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• W2144857144 abstract "We examined the contribution of cyclooxygenase (COX)-1 and -2 to the generation of prostacyclin, thromboxane (Tx) A(2), and 8-epi prostaglandin (PG) F(2alpha) during percutaneous transluminal coronary angioplasty (PTCA).Both TxA(2) and 8-epi PGF(2alpha) activate platelets and are mitogenic, whereas prostacyclin is a platelet inhibitor, and therefore may influence the outcome of PTCA.Twenty-one patients undergoing PTCA while receiving aspirin 300 mg daily or aspirin plus the selective COX-2 inhibitor nimesulide were compared with 13 patients treated only with fradafiban, a glycoprotein IIb/IIIa antagonist. Urine was analyzed for the metabolites of TxA(2) (Tx-M) and prostacyclin (PGI-M) and for the isoprostane, 8-epi PGF(2alpha).In the fradafiban group, there was a marked increase in Tx-M during PTCA (mean, 1973; 95% confidence interval [CI] 112 to 3834 rising to mean 7645; 95% CI 2,009 to 13281 pg/mg creatinine, p = 0.018). The Tx-M excretion was similarly reduced by aspirin and the combination of aspirin and nimesulide. In contrast, the combination of nimesulide and aspirin inhibited PGI-M excretion to a greater extent than aspirin (p = 0.001). Urinary 8-epi PGF(2alpha) excretion was elevated following PTCA compared with normal subjects (p = 0.002) and appeared to be unaffected by any of the treatments.The increase in TxA(2) during PTCA is primarily COX-1 dependent, and aspirin alone is effective in suppressing its formation. In contrast, prostacyclin generation is both COX-1 and COX-2 dependent. The inhibition of COX-1 and COX-2 did not prevent the production of 8-epi PGF(2alpha), suggesting that this is not enzymatically derived. The persistent generation of 8-epi PGF(2alpha) may contribute to the thrombosis and restenosis that complicate PTCA." @default.
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• W2144857144 date "2004-02-01" @default.
• W2144857144 modified "2023-09-23" @default.
• W2144857144 title "Optimal suppression of thromboxane a2formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor" @default.
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• W2144857144 doi "https://doi.org/10.1016/j.jacc.2003.09.041" @default.
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