[Variable extent of platelet responsiveness to clopidogrel inhibition: "clopidogrel resistance"?]

O Morel1, P Ohlmann, L Jesel

  • 1Fédération de cardiologie des hôpitaux universitaires de Strasbourg, France. Olivier.Morel@chru-strasbourg.fr

Annales De Cardiologie Et D'Angeiologie
|August 18, 2005
PubMed

Insights

Clopidogrel resistance, a factor in stent thrombosis despite aspirin and clopidogrel use, may be identified by lab tests. These tests can help manage patients at high risk for thrombotic events.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Percutaneous coronary angioplasty (PCA) with stenting reduces thrombotic occlusion risk using clopidogrel and aspirin.
  • Despite dual antiplatelet therapy, acute/subacute stent thrombosis occurs in 1-2% of patients.
  • Significant interindividual variability in clopidogrel response suggests "clopidogrel resistance."

Purpose of the Study:

  • To explore the concept of "clopidogrel resistance" and its association with thrombotic events post-PCA.
  • To identify factors contributing to variable clopidogrel responsiveness.
  • To evaluate the utility of laboratory tests for assessing "clopidogrel resistance."

Main Methods:

  • Review of literature on clopidogrel responsiveness and stent thrombosis.
  • Analysis of factors influencing clopidogrel metabolism and platelet function.
  • Discussion of diagnostic laboratory tests for "clopidogrel resistance."

Main Results:

  • "Clopidogrel resistance" is linked to an increased risk of thrombotic events after coronary angioplasty.
  • Factors like enteric absorption, CYP3A4 metabolism, P2Y12 receptor variations, and comorbidities (diabetes) contribute to resistance.
  • Laboratory tests may identify patients with "clopidogrel resistance."

Conclusions:

  • "Clopidogrel resistance" is a significant clinical issue in patients undergoing PCA.
  • Identifying resistant patients via laboratory testing could enable personalized antiplatelet therapy.
  • Higher clopidogrel doses may improve platelet inhibition in resistant individuals, potentially reducing thrombotic risk.

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