Why might lipids induce venous thrombosis?
Before the routine use of acetylsalicylic acid (ASA) and heparin, patients with acute myocardial infarction previously experienced high rates of VTE, often independent of their degree of immobilization during the recovery period [16,17,18]. Since then, systemic factors such as homocysteine [19,20,21] and antiphospholipid antibodies [22,23] have been shown to activate the coagulation cascade or impair the process of fibrinolysis, resulting in both arterial and venous thrombosis [21,22]. Similarly, if dyslipidemia is a risk factor for VTE, just as for arterial thrombosis, then the underlying mechanism is also probably best conceptualized as a systemic, rather than merely a depositional or ‘venosclerotic’ [24], disorder within the vessel wall.
