Objective: To assess the prevalence of a lacking aspirin effect on cyclooxygenase-1 (COX-1) ("aspirin resistance") in patients with symptomatic, stable coronary heart disease (CHD) using test methods directly reflecting inhibition of COX-1.
Material and methods: Arachidonic acid (AA)-induced platelet aggregation and plasma thromboxane B2 (TXB2) were determined twice 3 weeks apart - prior to elective coronary angiography - in 289 patients on 75 or 160 mg aspirin daily, all prompted to take aspirin before testing. Subjects who demonstrated lacking any effect of aspirin (>/=20 % AA-induced aggregation) on one or both occasions were later given a third test. Forty-two patients not taking aspirin were used as TXB2 controls.
Results: Eleven (3.8 %) had aggregation > or = 20 % in at least one of the two initial tests, but only two on both occasions. During the third test, all 11 patients had aggregation <20 %. The TXB2 distributions in controls and study patients differed markedly (mean 173 versus 19 pg/mL). Taking 45 pg/mL as the TXB2 cut-off level, sensitivity and specificity for detecting subjects taking aspirin were 90 % and 89 %, respectively. The area under the ROC curve was 0.96.
Conclusion: Repeated AA-induced platelet aggregometry showed that COX-1 could be blocked by low-dose aspirin in all 289 tested patients, suggesting that aspirin resistance is rare in patients with stable CHD.