BACKGROUND AND AIM: Controversial reports have been published about the efficiency of potent platelet inhibitors in patients with coronary artery syndrome (CAS). We therefore questioned whether a functional change in platelets affects the patient's response to ASA. STUDY DESIGN AND METHODS: Nineteen consecutive patients presenting with unstable coronary syndrome and 15 healthy volunteers were included. No platelet inhibitory drugs or coumarin were used in either group before the study. Platelet aggregation tests were performed on baseline samples and after a single dose of ASA. Afterwards, all patients underwent coronary angiography to exclude non-CAS. RESULTS: In the patient group (n=15 after exclusion) no significant increase in bleeding constant was found after ASA, using a PFA analyser, in contrast to the control group. The maximal velocity and the maximal percentage optical platelet aggregation using ADP was significantly more reduced in the control group. ASA did not significantly reduce the thromboxane B2 production in the patient group. CONCLUSION: ASA has less platelet inhibitory effects in patients with unstable CAS in comparison with healthy volunteers. Platelets, in the hyperactive state of unstable CAS, prove to be less subject to inhibition. This might add to the explanation of the lack of efficiency of platelet inhibitory drugs to prevent thrombotic complications after PTCA and platelet aggregation onto stent surfaces in patients with acute CAS.
BACKGROUND AND AIM: Controversial reports have been published about the efficiency of potent platelet inhibitors in patients with coronary artery syndrome (CAS). We therefore questioned whether a functional change in platelets affects the patient's response to ASA. STUDY DESIGN AND METHODS: Nineteen consecutive patients presenting with unstable coronary syndrome and 15 healthy volunteers were included. No platelet inhibitory drugs or coumarin were used in either group before the study. Platelet aggregation tests were performed on baseline samples and after a single dose of ASA. Afterwards, all patients underwent coronary angiography to exclude non-CAS. RESULTS: In the patient group (n=15 after exclusion) no significant increase in bleeding constant was found after ASA, using a PFA analyser, in contrast to the control group. The maximal velocity and the maximal percentage optical platelet aggregation using ADP was significantly more reduced in the control group. ASA did not significantly reduce the thromboxane B2 production in the patient group. CONCLUSION:ASA has less platelet inhibitory effects in patients with unstable CAS in comparison with healthy volunteers. Platelets, in the hyperactive state of unstable CAS, prove to be less subject to inhibition. This might add to the explanation of the lack of efficiency of platelet inhibitory drugs to prevent thrombotic complications after PTCA and platelet aggregation onto stent surfaces in patients with acute CAS.
Authors: C Bihour; C Durrieu-Jaïs; L Macchi; C Poujol; P Coste; P Besse; P Nurden; A T Nurden Journal: Arterioscler Thromb Vasc Biol Date: 1999-02 Impact factor: 8.311
Authors: J H Alexander; R A Harrington; R H Tuttle; L G Berdan; A M Lincoff; J W Deckers; M L Simoons; A Guerci; J S Hochman; R G Wilcox; M M Kitt; P R Eisenberg; R M Califf; E J Topol; K Karsh; W Ruzyllo; J Stepinska; P Widimsky; J B Boland; P W Armstrong Journal: Am J Cardiol Date: 1999-04-15 Impact factor: 2.778
Authors: M Capanni; D Prisco; E Antonucci; L Chiarugi; V Boddi; R Abbate; C Giglioli; R P Dabizzi; M Margheri; I Simonetti; G F Gensini Journal: Int J Clin Lab Res Date: 1999