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From the Department of Neurology (Dr. Hess), Medical College of Georgia and Veterans Affairs Medical Center, Augusta, GA; the Seaman Family MR Research Centre (Dr. Demchuk), Calgary, AB, Canada; the Department of Neurology (Dr. Brass), University of Texas-Houston Medical School, Houston, TX; and the Department of Neurology (Dr. Yatsu), Yale University School of Medicine and Veterans Affairs Medical Center, New Haven, CT.
Address correspondence and reprint requests to Dr. David C. Hess, Neuroscience (27), VA Medical Center, Augusta, GA 30904; e-mail: dhess{at}neuro.mcg.edu
Statins represent a promising class of agents to prevent stroke. In randomized trials of middle-aged patients with coronary artery disease, statins reduce the incidence of stroke. The reduction in stroke may not be solely related to cholesterol or low-density lipoprotein reduction but may involve nonsterol mechanisms effects on endothelial cells, macrophages, platelets, and smooth muscle cells. Statins also reduce the size of cerebral infarction in a murine stroke model, suggesting a neuroprotective effect. The best current evidence for stroke prevention is with pravastatin and simvastatin. Pravastatin reduces the risk of stroke in patients with coronary artery disease and average cholesterol levels; simvastatin reduces the risk of the combined endpoint of stroke and transient ischemic attack in hypercholesterolemic patients with coronary artery disease. Future studies of statins are needed in stroke populations, particularly the elderly.
Key words: HMG—CoA reductase inhibitors—Statins—Cholesterol—Stroke—Prevention
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