High on-treatment platelet reactivity (HPR): What does it mean, and does it matter?

摘要: 2013; 109: 347-355. In this issue of Thrombosis and Haemostasis, Saucedo et al. (1) demonstrate that the prevalence high on-treatment platelet reactivity was decreased after changing clopidogrel to prasugrel. It is perhaps appealing patients with adverse “high (HPR)” reduced when switched From a scientific point view, meaning “HPR” still unclear. This uncertainty derived from an arguably confusing clinical development history thienopyridine-type antiplatelet agents (ticlopidine, clopidogrel, prasugrel). Indeed, use these greatly expanded based on experience, rather than their mechanistic understanding. A randomised, blinded, trial versus aspirin in at risk ischaemic events (CAPRIE)was published 1996 (2). However, precise mechanism action exerted by clarified only cloning target ADP receptor P2Y12 2001 (3). Moreover, extent blockade active metabolite individual patient, which should be real bio-marker for drug, has been measured very limited number studies (4). Nonetheless, some remains about how much percentage blocked achieve appropriate antithrombotic effects patients. Obviously, goal not 100% inhibition because deficiency manifests as bleeding disorder (5). Perhaps focus drugs per se. Both prasugrel are pro-drugs. The chemical structure metabolite(s) detected 2002 (6). Since labile character reactive thiol function, it most likely majority produced easily binds receptors platelets circulating liver, where (▶ Figure 1A) Thus, plasma concentrations se would necessarily good pharmaco-dynamic marker(s) (8). blockage, once achieved liver circulation, same peripheral blood.