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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
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Published on: April 1, 2019

Does glycoprotein IIIa gene (Pl(A)) polymorphism influence clopidogrel resistance? : a study in older patients

Elod Papp1, Viktoria Havasi, Judit Bene

  • 1First Department of Medicine, School of Medicine, University of Pecs, Pecs, Hungary.

Drugs & Aging
|April 17, 2007
PubMed

Insights

The Pl(A2) allele does not increase clopidogrel resistance risk. Patients with Pl(A2) homozygosity may benefit more from clopidogrel than aspirin therapy.

Area of Science:

  • Pharmacogenomics
  • Cardiovascular Medicine
  • Clinical Pharmacology

Background:

  • Clopidogrel is a key antiplatelet agent for secondary prevention of cardiovascular events.
  • Aspirin intolerance or resistance necessitates clopidogrel monotherapy.
  • Glycoprotein IIIa gene Pl(A) polymorphism influences antiplatelet drug response.

Purpose of the Study:

  • To investigate the Pl(A2) allele's impact on platelet aggregation in patients on long-term clopidogrel.
  • To determine if Pl(A2) allele carriers exhibit clopidogrel resistance.

Main Methods:

  • Assessed Pl(A2) allele prevalence in clopidogrel-resistant (n=38) and responsive (n=59) patients.
  • Utilized polymerase chain reaction-restriction fragment length polymorphism for Pl(A) genotyping.
  • Measured adenosine diphosphate-induced platelet aggregation using a Carat TX4 optical aggregometer.

Main Results:

  • No significant difference in Pl(A2) allele prevalence between clopidogrel-resistant (0.09) and responsive (0.13) groups.
  • Combination antiplatelet therapy was more common in the resistant group (50% vs 30%).
  • Prevalence remained non-significant after adjusting for combination therapy and risk factors.

Conclusions:

  • Pl(A2) allele carriers do not face an elevated risk of clopidogrel resistance.
  • Pl(A2) homozygosity may indicate a preference for clopidogrel over aspirin for antiplatelet therapy.
Abstract

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