The HMG CoA reductase inhibitors reduce levels of low-density lipoproteins, raise high-density lipoproteins, and lower triglycerides. However, there are other pharmacological effects derived from HMG CoA reductase inhibitor therapy. Certain HMG CoA reductase inhibitors affect atherosclerotic plaque composition, endothelial function, platelet and clotting factors, and immune functioning. The unique extrahepatic pharmacological profile of agents in this class has not been fully characterized. All of the HMG CoA reductase inhibitors studied have improved endothelium-dependent vasodilatation. Vascular smooth muscle proliferation is not significantly affected by pravastatin but is by the other agents. Of all the HMG CoA reductase inhibitors, cerivastatin is the most potent inhibitor of vascular smooth muscle proliferation. Pravastatin is the only agent proven to significantly reduce platelet-thrombus formation and fibrinogen levels. Simvastatin has no effect on platelet-thrombus formation or fibrinogen levels, while atorvastatin and lovastatin have been shown to increase fibrinogen in some studies. Plasminogen activator inhibitor-1 levels are decreased by pravastatin, are not affected by atorvastatin, and are significantly increased by lovastatin and simvastatin. Pravastatin also has clinical benefits in transplant medicine as a result of inhibiting natural killer cell function, an effect that has not been explored with other HMG CoA reductase inhibitors.