Abstract 18621: Platelet Aggregation is Heightened in Those With Metabolic Syndrome and Less Effectively Mediated by Aspirin Therapy

Abstract

Background: Patients with metabolic syndrome (MetS) are at a higher risk of developing cardiovascular disease (CVD); however, interventions to mitigate this risk are not fully known. Platelets play a significant role in atherothrombosis, and aspirin is an important, yet controversial therapy used for the primary prevention of CVD. In this study, we examined platelet phenotype in MetS and degree of inhibition from ex vivo aspirin administration. Methods: In a study examining the mechanisms of atherothrombosis in pro-inflammatory conditions, patients without clinical CVD were enrolled and underwent phenotyping. Patients with MetS (n = 34, age 53.3 ± 13 years, 59% male) were compared to patients with no MetS (n = 63, age 41.1 ± 16 years, 52% male). Platelet aggregation of freshly isolated platelets was measured via light transmission aggregometry (LTA) in resting and stimulated conditions, in response to agonists adenosine diphosphate (ADP), high and low dose of arachidonic acid (AA), and after ex vivo aspirin (ASA) administration. Results: MetS patients were older and similar in sex and race (Figure 1A). As expected, patients with MetS had higher individual components of MetS, yet similar LDL-C (Figure 1A). Platelet aggregation to low dose ADP (p=0.09) and AA (p=0.04) was significantly increased in MetS (Figure 1B). Platelet aggregation in response to AA and coincubation with ASA was significantly lower in the no MetS cohort (Figure 1C). The efficacy of aspirin therapy was significantly lower in MetS (Figure 1D). In response to high dose AA after ASA treatment, platelet aggregation increased as number of MetS parameters also increased (Figure 1E). However, no individual metabolic syndrome parameter appeared to be driving these findings (Figure 1E). Conclusion: Among MetS patients, platelet aggregation is heightened and less inhibited by aspirin than those with no MetS. Additional research is warranted to explore possible anti-platelet strategies in patients with MetS.