Non-compliance is the predominant cause of aspirin resistance in chronic coronary arterial disease patients

Abstract

Background: Our previous publication showed that 9% of patients with a history of myocardial infarction MI. could be labeled as aspirin resistant; all of these patients were aspirin resistant because of non-compliance. This report compares the relative frequency of aspirin resistance between known compliant and non-compliance subjects to demonstrate that non-compliance is the predominant cause of aspirin resistance.

Methods: The difference in the slopes of the platelet prostaglandin agonist (PPA) light aggregation curves off aspirin and 2 hours after observed aspirin ingestion was defined as net aspirin inhibition.

Results: After supposedly refraining from aspirin for 7 days, 46 subjects were judged non-compliant with the protocol. Of the remaining 184 compliant subjects 39 were normals and 145 had a past history of MI. In known compliant subjects there was no difference in net aspirin inhibition between normal and MI subjects. Net aspirin inhibition in known compliant patients was statistically normally distributed. Only 3% of compliant subjects (2 normals and 5 MI) had a net aspirin inhibitory response of less than one standard deviation which could qualify as a conservative designation of aspirin resistance. A maximum of 35% of the 191 post MI subjects could be classified as aspirin resistant and/or non-compliant: 9% aspirin resistant because of non-compliance, 23% non-compliant with the protocol and possibly 3% because of a decreased net aspirin inhibitory response in known compliant patients.

Conclusion: Our data supports the thesis that the predominant cause of aspirin resistance is noncompliance.

Figure 1

Note that PPA demonstrates a gradual return of platelet aggregation to normal over 3 days. This characteristic of PPA stimulated aggregation makes it useful for measuring gradations of aspirin induced platelet inhibition. AA aggregation remains unresponsive for 3 days and returns to normal function between days 3 and 4. AA stimulated platelet aggregations were used to show if aspirin platelet inhibition was present or absent [31].

Figure 2

When the single point with the largest aspirin response is removed as a statistical outlier, the net aspirin inhibitory response distribution curve is judged to be normally distributed.

Figure 3

The seven subjects with less than 1 standard deviation decrease in their on aspirin slopes are depicted by open squares (□), those with a decrease in PPA slope between 1 and 2 standard deviations by solid diamonds (◆) and those with a greater than 3 standard deviation decrease by open circles (○). A direct relationship is observed between PPA slope off aspirin and the net aspirin inhibitory response. (p < 0.001).