Platelet Rna As a Novel Biomarker for the Response to Antiplatelet Therapy

Abstract

9 ISSN 1479-6678 10.2217/FCA.13.90 © 2014 Future Medicine Ltd Future Cardiol. (2014) 10(1), 9–12 Antiplatelet agents, such as aspirin, or P2Y 12 inhibitors, such as clopidogrel, prasugrel or ticagrelor, are widely prescribed to prevent ischemic events [1]. The combination of aspirin and a P2Y 12 inhibitor is endorsed by international guidelines in patients at high risk of ischemic events, while aspirin monotherapy is the backbone of preventative therapy for patients with established vascular disease [2–6]. Despite convincing evidence of its effectiveness, the efficacy of aspirin in certain individuals may vary and recurrence rates are high [2]. For example, in patients with established cardio vascular disease or multiple risk factors who use aspirin, 15–20% will suffer a future cardiovascular event (myocardial infarction [MI] or stroke), hospitalization for revascularization or death over 28 months [7]. Similarly, patients with Type 2 diabetes, a powerful magnifier of cardiovascular risk, are at equivalent risk of a first MI as nondiabetics with a prior MI (each 19–20% over 7 years) [8]. Consequently, aspirin is recommended in patients with Type 2 diabetes, especially if other cardiovascular risk factors are present [2,9]. However, two randomized trials of low-dose aspirin as primary prevention in more than 3000 diabetics each failed to significantly reduce MI or stroke [10,11], thereby suggesting that the benefits of aspirin are not uniform and may fail in certain high-risk individuals. Further more, antiplatelet agents are accompanied by an increase in bleeding events [2,12], which may offset any potential benefits, particularly in low-risk populations. Therefore, certain individuals may fail to benefit from aspirin, and others may be exposed to an increased risk of bleeding. The vast majority of clinicians and researchers lack reliable methods of identifying individuals with inadequate or unanticipated responses to antiplatelet drugs, and thus the tools for tailoring antiplatelet therapy. This need is greatest in the primary care setting where aspirin is widely used, but no method to assess drug response is accessible. Platelet function tests are available in certain settings and capture the large interindividual variability in response to aspirin, despite complete suppression of aspirin’s putative target, platelet COX-1 [13–16].