Association between high on-treatment platelet reactivity and occurrence of cerebral ischemic events in patients

A Komosa1, J M Siller-Matula2, M Lesiak1

  • 11st Department of Cardiology, Poznan University of Medical Sciences, Poland.

Thrombosis Research
|January 31, 2016
PubMed

Insights

High on-treatment platelet reactivity (HTPR) despite clopidogrel treatment increases the risk of ischemic cerebral events in patients undergoing coronary stenting. CYP2C19*2/*2 allele carriers also face a higher risk of these events.

Area of Science:

  • Cardiology
  • Pharmacogenomics
  • Interventional Cardiology

Background:

  • Percutaneous coronary angioplasty (PCI) with drug-eluting stents (DES) and dual antiplatelet therapy are standard for coronary artery disease.
  • Newer DES and antiplatelet strategies have improved outcomes and reduced stent thrombosis risk.

Purpose of the Study:

  • To determine if high on-treatment platelet reactivity (HTPR) during clopidogrel therapy is linked to ischemic cerebral events.
  • To investigate the association between HTPR, measured by Multiplate Electrode Aggregometer (MEA), and adverse cerebral events.

Main Methods:

  • 249 patients with coronary artery disease undergoing PCI for stable angina or acute coronary syndrome were enrolled.
  • Platelet aggregation was assessed using MEA, and CYP2C19 genetic polymorphism was analyzed in 150 patients via HRM Real-Time PCR.

Main Results:

  • Patients with HTPR had a significantly higher incidence of ischemic stroke (OR=16.8) and other cerebral ischemic events (OR=6.5).
  • The CYP2C19*2/*2 allele was associated with an increased risk of cerebral ischemic events (OR=10).
  • No statistical significance was found for the cumulative assessment of all ischemic and hemorrhagic events.

Conclusions:

  • HTPR, measured by MEA, is a significant risk factor for ischemic cerebral events in patients treated with clopidogrel post-coronary stenting.
  • CYP2C19*2/*2 allele carriers exhibit an elevated rate of ischemic cerebral events, reinforcing the genetic influence on treatment response.
Abstract

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