Abstract 4538: Poor Response to Aspirin in Patients with Peripheral Arterial Disease Enrolled in the Effect of Lipid Modification on Peripheral Arterial Disease after Endovascular Intervention Trial (ELIMIT)
Background: Increased platelet aggregation and variable response to aspirin (ASA) have been reported in patients with peripheral arterial disease (PAD). We examined the prevalence of poor response to ASA defined as arachidonic acid (AA) induced platelet aggregation >30% in patients with PAD enrolled in the ELIMIT.
Methods: PAD patients (n=45), on ASA, with baseline platelet function tests were included. Platelet function was measured by optical aggregometry with agonists including epinephrine, adenosine diphosphate (ADP), collagen and AA (0.5 mg/ml). Also, the time for a platelet plug to close an aperture in a Platelet Function Analyzer (PFA)-100 with collagen/epinephrine (CEPI) and collagen/ADP (CADP) cartridges was measured.
Results: In all, 24.4% (n=11) of the patients had AA aggregation >30%. Patients with AA aggregation >30% had shorter closure time in the CEPI cartridge (136 ± 21.9 vs. 253.4 ± 13.6 seconds; p<0.001) and a higher percent aggregation with fibrillar type I collagen (89.6 ± 3.1 vs. 75.1±3.3%; p=0.02). Significant association was observed between AA aggregation >30% and CEPI closure time <164 sec (χ2 statistic 9.7; p=0.002), but no association was noted with ADP induced aggregation >70% ( χ2 statistic 1.7; p=0.18) (other suggested markers of poor response to ASA). A CEPI closure time <164 sec identified 7/10 patients with AA aggregation ≥30% while the ADP aggregation >70% identified only 5/11 patients. No association was noted with CADP closure time (p=0.93) or epinephrine induced aggregation (p=0.91).
Conclusion: There are a significant number of PAD patients with evidence of poor ASA response, although non compliance cannot be excluded. Patients enrolled in ELIMIT will have multiple follow up visits which will enable differentiating true non responders and non compliance. AA induced aggregation was significantly associated with PFA-100 thrombosis closure time measured with CEPI, but not CADP. Our data suggests that poor response to ASA may be a significant problem in PAD patients and common methods to identify poor ASA response are not always correlated. Experimental validation of these different methods and further definition of poor response to ASA in PAD patients should be pursued.