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Grand Rounds | Clinician's Corner

Antiplatelet Therapy in Non–ST-Segment Elevation Acute Coronary Syndromes

Steven P. Schulman, MD
JAMA. 2004;292(15):1875-1882. doi:10.1001/jama.292.15.1875.
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Acute coronary syndromes are a frequent cause of hospital admission for patients with coronary artery disease. The pathophysiology of acute coronary syndromes often involves plaque rupture or fissure with platelet aggregation. Recognition of the importance of platelet aggregation resulted in several large randomized trials testing 3 types of platelet antagonists, aspirin, glycoprotein IIb/IIIa inhibitors, and adenosine diphosphate inhibitors. A thorough understanding of the data, risks, and benefits of these therapies is important to optimize treatment of the patient with an acute coronary syndrome. Recognition that there is a great deal of interpatient variability in response to these antiplatelet therapies highlights the need for future research in this area.

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Figure 1. Electrocardiogram on Patient Admission Demonstrating Diffuse Ischemic ST Depression and ST-Segment Elevation in Lead aVR
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Figure 2. Sites of Action of Antiplatelet Therapy on Mechanisms of Platelet Activation and Aggregation
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The final event in the pathway of platelet aggregation is binding of fibrinogen by activated glycoprotein (Gp) IIb/IIIa receptors on adjacent platelets. Thienopyridines—which inhibit stimulation of the adenosine diphosphate (ADP) receptor, P2Y12, and aspirin, which inhibits thromboxane A2 (TxA2) production resulting in decreased stimulation of the TxA2 receptor—interfere with steps leading to activation of Gp IIb/IIIa receptors. Glycoprotein IIb/IIIa inhibitors directly inhibit platelet aggregation at the Gp IIb/IIIa receptor. Factors that may limit the effectiveness of specific antiplatelet therapies are shown in the blue boxes. Ca indicates calcium; COX, cyclooxygenase.

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