg²,

Middeldorp³

2012

ATVB

175

138

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Abstract-Venous thromboembolism is an episodic disease with an annual incidence of 2 to 3/1000 per year that is associated with a high morbidity and mortality. Risk factors for venous thromboembolism come in many guises. They fit into an extended version of Virchow's triad and they tilt the hemostatic balance toward clot formation. This can be achieved by decreasing blood flow and lowering oxygen tension, by activating the endothelium, by activating innate or acquired immune responses, by activating blood platelets, or by increasing the number of platelets and red blood cells or modifying the concentrations of pro-and anticoagulant proteins in the blood. In this narrative review we will discuss the known common risk factors within this pathophysiological framework. (Arterioscler Thromb Vasc Biol. 2012;32:563-568.)Key Words: endothelium Ⅲ platelets Ⅲ pulmonary embolism Ⅲ risk factors Ⅲ Venous thrombosis V enous thromboembolism (VTE) is the third most common vascular disease after myocardial infarction and ischemic stroke. The annual incidence of symptomatic and objectively confirmed VTE, the collective term generally used for deep venous thrombosis, pulmonary embolism or both, is 2 to 3 per thousand inhabitants. 1 The incidence varies strongly with age from 0.1 in adolescence to 8 per 1000 in those above the age of 80 years. 1 The mechanistic framework that helps to understand and group the causes of VTE is an extension of the triad of Virchow, which postulates that thrombosis is caused by changes in (1) blood flow, (2) the state of the vessel wall, and/or (3) the composition of blood. 2 In a more current reductionist's view, stasis and low oxygen tension, activation of the endothelium, activation of innate (involving monocytes and granulocytes) and acquired immunity, activation of blood platelets, the concentration and nature of microparticles (MPs), and the individual concentrations of pro-and anticoagulant proteins all claim a role (see the Figure). In addition, red blood cells are present in venous clots. We will use this reductionist's framework to group and discuss the known common risk factors for VTE that are summarized in Table. Blood Flow, Oxygen Tension, and Endothelial Activation Prolonged stasis in a vein, in particular in deepest parts of the pocket of a venous valve, causes lowered oxygen tension. 3 This oxidative stress will lead to the upregulation of multiple stress-response genes including hypoxia inducible factor 1-alpha, P-selectin (CD62), and other adhesion receptors. 4,5 The resulting proinflammatory state of the endothelium supports the local recruitment of monocytes, granulocytes, platelets, and MPs. The recruitment of these actors and their activation may lead to the local exposure of tissue factor (TF), 6 thus initiating the extrinsic pathway of coagulation. When damaged granulocytes start releasing neutrophil extracellular traps, DNA, and RNA, factor XII may become activated thus triggering the intrinsic pathway of coagulation and further facilitating the formation of a thrombus. 7,8 T...

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Thrombosis and embolism after injury.

Cited by 21 publications

References 44 publications

Sonographic Elasticity Imaging of Acute and Chronic Deep Venous Thrombosis in Humans

Sonographic Elasticity Imaging of Acute and Chronic Deep Venous Thrombosis in Humans

Epidemiology and pathophysiology of venous thromboembolism: similarities with atherothrombosis and the role of inflammation

Mechanistic View of Risk Factors for Venous Thromboembolism

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