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e0635 The evaluation to the efficacy and safety of tirofiban in acute coronary syndrome patients with clopidogrel resistance during percutaneous coronary intervention

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Objective To assess the efficacy and safety of the tirofiban in acute coronary syndrome patients with clopidogrel resistance undergoing selective percutaneous coronary intervention (PCI). Methods A total of 90 acute coronary syndrome patients with clopidogrel resistance were randomised into two groups, the high maintenance clopidogrel group (HMCG, n=50) and the tirofiban group (TG, n=40). All the patients underwent PCI after 7-10 day's medical treatment. Clinical information was collected. The platelet aggregation rate (PAR) were measured, and the markers of platelet activation, PAC-1 and CD62P were measured. Result There was no significant difference in baseline data between two groups. The expression rate of CD62P and PAC-1 in HMCG and TG were higher than the normal control group, but no difference between clopidogrel group and the tirofiban group. After the medical treatment the expression rate of CD62P and PAC-1 in TG is higher than that in HMCG (p<0.05). At the time of 0.5 h after PCI, the expression rate of CD62P and PAC-1 is higher than that before PCI (p<0.05). Until 12 h after PCI the expression rate of CD62P and PAC-1 is dropped down to the level before PCI. There were less MACE cases in TG than that in HMCG in hospital (p<0.05), but no significant difference in haemorrhage events between two groups. Conclusion 150 mg/d clopidogrel can inhibit the activation of platelet but 75 mg/d clopidogrel can't in patients of ACS with clopidogrel resistance. Tirofiban can decreases the MACE cases of patient with clopidogrel resistant during PCI but do not increase the haemorrhage events.
Title: e0635 The evaluation to the efficacy and safety of tirofiban in acute coronary syndrome patients with clopidogrel resistance during percutaneous coronary intervention
Description:
Objective To assess the efficacy and safety of the tirofiban in acute coronary syndrome patients with clopidogrel resistance undergoing selective percutaneous coronary intervention (PCI).
Methods A total of 90 acute coronary syndrome patients with clopidogrel resistance were randomised into two groups, the high maintenance clopidogrel group (HMCG, n=50) and the tirofiban group (TG, n=40).
All the patients underwent PCI after 7-10 day's medical treatment.
Clinical information was collected.
The platelet aggregation rate (PAR) were measured, and the markers of platelet activation, PAC-1 and CD62P were measured.
Result There was no significant difference in baseline data between two groups.
The expression rate of CD62P and PAC-1 in HMCG and TG were higher than the normal control group, but no difference between clopidogrel group and the tirofiban group.
After the medical treatment the expression rate of CD62P and PAC-1 in TG is higher than that in HMCG (p<0.
05).
At the time of 0.
5 h after PCI, the expression rate of CD62P and PAC-1 is higher than that before PCI (p<0.
05).
Until 12 h after PCI the expression rate of CD62P and PAC-1 is dropped down to the level before PCI.
There were less MACE cases in TG than that in HMCG in hospital (p<0.
05), but no significant difference in haemorrhage events between two groups.
Conclusion 150 mg/d clopidogrel can inhibit the activation of platelet but 75 mg/d clopidogrel can't in patients of ACS with clopidogrel resistance.
Tirofiban can decreases the MACE cases of patient with clopidogrel resistant during PCI but do not increase the haemorrhage events.

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