Key result
Higher urinary 11-dehydro thromboxane B2 linked to ~80% greater risk of major CV events on aspirin.
Why the study?
It was uncertain whether aspirin resistance, defined by failure to suppress thromboxane generation, increases cardiovascular event risk in high-risk patients.
Does elevated urinary 11-dehydro thromboxane B2 (aspirin resistance) increase the risk of myocardial infarction, stroke, or cardiovascular death in high-risk patients treated with aspirin?
Comparison
Upper quartile vs lower quartile of urinary 11-dehydro thromboxane B2 levels
Design
Nested case-control study
Follow-up
5 years
Authors
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Should not yet change aspirin therapy; leaves open whether 11-dehydro thromboxane B2 identifies modifiable risk.
Case-Control (n=976)
Does elevated urinary 11-dehydro thromboxane B2 (aspirin resistance) increase the risk of myocardial infarction, stroke, or cardiovascular death in high-risk patients treated with aspirin?
Effect estimate: OR 1.8 (95% CI 1.2 to 2.7)
p-value: p=0.009
Elevated urinary 11-dehydro thromboxane B2 levels in aspirin-treated patients predict a higher risk of future myocardial infarction or cardiovascular death, suggesting aspirin resistance.
Eikelboom et al. (2002) conducted a case-control in High risk for cardiovascular events (n=976). Upper quartile of urinary 11-dehydro thromboxane B2 vs. Lower quartile of urinary 11-dehydro thromboxane B2 was evaluated on Composite outcome of myocardial infarction, stroke, or cardiovascular death (OR 1.8, 95% CI 1.2 to 2.7, p=0.009). Aspirin-treated patients in the upper quartile of urinary 11-dehydro thromboxane B2 had a higher risk of MI, stroke, or CV death than those in the lower quartile (OR 1.8; 95% CI 1.2-2.7; P=0.009).
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