No case of COX‐1‐related aspirin resistance found in 289 patients with symptoms of stable CHD remitted for coronary angiography

Abstract

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 ⩾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.

• Aspirin resistance
• coronary heart disease
• drug adherence
• platelet aggregation
• platelet function tests

Acknowledgements

Professor emeritus Sigurd Nitter‐Hauge, Department of Cardiology, The National University Hospital, Oslo, Norway is acknowledged.