Physicians' Academy for Cardiovascular Education

Increased platelet reactivity in HIV patients with ACS on dual antiplatelet therapy

Platelet reactivity in human immunodeficiency virus infected patients on dual antiplatelet therapy for an acute coronary syndrome: the EVERE2ST-HIV study

Hauguel-Moreau M, Boccara F, Boyd A, et al. - Eur Heart J 2017; published online ahead of print

Background

HIV-infected patients are at higher coronary heart disease (CHD) risk compared with the general population, due to a higher prevalence of cardiovascular (CV) risk factors and the cardiometabolic effects of antiretroviral drugs [1-3]. However, the underlying mechanisms leading to increased CHD risk in HIV patients have not been fully explored. One explanation might be the higher on-treatment platelet reactivity in HIV patients, which was shown to be an independent risk factor of major adverse CV events after acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI) [4,5].

In the EVERE2ST-HIV study (EValuation of REsidual Platelet Reactivity after acute coronary syndrome, STþ/ST-, in HIV study), platelet reactivity was evaluated in HIV- (n=80) and non-HIV (n=160) patients with a first episode of ACS on dual antiplatelet therapy (DAPT). Platelet reactivity was evaluated by measuring residual platelet aggregation (RPA) with light transmission aggregometry (LTA), VerifyNow aspirin assay (ARU), and P2Y12 assay (PRU) and with the Vasodilator-stimulated phosphoprotein (VASP) platelet reactivity index (VASP-PRI). Most patients were on clopidogrel (68%), others were on prasugrel (31%) or ticagrelor (1%) and all took aspirin.

Main results

Conclusion

In 80 ACS patients with HIV, the levels of platelet reactivity and the prevalence of HPR were increased when treated with P2Y12 receptors inhibitors and aspirin, compared with 160 ACS patients without HIV. Moreover, patients treated with protease inhibitors had an increase in platelet reactivity. These findings provide an explanation for the poor prognosis of ACS patients with HIV, and raise the question of the most effective combination of antiplatelet and antiretroviral agents.

Editorial comment

In their editorial article, Gurbel et al describe the pathophysiological ‘thrombotic storm’ that results from the combination of ACS, PCI, and HIV-infection, which are all associated with inflammation, hypercoagulability, and increased platelet reactivity. They also discuss the finding of increased platelet reactivity in patients who were treated with protease inhibitors, and suggest careful consideration regarding the use of these agents after an ACS, until further follow-up data are available. Finally, they conclude: ‘In summary, the authors present part of the forecast for the perfect ‘thrombotic storm’—high ex vivo platelet reactivity in an atmosphere of hypercoagulability and heightened inflammation. The ultimate goal of all studies employing a surrogate marker (high ex vivo platelet reactivity) is to identify the risk of an in vivo event (coronary thrombosis) in order to determine the optimal antiplatelet regimen in the individual patient. We agree with the authors that their finding of high ex vivo platelet reactivity in HIV-infected ACS patients potentially provides part of the mechanism to explain the higher risk of these patients. Avoiding the perfect storm in these high-risk patients requires complex navigational skills. Based on the preliminary findings of this provocative study, it appears that platelet function testing may be one of those skills.’

References

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Find this article online at Eur Heart J