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J Am Coll Cardiol, 2005; 46:1425-1433, doi:10.1016/j.jacc.2005.05.086
© 2005 by the American College of Cardiology Foundation
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The Potential Relevance of the Multiple Lipid-Independent (Pleiotropic) Effects of Statins in the Management of Acute Coronary Syndromes

Kausik K. Ray, MRCP, MD* and Christopher P. Cannon, MD, FACC

Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts



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  		Figure 1 "Pathological vascular triad" implicated in acute coronary syndrome. Illustration by Rob Flewell.

 


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  		Figure 2 Molecular pathway. Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibits cholesterol synthesis and isoprenoid production (geranyl-geranyl pyrophosphate and farnesyl pyrophosphate). This in turn reduces prenylation of G proteins such as Rho, and hence membrane binding. Illustration by Rob Flewell.

 


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  		Figure 3 Endothelial abnormalities in acute coronary syndrome. ET = endothelin; ICAM = intercellular adhesion molecule; NO = nitric oxide; PAI = plasminogen activator inhibitor; t-PA = tissue plasminogen activator; TF = tissue factor; TM = thrombomodulin; VCAM = vascular cellular adhesion molecule. Illustration by Rob Flewell.

 


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  		Figure 4 Inflammatory changes in acute coronary syndrome. CRP = C-reactive protein; IFN = interferon; IL = interleukin; MCP = monocyte chemoattractant protein; MMP = matrix metalloproteinases; MPO = myeloperoxidase; TNF = tumor necrosis factor. Illustration by Rob Flewell.

 




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Copyright © 2005 by the American College of Cardiology Foundation.