Peri-Procedural Platelet Function and Platelet Inhibition in Percutaneous Coronary Intervention
Dean J. Kereiakes, MD, FACC*,*,
Paul A. Gurbel, MD, FACC
* Christ Hospital Heart and Vascular Center/the Lindner Research Center, Cincinnati, Ohio
Sinai Center for Thrombosis Research, Sinai Hospital of Baltimore, Baltimore, Maryland.
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Figure 1 Mechanisms of Platelet Activation and Inhibition
Platelet activation and mechanism of action of antiplatelet agents. ADP = adenosine diphosphate; ATP = adenosine triphosphate; CD40L = CD 40 ligand; COX = cyclooxygenase; GP = glycoprotein; PAI = plasminogen activator inhibitor; PDGF = platelet-derived growth factor TXA2 = thromboxane A2; vWF = von Willebrand factor. Adapted from Mehta SR, Yusuf S. Short- and long-term oral antiplatelet therapy in acute coronary syndromes and percutaneous coronary intervention. J Am Coll Cardiol 2003;41 Suppl S:79S–88S.
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Figure 2 Response Distribution to Clopidogrel
Normal distribution of the absolute change in 20-µmol/l adenosine diphosphate (ADP)-induced aggregation ( A). All of the patients under the double-headed arrow meet the definition for nonresponsiveness (NR). The distribution is shifted rightward in the 600-mg group indicating greater inhibition (responsiveness to clopidogrel). Reproduced with permission from the American College of Cardiology (72).
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