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(Stroke. 2004;35:1121.)
© 2004 American Heart Association, Inc.

Original Contributions

Editorial Comment—Statins, Stroke Outcome, and Stroke Prevention: When Should We Start Treatment?

Neurology Department, Rabin Medical Center, Petach Tikva and Tel Aviv University, Israel

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Statins or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are a group of potent hypocholesterolemic agents that are widely used throughout the world. Many long-term clinical studies have demonstrated that statin therapy is associated with a reduced risk of vascular events—mainly coronary—even in so-called normocholesterolemic patients. Accordingly, guidelines for cholesterol treatment have been and are being modified, particularly for patients with ischemic heart disease (IHD). The magnitude of the effects is large. A recent meta-analysis¹ has demonstrated that a decrease in low-density lipoprotein cholesterol levels by 1.8 mmol/L reduces the risk of IHD by 61% and the risk of stroke by 17%, preventing thromboembolic but not hemorrhagic strokes. The benefit of statins treatment has also been shown for patients with hypertension,² diabetes mellitus,³ severe aortic arch plaques,⁴ and for high-risk patients in general.⁵ For secondary stroke prevention, however, the data are still somewhat circumstantial⁶ and a specific study is underway.⁷ In many of the studies, the beneficial effects of the statins were not directly related to their lipid-lowering properties, and data on many other effects of statins is accumulating.^8,9 On the vascular wall, statins exert vasodilatation and plaque stabilizing effects by many ways, such as upregulation of endothelial nitric oxide synthase (eNOS), suppression of heightened macrophage activity with subsequent reduced production of several matrix metalloproteins and proinflammatory cytokines TNF, IL-6, CRP, and reduction of vascular expression of adhesion molecules. Because all these factors enhance the thrombogenic potential of the atherosclerotic plaque, statins have a role in ameliorating this risk. Antiatherogenic . . . [Full Text of this Article]

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