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Clopidogrel "resistance": pre- vs post-receptor determinants.

N L Hurst1, V B Nooney, B Raman

  • 1Department of Cardiology and Pharmacology, The Queen Elizabeth Hospital, Woodville South, Australia; The University of Adelaide, Basil Hetzel Institute, Woodville South, Australia.

Vascular Pharmacology
|October 22, 2013
PubMed
Summary

Clopidogrel resistance, impacting its antiplatelet efficacy, stems from genetic and non-genetic factors affecting its metabolism and action. Understanding these mechanisms is crucial for optimizing treatment in high-risk cardiovascular patients.

Keywords:
Anti-platelet agentsClopidogrelP2Y(12) inhibitorsPlateletsThrombosis

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Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Clopidogrel's antiplatelet effect, crucial for preventing thrombotic events, is mediated by P2Y12 receptor antagonism.
  • Limited clopidogrel efficacy, termed 'resistance,' is linked to increased risk of stent thrombosis.

Purpose of the Study:

  • To explore the multifaceted mechanisms underlying clopidogrel resistance.
  • To differentiate between genetic and non-genetic contributors to clopidogrel resistance.
  • To inform therapeutic strategies for high-risk cardiovascular patients.

Main Methods:

  • Review of existing literature on clopidogrel efficacy, resistance, and associated factors.
  • Analysis of pharmacogenetic, pharmacokinetic, and intracellular biochemical mechanisms.
  • Speculation on non-genetic causes involving intracellular signaling pathways.

Main Results:

  • Clopidogrel resistance is attributed to reduced active metabolite levels and impaired downstream signaling.
  • CYP2C19 loss-of-function mutations and drug-drug interactions impair bioactivation.
  • Non-genetic factors, including obesity and diabetes, are associated with increased resistance.

Conclusions:

  • Clopidogrel resistance involves complex pharmacogenetic, pharmacokinetic, and biochemical interactions.
  • Non-genetic resistance mechanisms may affect other P2Y12 inhibitors, independent of bioactivation.
  • Identifying non-genetic resistance components is key to developing improved therapies for cardiovascular patients.