Aspirin resistance.
Aspirin resistance is the inability of aspirin to reduce platelet production of thromboxane A2 and thereby platelet activation and aggregation. Increasing degrees of aspirin resistance may correlate independently with increasing risk of cardiovascular events. Aspirin resistance can be detected by laboratory tests of platelet thromboxane A2 production or platelet function that depend on platelet thromboxane production. Potential causes of aspirin resistance include inadequate dose, drug interactions, genetic polymorphisms of COX-1 and other genes involved in thromboxane biosynthesis, upregulation of non-platelet sources of thromboxane biosynthesis, and increased platelet turnover. Aspirin resistance can be overcome by treating the cause or causes, and reduced by minimising thromboxane production and activity, and blocking other pathways of platelet activation. Future research is aimed at defining aspirin resistance, developing reliable tests for it, and establishing the risk of associated cardiovascular events. Potential mechanisms of aspirin resistance can then be explored and treatments assessed.
Department of Neurology, Royal Perth Hospital and School of Medicine and Pharmacology, University of Western Australia, Perth, WA, Australia.
Graeme J
GJ
Hankey
John W
JW
Eikelboom
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000493:pharmacokinetics / Q000627:therapeutic use*; D001241:Aspirin / Q000493:pharmacokinetics / Q000627:therapeutic use*; D001682:Biological Availability; D004351:Drug Resistance / Q000502:physiology*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D015995:Prevalence; D011379:Prognosis
D000894:Anti-Inflammatory Agents, Non-Steroidal; D001241:Aspirin