Redefining Risk in Acute Coronary Syndromes Using Molecular Medicine
Saif Anwaruddin, MD*,
Arman T. Askari, MD, FACC* and
Eric J. Topol, MD, FACC ,1,*
* Department of Cardiovascular Medicine, The Cleveland Clinic, Cleveland, Ohio
Division of Cardiovascular Diseases, Scripps Clinic, La Jolla, California.
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Figure 1 Platelets: Key Mediators of Inflammation
CD40R = CD40 receptor; GP-1b = glycoprotein 1b receptor; IL-8 = interleukin 8; MCP-1 = monocyte chemoattractant protein-1; PSGL = P-selectin glycoprotein ligand; sCD40 = soluble CD40; vWF = von Willebrand factor.
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Figure 2 Leukocyte Secretory Products
HGF = hepatocyte growth factor; IFN- = interferon gamma; IL-18 = interleukin-18; LDL = low-density lipoprotein; MCP-1 = monocyte chemoattractant protein-1; MMPs = matrix metalloproteinases; MPO = myeloperoxidase; NO = nitric oxide; VCAMs = vascular cell adhesion molecule.
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Figure 3 A Model of Risk Stratification Based on a Representative Panel of Molecular and Genetic Factors
ACS = acute coronary syndrome; CRP = C-reactive protein; EPC = endothelial progenitor cell; FLAP = 5-lipoxygenase activating protein pathway; fn = platelet function; IL = interleukin; LTA4 = leukotriene A4 pathway; MMPs = matrix metalloproteinases; MPO = myeloperoxidase; PAI-1 = plasminogen activator inhibitor; PAPP-A = pregnancy-associated plasma protein A; sCD40L = soluble CD40 ligand; TNF- = tumor necrosis factor alpha; VEGF = vascular endothelial growth factor; vWF = Von Willebrand factor.
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