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(Circulation. 2002;106:2041.)
© 2002 American Heart Association, Inc.

Editorial

Statins as Potent Antiinflammatory Drugs

David J. Lefer, PhD

From the Department of Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, La.

Correspondence to David J. Lefer, PhD, Department of Molecular and Cellular Physiology, 1501 Kings Highway, Shreveport, LA 71130. E-mail dlefer@lsuhsc.edu

Key Words: Editorials • statins • nitric oxide synthase • leukocytes

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

Statin drugs have previously been shown to very significantly reduce cardiovascular disease events in a number of large clinical trials.¹ As a result, statins are now considered to represent one of the most powerful classes of agents for the treatment of cardiovascular diseases.² Statins are rapidly becoming frontline therapy for diabetes mellitus, hypertension, and other known cardiovascular disease risk factors. Originally, reductions in cardiovascular disease events and mortality and overall improved outcomes were attributed to dramatic reductions in circulating serum lipid levels that were mediated by inhibition of liver 3-hydroxy 3-methyl glutaryl coenzyme A (HMG-CoA) reductase.¹ However, more recent experimental and clinical investigations have revealed that statins can exert a number of cholesterol-independent, cardioprotective actions. In this regard, statins are potent modulators of endothelial cell nitric oxide synthase (eNOS) function and have been shown to upregulate eNOS enzyme levels and nitric oxide (NO) synthesis.^3–5

See p 2104

Pruefer and colleagues⁶ now demonstrate in this issue of Circulation powerful antiinflammatory properties of simvastatin in the setting of Staphylococcus aureus -toxin infection. Endotoxemia represents a potent stimulus for vascular inflammation that is characterized by enhanced leukocyte recruitment to the microvascular endothelium. The report by Pruefer et al⁶ elegantly demonstrates that pretreatment with clinically relevant doses of simvastatin attenuates endotoxin-induced leukocyte rolling and transmigration in the rat mesentery. Simvastatin was administered 18 hours before administration of endotoxin. Simvastatin therapy also resulted in a 50% upregulation of eNOS expression in the endothelium and a 50% decrease in endothelial cell P-selectin expression. Circulating cholesterol levels . . . [Full Text of this Article]

Related Article:

Simvastatin Inhibits Inflammatory Properties of Staphylococcus aureus -Toxin

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Circulation 2002 106: 2104-2110. [Abstract] [Full Text]

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