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Statin use in acute coronary syndromes: cellular mechanisms and clinical evidence
Robert S Rosenson1, Alan S Brown
1Preventive Cardiology Center, Division of Cardiology, Department of Medicine, Northwestern University, The Feinberg School of Medicine, Chicago, IL 60611, USA. r-rosenson@nothwestern.edu
Purpose Of Review:
Review the cellular mechanisms and clinical evidence for the use of statins in patients with unstable coronary syndromes.
Recent Findings:
Clinical trials of statin therapy in acute coronary syndromes demonstrate a rapid improvement in endothelial function, improved perfusion to ischemic myocardium, and an early reduction in cardiovascular events. The early benefit of statin therapy is related to a combination of molecular mechanisms that involve the oxidized LDL receptor (LOX-1), endothelial localized nitric oxide synthase, inflammatory cytokines, interstitial collagenases, and tissue factor expression. In human atheroma, 3 months' use of statin (pravastatin) therapy reduced the content of oxidized LDL, inflammatory cells (macrophage, T cells) infiltrates, and improved plaque stability by increasing the collagen content of the fibrous cap.
Summary:
The antiatherothrombotic effects of statin therapy appear to have important clinical relevance to patients with impaired myocardial perfusion and acute coronary syndrome.