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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