Semin Thromb Hemost 1997; 23(4): 349-356
DOI: 10.1055/s-2007-996108
Copyright © 1997 by Thieme Medical Publishers, Inc.

Aspirin and Platelets: The Antiplatelet Action of Aspirin and Its Role in Thrombosis Treatment and Prophylaxis

Karsten Schrör
  • From the Institut für Pharmakologie, Heinrich-Heine-Universität Düsseldorf Düsseldorf, Germany.
Further Information

Publication History

Publication Date:
08 February 2008 (online)


The antithrombotic action of aspirin (acetylsalicylic acid) is due to inhibition of platelet function by acetylation of the platelet cyclooxygenase (COX) at the functionally important amino acid serine529. This prevents the access of the substrate (arachidonic acid) to the catalytic site of the enzyme at tyrosine385 and results in an irreversible inhibition of platelet-dependent thromboxane formation. Aspirin is an approximately 150- to 200-fold more potent inhibitor of the (constitutive) isoform of the platelet enzyme (COX-1) than the (inducible) isoform (COX-2) which is expressed by cytokines, inflammatory stimuli, and some growth factors. This explains the different dosage requirements of aspirin as an antithrombotic (COX-1) and an anti-inflammatory drug (COX-2), respectively.

Aspirin is the “gold standard” antiplatelet agent for prevention of arterial thromboses. The optimum dose of aspirin as an antithrombotic drug can differ in different organ circulations. While 100 mg/day is sufficient for prevention of thrombus formation in the coronary circulation, higher doses may be required for the prevention of vascular events in the cerebral and peripheral circulation. However, any effective antiplatelet dose of aspirin is associated with an increased risk of bleeding. Therefore, the individual benefit/risk ratio determines the administration of the compound.

There are no known prostaglandin-independent mechanisms for the antithrombotic action of aspirin in clinical use. Thus, platelet activation caused by other factors remains unchanged and might result in a resistance against inhibition of platelet function by aspirin. This involves platelet activation by shear stress and ADP. Additionally, there is no “sparing” of endothelial prostacyclin synthesis in clinical conditions of atherosclerotic endothelial injury. In this case, inhibition of COX-1 by aspirin will also reduce the amount of precursors for vascular prostacyclin synthesis, provided, for example, from adhering platelets.