Abstract 368: Increased Platelet Activity in HIV-Infected Subjects on Antiretroviral Therapy Is Inhibited with Low-Dose Aspirin

Introduction: HIV-infected adults are at increased risk for cardiovascular events and increased platelet activity may contribute to this risk. Hypothesis: Platelet activity measurements are increased in subjects with HIV on fully suppressive antiretroviral therapy (ART) and low-dose aspirin attenuates this increase in platelet activity. Methods: We studied platelet aggregation in 25 HIV infected subjects on ART with undetectable plasma HIV-1 RNA and median CD4 521 cells/mm 3 and 29 healthy HIV seronegative controls in response to submaximal adenosine diphosphate (ADP, 0.4uM), collagen (0.05ug/ml), epinephrine (0.1uM ), arachidonic acid (AA, 0.15mM) and without agonist (spontaneous platelet aggregation [SPA]). The effects of a 1-week course of aspirin 81mg daily on platelet activity were also investigated. Results are presented as median (interquartile range) and analyzed using the Mann-Whitney U test. Results: Compared to controls, subjects with HIV had increased platelet aggregation in response to ADP (13.5% [6.8, 81.6] vs 6.4% [2.8, 10.7], p<0.01), collagen (13.5% [6.8, 81.6] vs 6.4% [2.8, 10.7], p=0.01), AA (81.9% [9.4, 90.2] vs 9.6% [2.8, 77], p<0.01), and SPA, 8.2% [4.7, 13.2] vs 4.5% [2.2, 8.9], p=0.04). There was no difference in baseline aggregation in response to epinephrine. Following aspirin therapy, percent aggregation in response to AA decreased more in subjects with HIV (-43% vs -20%, P=0.04), yet remained significantly higher in subjects with HIV versus controls (9.8% [5.8, 16.6] vs 7.4 [4.4, 9.8], P=0.02). In response to ADP, collagen, epinephrine, and SPA, subjects with HIV experienced numerically greater platelet inhibition than controls and residual platelet aggregation was not significantly different between groups. Conclusions: Baseline platelet activity is increased in subjects with HIV infection virologically suppressed on ART which may contribute to the excess cardiovascular risk commonly observed in this population. Subjects with HIV experienced greater decreases in platelet activity in response to aspirin, retaining modestly more platelet activity compared to controls. Cardiovascular prevention studies of aspirin in subjects with HIV are warranted.