Among the various hypolipidemic drugs, 3-hydroxy-3-methyl-glutaryl-coenzyme A 
(HMG-CoA) reductase inhibitors (also known as "statins") belong to a 
heterogeneous class of compounds, sharing an identical hypocholesterolemic 
effect that develops through direct inhibition of a rate-limiting step in 
endogenous cholesterol synthesis. Their mechanism of action entails competitive 
inhibition of HMG-CoA reductase. Several lines of evidence suggest that the 
pleiotropic effects of statins may also play a role in prevention of venous 
thrombosis, wherein hypercholesterolemic patients are characterized by enhanced 
thrombin generation, increased susceptibility to endothelial dysfunction and 
platelet hyperreactivity, so that limiting or counteracting the burden of one or 
more of these mechanisms would provide an effective means of prophylaxis. 
Plausible biological links can also be found between statin therapy and 
reduction of thrombotic risk, mainly targeting immune system, blood coagulation, 
endothelium, lipid metabolism, and inflammation. The earlier JUPITER 
(Justification for the Use of Statins in Primary Prevention) trial provided 
appealing evidence that the risk of venous thrombosis may be lowered by statins. 
The results of the following studies and those of recent meta-analyses have, 
however, questioned this assumption. Currently, it seems thereby cautious to 
conclude that the use of statins as part of the approach used for preventing 
venous thromboembolism appears unwarranted. This is due to the existence of 
controversial clinical evidence, to the large number of patients who would need 
to be treated to prevent one case of venous thrombosis, as well as to the 
tangible risk of side effects. More randomized and the larger studies are needed 
before definitive conclusions can be drawn.