The Role of Statins in Preventing Stroke

Nenad Trubelja, MD; Carl Vaughan, MD; Neil L. Coplan, MD


Prev Cardiol. 2005;8(2):98-101. 

In This Article

Anti-Inflammatory Actions of Statins

There is not a strong epidemiological association between hyperlipidemia and stroke. Studies that show statin therapy is associated with reduced incidence of stroke may be due to the effect of statins on factors such as inflammation. Engstrom et al.[26] demonstrated that patients with hyperlipidemia and elevated inflammatory markers (such as fibrinogen and haptoglobin) are at increased risk for ischemic stroke over long-term follow-up, but in the absence of these inflammation-sensitive proteins, hyperlipidemia was not a risk factor for stroke. Statin therapy suppresses T-cell activation and inhibits the release of proinflammatory cytokines[5,24,25] that are critical mediators of inflammatory and immunological responses in the brain and are produced by neurons, glial cells, and the endothelium.[26] Statin therapy also influences C-reactive protein levels, which is another important marker of inflammation that also appears to be an independent risk factor for the development of ischemic stroke.[27,28,29] Statin therapy reduces C-reactive protein level independent of its effect on serum LDL cholesterol. For example, in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS),[29] lovastatin appeared to be highly effective in reducing the risk of acute coronary events in participants with elevated C-reactive protein levels but no hyperlipidemia. Therefore, statins may be more effective in reducing cardiovascular events in patients with a high compared with low C-reactive protein level.[29]