Platelet reactivity to adenosine diphosphate and long-term ischemic event occurrence following percutaneous coronary intervention: A potential antiplatelet therapeutic target
- 1 January 2008
- journal article
- Published by Informa UK Limited in Platelets
- Vol. 19 (8), 595-604
- https://doi.org/10.1080/09537100802351065
Abstract
Platelets play a central role in the genesis of post-percutaneous coronary intervention (PCI) ischemic events. High post-procedural platelet reactivity to adenosine diphosphate (HPR(ADP)) may be a risk factor for ischemic events after PCI. The study was designed to evaluate a cutpoint of platelet reactivity that is associated with the occurrence of ischemic events after PCI. Post-procedural platelet reactivity to ADP was measured by conventional aggregometry in 297 consecutive patients undergoing non-emergent PCI. Patients were prospectively followed for up to 2 years for post-discharge ischemic events. All patients had received clopidogrel and aspirin therapy at the time of aggregation measurements. Eighty-one patients (27%) suffered ischemic events. Patients with ischemic events had higher 5 microM ADP-induced platelet aggregation (46 +/- 14% vs. 30 +/- 17%, p < 0.001) and 20 microM ADP-induced platelet aggregation (60 +/- 13% vs. 43 +/- 19%, p < 0.001) compared to patients without ischemic events. Using a combined receiver operator curve analysis, cutpoints of >46% aggregation following 5 microM ADP stimulation and >59% aggregation following 20 microM ADP stimulation (HPR(ADP)) were associated with 58 and 54% of ischemic events, respectively. Multivariate Cox regression demonstrated a significant relation between event occurrence and post-procedural HPR(ADP) cutpoints (5 microM ADP, OR=3.9, and 20 microM ADP, OR=3.8, p < 0.001 for both). High post-procedural platelet reactivity to ADP is an independent risk factor for ischemic events within 2 years of non-emergent PCI. These data support a potential therapeutic target for antiplatelet therapy based on the results of an ex vivo platelet function test. The study is a step towards a personalized medicine approach to guide the intensity of antiplatelet therapy.Keywords
This publication has 31 references indexed in Scilit:
- Adjusted Clopidogrel Loading Doses According to Vasodilator-Stimulated Phosphoprotein Phosphorylation Index Decrease Rate of Major Adverse Cardiovascular Events in Patients With Clopidogrel ResistanceJournal of the American College of Cardiology, 2008
- Prasugrel versus Clopidogrel in Patients with Acute Coronary SyndromesNew England Journal of Medicine, 2007
- ADP-induced platelet aggregation and platelet reactivity index VASP are good predictive markers for clinical outcomes in non-ST elevation acute coronary syndromeThrombosis and Haemostasis, 2007
- A Randomized Comparison of High Clopidogrel Loading Doses in Patients With Non–ST-Segment Elevation Acute Coronary SyndromesJournal of the American College of Cardiology, 2006
- Absorption, Metabolization, and Antiplatelet Effects of 300-, 600-, and 900-mg Loading Doses of ClopidogrelCirculation, 2005
- Platelet Reactivity in Patients and Recurrent Events Post-StentingJournal of the American College of Cardiology, 2005
- Overestimation of Platelet Aspirin Resistance Detection by Thrombelastograph Platelet Mapping and Validation by Conventional Aggregometry Using Arachidonic Acid StimulationJournal of the American College of Cardiology, 2005
- Compliance as a critical consideration in patients who appear to be resistant to aspirin after healing of myocardial infarctionThe American Journal of Cardiology, 2005
- Clopidogrel Loading With Eptifibatide to Arrest the Reactivity of PlateletsCirculation, 2005
- Clopidogrel for Coronary StentingCirculation, 2003