Abstract 5067: Responsiveness to Low Dose Aspirin Influences Levels of Inflammatory Biomarkers
Platelets participate in cellular and humoral immunity; however the effect of low dose aspirin (ASA) therapy on platelet-mediated inflammation is unknown. Healthy family members (N=1934) of patients with premature coronary artery disease (CAD) participated in a 14-day trial of ASA 81 mg/day. Urinary 11-dehydro thromboxane B2 (uTxM), which reflects in vivo platelet activation, was measured at baseline and after ASA. Subjects were dichotomized by post-ASA uTxM levels into ASA responsive (lower quartile) and ASA resistant (upper quartile) groups based on previous studies showing an association between the upper quartile and incident CAD events. Levels of the inflammatory biomarkers, plasma hs-CRP and IL-6, were measured at both time points and compared between the two quartile extremes using multivariable-adjusted models. The study sample had 967 participants (females, 59%; blacks, 43%, age, 43.9±13 years). At baseline, plasma hs-CRP levels were similar between the upper and the lower uTxM quartiles, but IL-6 levels were significantly higher in the upper quartile (Table⇓). After ASA therapy, hs-CRP and IL-6 decreased in the lowest quartile, but increased in the upper (resistant) quartile, and the between-quartile difference (post-adjusted for pre) became significant for both inflammatory markers. Compared to ASA responsive subjects, those who are ASA “resistant” have higher levels of plasma inflammatory markers after ASA therapy and demonstrate lesser reductions in inflammatory markers from baseline. These extreme quartile differences in hs-CRP and IL-6 may reflect differences in ASA’s ability to suppress platelet-mediated inflammation, and may contribute to the increased CAD risk observed in aspirin resistant persons.