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CYP2C19 genotype-guided antiplatelet therapy in a patient with clopidogrel resistance

Mridula Rai1, Richard L Seip, Ankur Gupta

  • 1Hartford Hospital, Hartford, USA. mrai@harthosp.org

Connecticut Medicine
|June 13, 2012
PubMed

Insights

Switching antiplatelet medication based on genetic testing and platelet function improved outcomes for a patient with coronary artery disease. Personalized therapy reduced cardiovascular events by addressing clopidogrel resistance.

Area of Science:

  • Cardiology
  • Pharmacogenomics

Background:

  • Severe coronary arterial disease necessitates antiplatelet therapy, often with clopidogrel, to prevent stent thrombosis.
  • Clopidogrel efficacy is dependent on activation by the cytochrome P450 2C19 (CYP2C19) enzyme.

Observation:

  • A 74-year-old male with coronary artery disease exhibited high on-clopidogrel platelet reactivity despite long-term therapy.
  • The patient had undergone multiple percutaneous coronary interventions for stenosis and in-stent restenosis.

Findings:

  • CYP2C19 genotype testing revealed the patient was homozygous for the *2 null allele, classifying him as a poor metabolizer.
  • Switching to prasugrel, an antiplatelet agent not dependent on CYP2C19 activation, reduced platelet reactivity by 86%.

Implications:

  • Pharmacogenetic testing (CYP2C19 genotype) can identify patients with clopidogrel resistance.
  • Personalized antiplatelet therapy selection based on genotype and platelet function can optimize outcomes in patients with coronary artery disease.
  • This approach may reduce cardiovascular events in patients with poor clopidogrel metabolizer status.

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