Abstract 12698: Differential Impact of Inflammation on Five Laboratory Assays Detecting Aspirin Resistance
Objectives: Inflammation has been postulated to modify platelet response to aspirin treatment, thereby causing aspirin resistance. Both high inflammatory markers and aspirin resistance have been linked to adverse cardiovascular events. We aimed to study the differential impact of inflammation on various assays measuring aspirin sensitivity.
Methods: In 288 patients on dual antiplatelet therapy (aspirin and clopidogrel), the following assays were performed to detect aspirin resistance in response to arachidonic acid (AA) stimulation one day after stent implantation: light transmission aggregometry (LTA), VerifyNow aspirin assay, multiple electrode aggregometry (MEA), and Impact-R. Urinary 11-dehydro thromboxane B2 (d-TXB2), interleukin-6 (IL-6) and high sensitivity CRP (hsCRP) were determined by immunoassay. For statistical analyses, highly skewed variables were log transformed when appropriate.
Results: IL-6 was an independent predictor of platelet reactivity when determined by d-TXB2 (P<0.001), LTA (P<0.01), and in trend by MEA (P=0.08) using multiple linear regression analysis. Accordingly, patients with supra-median IL-6 had significantly higher platelet reactivity than patients with infra-median IL-6 when determined by d-TXB2 (median [IQR] 61.4ng/mmol [37.8, 111.4] vs. 45.0ng/mmol [26.7, 65.3], P<0.0001) and LTA (% maximal aggregation: 4.4 [1.9, 8.2] vs. 3.0 [1.1, 7.5], P=0.02). Supra-median IL-6 levels were associated with 3.4-fold (95%CI 1.9-5.9) increased risk of high on-aspirin-treatment residual platelet reactivity as defined by the upper fourth quartile of d-TXB2. No influence of IL-6 on other assays was observed. Results of hsCRP were in line with those of IL-6.
Conclusion: In patients on long-term aspirin treatment, increased inflammatory markers are independently associated with residual platelet reactivity. However, these effects were most pronounced for d-TXB2, while only modest or no effects were found for other assays suggesting that additional aspirin-insensitive thromboxane generation might play a role. The observed influence of inflammation could also contribute to the previously described predictive role of d-TXB2 for adverse cardiovascular events.
- © 2011 by American Heart Association, Inc.