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(Circulation. 2003;108:III-22.)
© 2003 American Heart Association, Inc.
From the The Lindner Center for Research and Education, Ohio Heart Health Center, Ohio State University, Cincinnati, Ohio.
Correspondence to Dean J. Kereiakes, M.D., F.A.C.C., The Lindner Center for Research and Education, 2123 Auburn Avenue, Suite 424, Cincinnati, OH 45219. Fax: 513-585-4858, E-mail: lindner{at}fuse.net
Vascular inflammation is central to the pathogenesis of acute coronary syndromes (ACS) and the response to vascular injury after percutaneous coronary intervention (PCI). For both ACS and PCI, the magnitude of vascular inflammation is linked to adverse late clinical outcomes (e.g., death, recurrent myocardial infarction [MI] or ischemia, and restenosis). Many pharmacologic therapies with demonstrated efficacy for the treatment of ACS have anti-inflammatory properties, which are distinct from their perceived primary mechanism of action. The anti-inflammatory effects of aspirin, clopidogrel, low-molecular-weight heparin (LMWH), platelet glycoprotein (GP) IIb/IIIa receptor inhibitors, statins, and angiotensin converting enzyme (ACE) inhibitors are reviewed, and the hypothesis is generated that modulation of vascular inflammation at least in part contributes a common basis for the long-term clinical benefit ascribed to these medications. A therapeutic algorithm based on clinical risk stratification and coronary revascularization strategy is proposed for incorporating the current American College of Cardiology (ACC)/American Heart Association (AHA) guideline recommendations for treatment of patients who present with non-ST-elevation ACS.
Key Words: inflammation angioplasty pharmacology
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