Statin therapy and levels of hemostatic factors in a healthy population: the Multi‐Ethnic Study of Atherosclerosis: a rebuttal

HMG CoA reductase inhibitors (statins) have become the cornerstone in prevention of atherosclerotic disease.[1] Beyond their undeniable risk reduction for cardiovascular events, statins have also been described to exert favourable effects on venous thromboembolism (VTE) incidence as well. In a direct comparison with placebo, rosuvastatin has been shown to reduce the risk for venous thrombosis by 43% in apparently healthy persons.[2] Although the mechanisms by which statins affect hemostasis are not fully elucidated, previous studies reported that statins induce a reduction of plasminogen activator inhibitor-1 (PAI-1), tissue factor (TF), tissue plasminogen activator (tPA) and factor VII.[3] Furthermore, a recent study in mice revealed a direct link between the function of the low density lipoprotein receptor (LDLR) and factor VIII levels,[4] which was further substantiated by the finding that patients with dysfunctional LDLR function due to molecular defects in the LDLR gene are characterized by high factor VIII levels.[5] This article is protected by copyright. All rights reserve