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CARDIOVASCULAR GENOMIC MEDICINE

Redefining Risk in Acute Coronary Syndromes Using Molecular Medicine

Saif Anwaruddin, MD^_*, Arman T. Askari, MD, FACC^_* and Eric J. Topol, MD, FACC^,_*

^_* Department of Cardiovascular Medicine, The Cleveland Clinic, Cleveland, Ohio
Division of Cardiovascular Diseases, Scripps Clinic, La Jolla, California

Manuscript received March 15, 2006; revised manuscript received August 28, 2006, accepted August 28, 2006.

^_* Reprint requests and correspondence: Dr. Eric J. Topol, Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037. (Email: etopol{at}scripps.edu).

Acute coronary syndromes represent a complex phenotype involving the interplay of many elements. The risk of developing an acute coronary syndrome and related complications has been defined by variables such as age, diabetes, smoking history, serum creatine phosphokinase, or electrocardiographic findings. However, in the past 5 years the wide-scale acceptance of a protein—troponin—has changed the diagnostic profile. With advances in molecular medicine, this protein is a segue to a panel of molecular assays that will improve screening and tailored intervention. We expound upon some of these factors and the potential they may carry in changing clinical medicine.

Abbreviations and Acronyms   ACS = acute coronary syndrome   CAD = coronary artery disease   CRP = C-reactive protein   EPC = endothelial progenitor cells   GP = glycoprotein   FLAP = 5-lipoxygenase activating protein pathway   LDL = low-density lipoprotein   MI = myocardial infarction

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