Risk of Recurrent Venous Thromboembolism After Provoked Venous Thromboembolism

2019-10-16 10:39:15 | BioPortfolio


Venous thromboembolism (VTE) is a common disease with an incidence of 1-2/1000 persons per year. VTE is a chronic disease with a considerable risk of recurrence. Patients with unprovoked VTE, i.e. VTE in the absence of a temporary risk factor including surgery, cancer or immobilisation, have a high recurrence risk and indefinite anticoagulation is generally recommended. The recurrence risk of patients with VTE provoked by a transient risk factor is regarded as low. Discontinuation of anticoagulation after three months is recommended because the benefit of reducing the recurrence risk further by prolonged anticoagulation is outweighed by the bleeding risk. However, the newer direct oral anticoagulants are potentially associated with a lower bleeding risk than vitamin K antagonists. Because they are also meanwhile widely available and are convenient there is a trend towards prolonging anticoagulation also in patients with a VTE after a transient provoking factor. However, the definition of transient provoking factors is imprecise and a distinct categorization according to the risk of recurrence is lacking. Preliminary evidence suggests that the recurrence risk varies considerably between the different transient provoking factors. In a prospective cohort study, the investigators will include patients with a deep vein thrombosis or pulmonary embolism provoked by a transient risk factor defined according to Guidance of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis (Kearon et al., J Thromb Haemost 2016; 14: 1480-3) after discontinuation of anticoagulation. The study endpoint is recurrent symptomatic VTE.

Study Design


Recurrent Venous Thrombosis


Medical University of Vienna




Medical University of Vienna

Results (where available)

View Results


Published on BioPortfolio: 2019-10-16T10:39:15-0400

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Medical and Biotech [MESH] Definitions

Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures.

The vitamin K-dependent cofactor of activated PROTEIN C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S; (PROTEIN S DEFICIENCY); can lead to recurrent venous and arterial thrombosis.

Formation or presence of a blood clot (THROMBUS) in the CRANIAL SINUSES, large endothelium-lined venous channels situated within the SKULL. Intracranial sinuses, also called cranial venous sinuses, include the superior sagittal, cavernous, lateral, petrous sinuses, and many others. Cranial sinus thrombosis can lead to severe HEADACHE; SEIZURE; and other neurological defects.

An autosomal dominant disorder showing decreased levels of plasma protein S antigen or activity, associated with venous thrombosis and pulmonary embolism. PROTEIN S is a vitamin K-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated PROTEIN C (also a vitamin K-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein C deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis. (From Harrison's Principles of Internal Medicine, 12th ed, p1511; Wintrobe's Clinical Hematology, 9th ed, p1523)

Impaired venous blood flow or venous return (venous stasis), usually caused by inadequate venous valves. Venous insufficiency often occurs in the legs, and is associated with EDEMA and sometimes with VENOUS STASIS ULCERS at the ankle.

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