Aspirin resistance: a review of diagnostic methodology, mechanisms, and clinical utility.

Ingestion of a daily aspirin in patients with coronary artery disease decreases the rate of occlusive atherosclerotic events by about 25 percent. Some patients whose platelets are minimally inhibited by aspirin are categorized as aspirin resistant. Three reports document an increased risk for future vascular events in aspirin resistant patients. Aspirin's platelet inhibitory effect is measured using a variety of techniques. The demarcation between minimal and expected aspirin inhibition of platelets is arbitrarily determined by each investigator which leads to confusion in translating these reports to patient care. The focus of this report is the relative merits of the different techniques and their utility for defining patients with minimal aspirin induced platelet inhibition. The clinically useful mechanisms underlying decreased aspirin induced platelet inhibition include failure of a patient to take their daily aspirin, poor compliance, and nonsteroidal anti-inflammatory drugs (NSAIDs) interference with aspirin's ability to get to its binding site on the cyclooxygenase enzyme-1 (COX-1)]. Compliance is best assessed by comparing the results obtained with arachidonic acid (AA) stimulated light aggregation at two time points. The first time point is while the patient is supposedly taking their usual daily aspirin and the second time point is 2 hours after the patient is observed to ingest 325 mg of aspirin. After observed ingestion of aspirin, those patients with minimal aspirin inhibition of platelets are best detected using light aggregation stimulated by a new platelet agonist platelet prostaglandin agonist (PPA). In order for the results of a particular technique to be clinically meaningful it must be shown that those patients with minimal aspirin inhibition of platelets have an increased risk for a future vascular event that is independent from known major cardiovascular risk factors.