title: On-treatment platelet reactivity: State of the art and perspectives.
abstract: High on-clopidogrel platelet reactivity (HcPR) during dual-antiplatelet therapy is a marker of vascular risk, in particular stent thrombosis, in patients with acute coronary syndromes (ACS). Genetic determinants (CYP2C19*2 polymorphism), advanced age, female gender, diabetes and reduced ventricular function are related to a higher risk to develop HcPR. In addition, inflammation and increased platelet turnover, as revealed by the elevated percentage of reticulated platelets in patients' blood, that characterize the acute phase of acute coronary syndromes, are associated with HcPR. To overcome the limitation of clopidogrel, new antiplatelet agents (prasugrel and ticagrelor) were developed and the demonstration of their superiority over clopidogrel was obtained in the two randomized trials, TRITON TIMI 38 and PLATO. Emerging evidence is accumulating on the role of high-on aspirin platelet reactivity (HaPR), especially in the clinical context of diabetes. Finally, the presence of new, potent antiplatelet drugs has shifted the focus from thrombotic to bleeding risk. Recent data document that low on-treatment platelet reactivity (LPR) is associated with a significantly higher bleeding risk. Due to the current possibility to choose between multiple antiplatelet strategies, the future perspective is to include in the management of ACS, in addition to clinical data and classical risk factors, the definition of platelet function during treatment in order to set a tailored therapy.
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy; Center for Aterothrombotic Diseases, AOU Careggi, Florence, Italy. Electronic address: rossella.marcucci@unifi.it.
authors.forename: Rossella
authors.initials: R
authors.lastname: Marcucci
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy; Center for Aterothrombotic Diseases, AOU Careggi, Florence, Italy.
authors.forename: Elisa
authors.initials: E
authors.lastname: Grifoni
authors.affiliation: Department of Experimental and Clinical Medicine, University of Florence, Italy; Center for Aterothrombotic Diseases, AOU Careggi, Florence, Italy.
authors.forename: Betti
authors.initials: B
authors.lastname: Giusti
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000188:drug therapy* / Q000201:enzymology; D000241:Adenosine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives / Q000493:pharmacokinetics / Q000627:therapeutic use; D000367:Age Factors; D001792:Blood Platelets / Q000187:drug effects*; D000077144:Clopidogrel; D065731:Cytochrome P-450 CYP2C19 / Q000235:genetics; D004347:Drug Interactions; D006470:Hemorrhage / Q000517:prevention & control; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000009:adverse effects* / Q000493:pharmacokinetics / Q000627:therapeutic use; D011110:Polymorphism, Genetic; D000068799:Prasugrel Hydrochloride / Q000008:administration & dosage / Q000009:adverse effects / Q000493:pharmacokinetics / Q000627:therapeutic use; D012737:Sex Factors; D015607:Stents; D013927:Thrombosis / Q000517:prevention & control; D000077486:Ticagrelor; D013988:Ticlopidine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives / Q000493:pharmacokinetics / Q000627:therapeutic use
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D000068799:Prasugrel Hydrochloride; D000077486:Ticagrelor; D000241:Adenosine; D013988:Ticlopidine