COMPARISON OF IMPEDANCE WHOLE BLOOD AGGREGATION AND OPTICAL PLATELET-RICH PLASMA AGGREGATION TO MEASURE THE ANTIPLATELET EFFECT OF ASPIRIN IN HEALTHY CONTROLS AND IN PATIENTS WITH PERIPHERAL ARTERY DISEASE (PAD)
Abstract number: P-T-361
Tran1 H.A., Anand2 S.S., Ginsberg2 J.S., Weitz2 J.I., Johnston3 M., Eikelboom2 J.W.
11Clinical Haematology, Australian Centre for Blood Diseases, Melbourne, Australia 22Medicine, McMaster University 33Hemostasis Reference Laboratory, Henderson Research Centre, Hamilton, Canada
How-to-cite Tran HA, Anand SS, Ginsberg JS, Weitz JI, Johnston M, Eikelboom JW. COMPARISON OF IMPEDANCE WHOLE BLOOD AGGREGATION AND OPTICAL PLATELET-RICH PLASMA AGGREGATION TO MEASURE THE ANTIPLATELET EFFECT OF ASPIRIN IN HEALTHY CONTROLS AND IN PATIENTS WITH PERIPHERAL ARTERY DISEASE (PAD). J Thromb Haemost 2007; 5 Supplement 2: P-T-361
Introduction: Clinical aspirin resistance (failure to prevent a thrombotic clinical event) probably occurs in some patients from sub-optimal inhibition of platelet function. Although contemporary studies suggest a relation between "laboratory" and clinical aspirin resistance, experts disagree about the best test to measure aspirin's anti-platelet effect. To assess the anti-platelet effect of aspirin, impedance-based whole blood aggregation (IPWBA) and optical-based platelet rich plasma aggregation (OBPRPA) were performed in healthy controls and patients with PAD.
Methods: 44 healthy controls (77% women, median age 44 years) received aspirin 81 mg/d for 3 weeks and 40 patients with PAD (18% women, median age 67 years) were taking ongoing aspirin 81 mg/day. Citrated blood was collected prior to initiation of, and after completion of 3 weeks of aspirin in controls, and during ongoing aspirin in patients. The agonist used in all aggregation studies was 0.5mM arachidonic acid (AA).
Results: Controls showed inhibition of OBPRPA (84.014.4% [baseline] to 4.112.3% [3 weeks]) and IPWBA (12.73.3W [baseline] to 0.62.8W [3 weeks]). There was no significant correlation or weak correlation between OBPRPA and IPWBA (r=0.10, p=0.53), and at 3 weeks results were consistent with the "post-therapy" controls. IPWBA showed complete inhibition of platelet aggregation in 91% of post-treatment controls and 85% of cases at 3 weeks. There was no significant correlation between IPWBA and OBPRPA at 3 weeks (r=-0.04, p=0.79).
Conclusions: OBPRPA and IPWBA are both highly responsive to the ant-platelet effects of low-dose (81 mg/day) aspirin. Further studies should be undertaken to determine whether clinically useful cut-points for these assays can be identified that identify aspirin resistance.
To cite this abstract use the following format:
Journal of Thrombosis and Haemostasis 2007; Volume 5, Supplement 2: abstract number
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