[Statins as Anti-Inflammatory Agents]

Statins modify cellular composition of atherosclerotic plaques decreasing their inflammatory elements capable to produce plaque destabilizing metalloproteinases and prothrombotic tissue factor. In humans long term administration of these drugs leads to decrease of levels of markers of inflammation notably of C-reactive protein. Possible mechanisms of anti-inflammatory action of statins include activation of peroxisome proliferator activated receptor alpha. Indirect evidence exists from studies with clinical end points that statins are effective in patients with elevated initial level of C-reactive protein (CARE) and that this phenomenon occurs irrespective of the initial LDL CH level (AFCAPS) and its changes during statin therapy. Thus administration of statins apparently is an intervention capable to selectively modify the harmful components of inflammation in the arteries and to create new avenue for the management of patients with cardiovascular disease who do not have hypercholesterolemia (R.Ross).