Statins in venous thrombosis: biochemical approaches to limiting vascular disease

Venous thrombosis (deep vein thrombosis or pulmonary embolism) is a common and potentially lethal disease that occurs each year in about 1–2 of 1000 people. (1) The condition can be prevented and treated with anticoagulants, but as a side effect, bleeding often occurs. (2) Currently, the duration of treatment of venous thrombosis with anticoagulants depends on whether the event was provoked or not. (3) Provoking risk factors, such as surgery, immobilization, and use of oral contraceptives, are transient causes. This will temporarily increase the “thrombotic potential” of a person which explains, for example, why recurrence risk is low (<1%) in patients who developed their first event after surgery. Patients with provoking risk factors are usually treated for 3–6 months only, while patients with unprovoked thrombosis are prescribed treatment for a longer period. This decision is based on the high incidence of venous recurrence in patients with unprovoked events (30% within 5 years after the 3–6 months of oral anticoagulation). (4 and 5) Only 40%–50% of patients can be classified as patients with provoked events, which leads to a dilemma in the other 50%–60% of patients: discontinuing treatment may lead to a new venous thrombotic event, while continuing oral anticoagulant treatment overtreats the majority of patients and is accompanied with a yearly 1%–3% risk of major bleeding. (2 and 6) Therefore, novel therapeutic strategies that are not associated with bleeding complications need to be sought.