Circulating tissue factor positive microparticles in patients with acute recurrent deep venous thrombosis

Ye, Runyi; Ye, Caisheng; Huang, Yongbo; Liu, Longshan; Wang, Shenming

doi:10.1016/j.thromres.2011.10.014

Cited by 53 publications

(52 citation statements)

References 35 publications

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“…TF-MP activity and concentrations in plasma unambiguously correlate with the risk of recurrent VTE. 41,47 Patients suffering from malignancy have a clearly elevated risk of VTE. Several studies indicate that cancer patients with VTE have significantly higher TF-MP activity and levels than cancer patients without VTE, 48 -51 and such an association between TF-MP and VTE is confirmed by mechanistic studies.…”

Section: Microparticlesmentioning

confidence: 99%

“…42,43 Several, but not all studies, found that either plasma TF-MP concentration or TF-MP procoagulant activity positively correlates with the risk of VTE. 41,[43][44][45][46] An explanation for these inconsistent findings may be that detection of MPs is often inaccurate because of their small size. With regard to the recurrence of VTE, a clearer picture emerges.…”

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confidence: 99%

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Mechanistic View of Risk Factors for Venous Thromboembolism

Reitsma

Versteeg²,

Middeldorp³

2012

ATVB

173

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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Section: Microparticlesmentioning

confidence: 99%

mentioning

confidence: 99%

Mechanistic View of Risk Factors for Venous Thromboembolism

Reitsma

Versteeg²,

Middeldorp³

2012

ATVB

173

138

View full text Add to dashboard Cite

show abstract

“…Interestingly, the highest levels of TF + -microparticles were observed in patients with functional class III-IV and/or the weakest 6-min test performance, suggesting a potential correlation between microparticles and functional status. Comparable results were observed in patients with recurrent deep venous thrombosis, a potential trigger for acute pulmonary embolism development [51].…”

Section: Procoagulant Properties Of Microparticlesmentioning

confidence: 88%

Cellular microparticles in the pathogenesis of pulmonary hypertension

et al. 2012

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Pulmonary hypertension (PH) is a fatal disease with no treatment options, characterised by elevated pulmonary vascular resistanzce and secondary right ventricular failure. The aetiology of pulmonary arterial hypertension is multiple and its pathogenesis is complex. Although the exact role of cellular microparticles remains partially understood, there is increasing evidence to suggest an active role for microparticles in PH pathophysiology. Patients with PH exhibited higher circulating levels of microparticles compared to control subjects and in vitro or in vivo generated microparticles can induce endothelial dysfunction, interfere with coagulation pathways or modulate inflammatory phenomenon. Whether or not these new conveyors of biological information contribute to the acquisition and/or maintenance of the altered endothelial phenotype is unexplored in PH and requires further study. @ERSpublications Patients with PH have elevated circulating levels of microparticles which may contribute to disease pathophysiology

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“…Therefore, the effects of MPs formation on the inception of VTE remain unclear. Studies on the long-term trend of MPs after the acute thrombotic event [50][51][52][53][54], despite the different assays used and the different aims and settings seem to suggest that the levels of MPs after a thrombotic event remain high despite adequate anticoagulation therapy. Moreover, therapy with low molecular weight heparin seems to reduce MPs levels more effectively than oral anticoagulant [54,55].…”

Section: Mps and Venous Thrombosismentioning

confidence: 99%

Modulating thrombotic diathesis in hereditary thrombophilia and antiphospholipid antibody syndrome: a role for circulating microparticles?

Campello

Radu

Spiezia

et al. 2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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Over the past decades, there have been great advances in the understanding of the pathogenesis of venous thromboembolism (VTE) in patients with inherited and acquired thrombophilia [mainly antiphospholipid antibody syndrome (APS)]. However, a number of questions remain unanswered. Prognostic markers capable of estimating the individual VTE risk would be of great use. Microparticles (MPs) are sub-micron membrane vesicles constitutively released from the surface of cells after cellular activation and apoptosis. The effects of MPs on thrombogenesis include the exposure of phopshatidylserine and the expression of tissue factor and MPs have been described in clinical studies as possible diagnostic and prognostic biomarkers for VTE. This review will provide a novel perspective on the current knowledge and research trends on the possible role of MPs in hereditary thrombophilia and APS. Basically, the published data show that circulating MPs may contribute to the development of VTE in thrombophilic carriers, both in mild and severe states. Moreover, the presence of endothelial-MPs and plateletMPs has been described in antiphospholipid syndrome and seems to be directly linked to antiphospholipid antibodies and not to other underlying autoimmune disorders or the thrombotic event itself. In conclusion, circulating MPs may constitute an epiphenomenon of thrombophilia itself and could be up-regulated in acute particular conditions, promoting a global prothrombotic state up to the threshold of the clinical relevant thrombotic event.

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Circulating tissue factor positive microparticles in patients with acute recurrent deep venous thrombosis

Cited by 53 publications

References 35 publications

Mechanistic View of Risk Factors for Venous Thromboembolism

Mechanistic View of Risk Factors for Venous Thromboembolism

Cellular microparticles in the pathogenesis of pulmonary hypertension

Modulating thrombotic diathesis in hereditary thrombophilia and antiphospholipid antibody syndrome: a role for circulating microparticles?

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