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Optimal suppression of thromboxane a₂ formation by aspirin during percutaneous transluminal coronary angioplasty: no additional effect of a selective cyclooxygenase-2 inhibitor

Dermot Kearney, MD^*, Anthony Byrne, MD^*, Peter Crean, MD, FRCPI, Dermot Cox, PhD^* and Desmond J. Fitzgerald, MD, FRCPI^*,*

^* Department of Clinical Pharmacology, RCSI, Dublin, Ireland
Department of Cardiology, St. James' Hospital, Dublin, Ireland

View larger version (15K): [in a new window]   Figure 1 Urinary excretion of 11-dehydro thromboxane B2 (Tx-M) in patients on fradafiban alone, aspirin alone, or aspirin plus nimesulide prior to and at selected intervals during and following percutaneous transluminal coronary angioplasty (PTCA). Urinary Tx-M was higher in the fradafiban group prior to PTCA than in normal subjects (p < 0.05) and increased markedly during the procedure compared with aspirin alone (p < 0.0001).

View larger version (17K): [in a new window]   Figure 2 Urinary excretion of 8-epi PGF2 in patients on fradafiban alone, aspirin alone, or aspirin plus nimesulide prior to and at selected intervals during and following percutaneous transluminal coronary angioplasty (PTCA). There were no differences between the treatment groups and normal control subjects before PTCA. Although there was no significant change in the groups individually, when all three groups were considered together, the level of urinary 8-epi PGF2 was elevated after PTCA compared to normal subjects (p = 0.002).

View larger version (14K): [in a new window]   Figure 3 Urinary excretion of 2,3 dinor-6-keto-PGF1 (PGI-M) in patients on aspirin or aspirin and nimesulide prior to and at selected intervals during and following percutaneous transluminal coronary angioplasty (PTCA). The addition of nimesulide caused a significant drop in PGI-M formation compared to aspirin alone prior to (p = 0.018) and over the period of sampling after PTCA (p = 0.001).