Why the study?
Does plain aspirin reduce thromboxane B2 and prostaglandin E2 compared to enteric-coated aspirin 81 mg in patients with chronic stable coronary disease?
Does plain aspirin reduce thromboxane B2 and prostaglandin E2 compared to enteric-coated aspirin 81 mg in patients with chronic stable coronary disease?
Plain aspirin significantly reduces TXB2 and PGE2 levels compared to baseline enteric-coated aspirin 81 mg, suggesting that low-dose enteric-coated aspirin may not effectively inhibit these markers of platelet activation.
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Plain aspirin suppresses TXB2 and PGE2 far more than enteric-coated aspirin; challenges enteric-coated formulations as standard in stable CAD.
Background: All usual daily doses of plain aspirin inhibit thromboxane B2 (TXB2) as well as prostaglandin E2 (PGE2). The role of 81-mg enteric-coated aspirin (ECA) is controversial. Method: In a randomized, double-blind trial, 37 patients (25 men and 12 women) with chronic stable coronary disease taking ECA 81 mg at baseline were assigned to plain aspirin 81, 162.5, 325, 650 or 1300 mg daily for 12 weeks. At baseline and 12 weeks, blood was tested for TXB2 and PGE2. Results: All doses of plain aspirin produced virtually identical reductions in TXB2 and PGE2. For all doses combined, the mean ratio of the 12-week to baseline value was 0.03 for TXB2 (p < 0.001) and 0.63 for PGE2 (p < 0.001). Conclusion: These data indicate that ECA 81 mg daily does not inhibit TXB2 and PGE2, markers of acute and systemic responses to aspirin. Randomized trials designed a priori to test this hypothesis are necessary.
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Hennekens et al. (2012) studied this question.
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