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Platelet reactivity to adenosine diphosphate and long-term ischemic event occurrence following percutaneous coronary

Paul A Gurbel1, Mark J Antonino, Kevin P Bliden

  • 1Sinai Center for Thrombosis Research, Department of Medicine, Sinai Hospital, Baltimore, Maryland 21215, USA. pgurbel@lifebridgehealth.org

Platelets
|November 18, 2008
PubMed

Insights

High platelet reactivity to adenosine diphosphate (ADP) after percutaneous coronary intervention (PCI) increases ischemic event risk. Identifying specific reactivity cutpoints can guide antiplatelet therapy and personalize treatment post-PCI.

Area of Science:

  • Cardiology
  • Hematology
  • Pharmacology

Background:

  • Platelets are crucial in post-percutaneous coronary intervention (PCI) ischemic events.
  • High post-procedural platelet reactivity to adenosine diphosphate (HPR(ADP)) is a potential risk factor.
  • Current antiplatelet therapies may require personalized adjustments.

Purpose of the Study:

  • To evaluate specific cutpoints of platelet reactivity to ADP associated with ischemic events after PCI.
  • To determine if HPR(ADP) is an independent risk factor for ischemic events.
  • To explore personalized medicine approaches for antiplatelet therapy intensity.

Main Methods:

  • 297 patients undergoing non-emergent PCI were studied.
  • Post-procedural platelet reactivity to ADP was measured using conventional aggregometry.
  • Patients were followed for up to 2 years for post-discharge ischemic events.

Main Results:

  • 81 patients (27%) experienced ischemic events.
  • Patients with events showed significantly higher 5 microM and 20 microM ADP-induced platelet aggregation.
  • Cutpoints of >46% (5 microM ADP) and >59% (20 microM ADP) identified HPR(ADP), associated with 58% and 54% of events, respectively.
  • HPR(ADP) was an independent risk factor (OR=3.9 for 5 microM, OR=3.8 for 20 microM ADP).

Conclusions:

  • High post-procedural platelet reactivity to ADP is an independent risk factor for ischemic events within 2 years of PCI.
  • These findings support using ex vivo platelet function tests to guide antiplatelet therapy.
  • The study represents a step towards personalized antiplatelet treatment strategies.

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