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While venous thrombosis of the legs is the most common form, venous thrombosis may occur in other veins. These may have particular specific risk factors: [5] Cerebral venous sinus thrombosis, cavernous sinus thrombosis and jugular vein thrombosis: thrombosis of the veins of the brain and head
The mainstay of VTE management is anticoagulation therapy, which prevents thrombus propagation and embolization. Such treatment reduces the risk of recurrence. [5] [4] [1] The choice and duration of anticoagulation depend on the individual patient's risk factors, bleeding risk, and preferences.
Dozens of genetic risk factors have been identified, [14] and they account for approximately 50 to 60% of the variability in VTE rates. [4] As such, family history of VTE is a risk factor for a first VTE. [88] Factor V Leiden, which makes factor V resistant to inactivation by activated protein C, [88] mildly increases VTE risk by about three times.
One of the goals of blood clot prevention is to limit venous stasis as this is a significant risk factor for forming blood clots in the deep veins of the legs. [6] Venous stasis can occur during the long periods of not moving. Thrombosis prevention is also recommended during air travel. [7]
Thrombosis may occur in veins (venous thrombosis) or in arteries (arterial thrombosis). Venous thrombosis (sometimes called DVT, deep vein thrombosis) leads to a blood clot in the affected part of the body, while arterial thrombosis (and, rarely, severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by ...
Mitral stenosis poses a high risk of forming emboli which may travel to the brain and cause stroke. [2] Endocarditis increases the risk for thromboembolism, [2] by a mixture of the factors above. Atherosclerosis in the aorta and other large blood vessels is a common risk factor, [2] both for thromboembolism and cholesterol embolism.
A 2006 meta-analysis showed only a 1.3-fold increased risk for coronary disease. [6] Deficiencies in the anticoagulants Protein C and Protein S further increase the risk five- to tenfold. [2] Behind non-O blood type [7] and factor V Leiden, prothrombin G20210A is one of the most common genetic risk factors for venous thromboembolism. [4]
Some other risk factors are poor ejection fraction (<35%), size of infarct, and the presence of AF. In the first three months after infarction, left-ventricle aneurysms have a 10% risk of emboli forming. Patients with prosthetic valves also carry a significant increase in risk of thromboembolism.
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