Statins decrease thrombin generation in patients with hypercholesterolemia.

Statins are cholesterol-lowering agents with antithrombotic effect possibly unrelated to their lipid-lowering properties. Traditional global coagulation tests failed, however, to reveal clinically relevant change after treatment. We therefore sought to investigate whether statins were able to modify thrombin generation in hypercholesterolemia. Fifty-one patients who needed treatment with statins were enrolled in this study. Thrombin generation, assessed as endogenous thrombin potential (the amount of thrombin generated after triggering coagulation with small amount of tissue factor) was measured at pre- and two months post-treatment with statins. The median (inter-quartile range) level of total cholesterol that was 325 mg/dL (278-405) decreased significantly [211 mg/dL (197-247)] at post-treatment (p<0.001); the median level of HDL cholesterol that was 49 mg/dL (43-56) increased significantly [55 mg/dL (47-66)] at post-treatment (p<0.001). The median endogenous thrombin potential (inter-quartile range) before treatment was 2372 nM·min (2008-2617) and decreased to 2,048 nM·min (1764-2375) (p<0.001) after treatment. The results support the hypothesis of a direct link between statins and coagulation through their capacity to lower thrombin generation in patients with hypercholesterolemia. The antithrombotic properties of statins could be mediated (at least in part) by their endogenous thrombin potential lowering effect. This interesting hypothesis warrants evaluation by clinical trials.