Biological efficacy of low against medium dose aspirin regimen after coronary surgery: analysis of platelet function. Export

@article{citeulike:630498, abstract = {The failure of aspirin to inhibit platelet function has been documented in patients undergoing coronary artery bypass graft (CABG) surgery, but the causes of "aspirin-resistance" remain uncertain. The aim of this study was to investigate the efficacy of aspirin in patients undergoing CABG surgery receiving either 100 mg or 325 mg of oral aspirin for 5-days. Platelet function was tested the day before surgery and on day +1 and day +5, and evaluated by changes in collagen-induced thromboxane-A2 (TxA2) release and platelet aggregation following stimulation with collagen, ADP and epinephrine. In all patients, baseline platelet aggregation was significantly inhibited by pre-incubation with in vitro aspirin (150 micromol/l), with a mean reduction in TxA2-release of >or=95.5\% (82.3,99.1). After 5-days of oral aspirin, platelet aggregation was significantly inhibited, and was not further inhibited by in vitro aspirin. Oral aspirin was also associated with a >or=99.5\% (97.8, 99.7) reduction in TxA2-release, and with the reversal of the second-phase of ADP-induced aggregation which is TxA2-dependent. In addition a single-dose of 325 mg aspirin on the first post-operative morning may have a greater inhibitory effect on collagen-induced aggregation than 100 mg aspirin. Western blot analysis provided no evidence for the presence of COX-2 in platelets, while the up-regulation of p38-MAPK following platelet-stimulation and surgery was seen. The inhibition of COX-2 (NS398) or p38-MAPK (SB203580) activity did not affect platelet aggregation and TxA2-release on day +5. In summary, there was no evidence for inherent or acquired aspirin-resistance in this surgical population, or for the involvement of either COX-2 or p38-MAPK.}, address = {Department of Clinical Pharmacology, Papworth Hospital NHS Trust, Cambridge, CB3 8RE, UK. jacqueline.cornelissen@papworth.nhs.uk}, author = {Cornelissen, J. and Kirtland, S. and Lim, E. and Goddard, M. and Bellm, S. and Sheridan, K. and Large, S. and Vuylsteke, A.}, citeulike-article-id = {630498}, citeulike-linkout-0 = {http://dx.doi.org/10.1267/THRO06030476}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/16525576}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=16525576}, doi = {10.1267/THRO06030476}, issn = {0340-6245}, journal = {Thromb Haemost}, keywords = {aas-resistencia}, month = {March}, number = {3}, pages = {476--482}, posted-at = {2006-05-14 04:52:28}, priority = {3}, title = {Biological efficacy of low against medium dose aspirin regimen after coronary surgery: analysis of platelet function.}, url = {http://dx.doi.org/10.1267/THRO06030476}, volume = {95}, year = {2006} }

TY - JOUR ID - citeulike:630498 L3 - citeulike-article-id:630498 N2 - The failure of aspirin to inhibit platelet function has been documented in patients undergoing coronary artery bypass graft (CABG) surgery, but the causes of "aspirin-resistance" remain uncertain. The aim of this study was to investigate the efficacy of aspirin in patients undergoing CABG surgery receiving either 100 mg or 325 mg of oral aspirin for 5-days. Platelet function was tested the day before surgery and on day +1 and day +5, and evaluated by changes in collagen-induced thromboxane-A2 (TxA2) release and platelet aggregation following stimulation with collagen, ADP and epinephrine. In all patients, baseline platelet aggregation was significantly inhibited by pre-incubation with in vitro aspirin (150 micromol/l), with a mean reduction in TxA2-release of >or=95.5% (82.3,99.1). After 5-days of oral aspirin, platelet aggregation was significantly inhibited, and was not further inhibited by in vitro aspirin. Oral aspirin was also associated with a >or=99.5% (97.8, 99.7) reduction in TxA2-release, and with the reversal of the second-phase of ADP-induced aggregation which is TxA2-dependent. In addition a single-dose of 325 mg aspirin on the first post-operative morning may have a greater inhibitory effect on collagen-induced aggregation than 100 mg aspirin. Western blot analysis provided no evidence for the presence of COX-2 in platelets, while the up-regulation of p38-MAPK following platelet-stimulation and surgery was seen. The inhibition of COX-2 (NS398) or p38-MAPK (SB203580) activity did not affect platelet aggregation and TxA2-release on day +5. In summary, there was no evidence for inherent or acquired aspirin-resistance in this surgical population, or for the involvement of either COX-2 or p38-MAPK. IS - 3 JF - Thromb Haemost SN - 0340-6245 AD - Department of Clinical Pharmacology, Papworth Hospital NHS Trust, Cambridge, CB3 8RE, UK. jacqueline.cornelissen@papworth.nhs.uk EP - 482 TI - Biological efficacy of low against medium dose aspirin regimen after coronary surgery: analysis of platelet function. VL - 95 SP - 476 KW - aas-resistencia AU - Cornelissen, J AU - Kirtland, S AU - Lim, E AU - Goddard, M AU - Bellm, S AU - Sheridan, K AU - Large, S AU - Vuylsteke, A PY - 2006/03// UR - http://dx.doi.org/10.1267/THRO06030476 ER -