Abstract 1187: The Metabolic Syndrome is Associated with Impaired Inhibition of Platelet Function by Low-Dose Aspirin
Aspirin (ASA) prophylaxis for coronary artery disease (CAD) is recommended for persons with the metabolic syndrome (MetS). We determined the extent to which persons with MetS who also have increased familial risk for CAD accrue the expected antiplatelet benefits from ASA. We examined 2089 apparently healthy persons (58% female, mean age 44 years, 60% white) with a family history of CAD for the components that comprise MetS according to the Adult Treatment Panel-III definition. We assayed whole blood for ex vivo platelet aggregation induced by 10 μM arachidonic acid (AA) and assessed a measure of in vivo platelet activation using urinary 11-dehydrothromboxane B2 (T×M), at baseline and after two week treatment with 81 mg/day aspirin. We used generalized estimating equation regression analysis accounting for intrafamilial correlation, and platelet measures are presented standardized for the average of the study sample. Post-ASA platelet measures were adjusted for pre-ASA levels to isolate the ASA effect. At baseline, in multivariable analyses adjusted for race, age, sex and risk factors, compared to persons without the metabolic syndrome, those with MetS had more aggregable platelets in response to AA and higher levels of T×M (Table⇓). Post-aspirin, nearly all individuals had complete suppression of platelet aggregation to arachidonic acid (median aggregation 0 Ohms). However, the odds for retention of any aggregation to AA were greater in those with MetS (Table⇓). T×M levels remained higher in those with MetS even post-ASA, adjusting for pre-ASA T×M levels. Among persons with an increased risk for CAD, the metabolic syndrome was associated with greater platelet aggregation and activation both before and following aspirin, suggesting that low dose aspirin therapy alone may not be sufficient to provide optimal antiplatelet protection in persons with the metabolic syndrome.