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Background—Unstable angina is associated with enhanced lipid peroxidation and reduced antioxidant defenses. We have previously reported aspirin failure in the suppression of enhanced thromboxane (TX) biosynthesis in a subset of episodes of platelet activation in this setting. We tested the hypothesis that the in vivo formation of the F₂-isoprostane 8-iso-prostaglandin (PG)F_2α, a bioactive product of arachidonic acid peroxidation, is enhanced in unstable angina and contributes to aspirin-insensitive TX biosynthesis.

Methods and Results—Urine samples were obtained from patients with unstable angina (n=32), stable angina (n=32), or variant angina (n=4) and from 40 healthy subjects for the measurement of immunoreactive 8-iso-PGF_2α and 11-dehydro-TXB₂. 8-Iso-PGF_2α excretion was significantly higher in patients with unstable angina (339±122 pg/mg creatinine) than in matched patients with stable …