Refers to the inability of aspirin to inhibit platelet thromboxane A2 and therefore platelet activation and aggregation.
May correlate with increasing risk of cardiovascular disease.
Detected by assaying thromboxane A2 production or determining platelet function that is dependent on thromboxane A2 production.
Recurrent stroke, myocardial infarction or vascular deaths more likely to occur in aspirin non-responders than in responders, 40% vs. 4.4%, respectively.
Laboratory studies indicating aspirin resistance by optical platelet aggregation studies associated with increased risk of cardiovascular deaths, myocardial infarction and stroke.
Failed platelet inhibition associated with reocclusion of peripheral arterial angioplasties in patients with claudication.
Potential causes include inadequate dosage, drug interactions, genetic polymorphisms of COX-1 and thromboxane biosynthesis and increased platelet turnover.
Can be overcome by treating the causes and decreasing thromboxane production and activity and blocking platelet activation.