Thrombus formation is a multi-factor process which is influenced by a group of genetic and environmental factors. The main characteristics of clinically common thrombosis patients are familial inheritance, recurrent recurrence, severity of symptoms, abnormal site of thrombosis, and younger onset time.
Suspicion of arterial or venous thrombosis or thromboembolism requires objective evidence. Angiography is the diagnostic reference, but skilfully performed ultrasound can also examine superficial blood vessels and the heart.
Genetic predisposition is present in 25% to 50% of patients with angiographic evidence of spontaneous deep vein thrombosis. A congenital defects anticoagulant mechanism (such as factor Ⅴ activated protein C resistance, homocysteine levels, protein C deficiency, lack of protein S, antithrombin deficiency, fibrinolysis dysfunction), when combined with a thrombosis of the stimulus (such as surgery, pregnancy, birth control pills, for antiphospholipid antibodies) enough to vte. Patients with an early history of multiple site thrombosis have significantly more frequent and severe episodes than those with a single thrombosis.
Antithrombotic therapy is the use of thrombolytic drugs, antiplatelet drugs and anticoagulants. When developing antithrombotic treatment strategies, the first attention should be paid to thrombolytic therapy, since thrombolytic drugs can remove an existing thrombi. Antithrombotic therapy should be diversified, depending on whether the site of involvement is the venous or arterial circulatory system, the degree and location of vascular involvement, the spread of thrombosis, the risk of embolization or recurrence, and the relative advantages and disadvantages of antithrombotic therapy versus bleeding.