Minimal Frequency of Aspirin Resistance after Observed Aspirin Ingestion.

Abstract

Poor compliance is an important cause of aspirin resistance. Our goal was to investigate amount of aspirin induced inhibition of platelets independent of compliance. We investigated the net amount of aspirin induced inhibition of platelets by comparing Platelet Prostaglandin Agonist (PPA) stimulated platelet aggregations before, off aspirin, with the platelet inhibition that occurred 2 hours after observed aspirin ingestion. 217 post-myocardial infarction patients who had taken aspirin for at least 30 days were evaluated at two time points. The first time point was 7 days after they had signed informed consent to stop taking aspirin as well as nonsteroidal anti-inflammatory drugs (NSAIDs). The second time point was 2 hrs after they were observed to ingest 325mg of aspirin. Platelets were evaluated using 2 different agonists in a light aggregometer. Arachidonic acid (AA) was used as a qualitative check to see if the patients at the first time point had really refrained from taking aspirin and NSAIDs for 7 days and PPA which mainly activates platelets via the prostaglandin pathway and can detect degrees of aspirin induced platelet inhibition. The slope of the PPA stimulated aggregation curve was used to measure aspirin induced platelet inhibition. The net aspirin response was calculated by determining the paired difference between the PPA slopes at the two time points. Compliance with the directive of not taking aspirin or NSAIDs before the first time point was checked with AA stimulated aggregometry and 45 patients were judged to be noncompliant. We defined aspirin resistance as a minimal change in PPA slope of 15 or less. Of the patients who had complied with the directive not to take aspirin or NSAIDs for 7 days as determined by AA aggregometry only 7 (3.2%) were aspirin resistant. The net aspirin response was directly related to the PPA slope off aspirin (p<0.001). When the 45 patients who were judged by AA aggregometry to be noncompliant with the directive to refrain from taking aspirin or NSAIDs were removed from the analysis, the direct relationship between the slope of the off aspirin PPA aggregation and the net aspirin response remained significant (p<0.001). The amount of platelet inhibition in the compliant group 42±16 was significantly larger than the platelet inhibition in the noncompliant group 36±16 (p=0.02). We conclude that: 1. a small percent of patients, 3.2%, whose net amount of aspirin induced platelet inhibition was less than 15 may be resistant to aspirin because of mechanisms unrelated to compliance and 2. The net amount of aspirin induced inhibition of platelets is directly related to the slope of the “off” aspirin PPA stimulated aggregation curve.