Chronic Application of Low-Dose Aspirin Affects Multiple Parameters of Three Blood Cellular Types and Antithrombin Activity: A 1:1:1 Propensity Score Matching Analysis

The mechanisms of aspirin antithrombotic actions have not been fully elucidated. We re-analyzed the data from the project Aspirin Resistance in Patients with Ischemic Atherothrombotic Diseases from April 2008 to June 2010. A total of 530 subjects were classified into 3 groups, including 40 patients without aspirin use, 24 patients taking 25-50 mg/d aspirin, and 466 patients taking 75-100 mg/d aspirin over 1 month. By 1:1:1 propensity score matching adjusting 15 primary clinical covariates, 51 patients (n = 17 per group) comprised the final sample. Hemostasis-related parameters and high platelet reactivity as measured by arachidonic acid-induced and adenosine diphosphate-induced light transmission aggregometry were compared in the 3 groups. A dose-dependent relationship was observed between aspirin and decreased high platelet reactivity incidence (PAA < 0.001, PADP < 0.01, respectively), decreased monocyte ratio (P = 0.052), increased antithrombin activity (P < 0.001), and increased platelet distribution width (P < 0.05). Aspirin at 25-50 mg/d is related to the lowest red blood cell (RBC) count, whereas 75-100 mg/d aspirin showed the highest RBC count among the 3 groups (4.52 ± 0.35 × 1012/L vs. 4.35 ± 0.57 × 1012/L vs. 4.80 ± 0.59 × 1012/L, P = 0.046). Our finding demonstrated that aspirin exerts its antithrombotic effects at least by antiplatelet function, enhancing antithrombin activity and suppressing monocytes in vivo. In addition, 3 blood cell types, namely RBCs, monocytes, and platelets, are involved in the aspirin antithrombotic mechanism. The cellular response to aspirin partially enhances the antithrombotic effects while partially inhibiting the effects.