Abstract
Aim: Anti-platelet therapy with aspirin (ASA) reduces nonfatal myocardial infarction, stroke, and cardiovascular death by irreversibly inhibiting platelet COX-1 and TxA2 production. However, variable TxA2 inhibition is common. We studied the relationship of urinary 11dhTxB2, an inactive TxA2 metabolite, with all-cause mortality in stable coronary artery disease (CAD) patients on ASA treatment.
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