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Association of FMO3 rs1736557 polymorphism with clopidogrel response in Chinese patients with coronary artery disease

Kong-Xiang Zhu1,2, Pei-Yuan Song1,2, He-Li1,2

  • 1Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, People's Republic of China.

European Journal of Clinical Pharmacology
|October 22, 2020
PubMed

Insights

The FMO3 rs1736557 AA genotype increases clopidogrel

Area of Science:

  • Pharmacogenomics
  • Cardiovascular Medicine
  • Molecular Biology

Background:

  • Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel is standard for coronary artery disease (CAD) patients post-percutaneous coronary intervention.
  • High on-treatment platelet reactivity (HTPR) during clopidogrel therapy increases risks of stent thrombosis and ischemic events.
  • CYP2C19 loss-of-function variants are known to cause HTPR; FMO3's role in platelet responsiveness is also noted.

Purpose of the Study:

  • To investigate the association between the FMO3 rs1736557 polymorphism and clopidogrel response in Chinese CAD patients.
  • To determine if FMO3 rs1736557 influences clopidogrel's antiplatelet potency.

Main Methods:

  • 522 Chinese CAD patients receiving DAPT were studied.
  • Platelet reactivity was measured using the vasodilator-stimulated phosphoprotein-phosphorylation assay after clopidogrel administration (loading or maintenance dose).
  • FMO3 rs1736557 and CYP2C19 polymorphisms (*2, *3) were genotyped using PCR-RFLP.

Main Results:

  • CYP2C19 poor and intermediate metabolizers exhibited significantly higher platelet reactivity than extensive metabolizers.
  • FMO3 rs1736557 AA homozygotes showed significantly lower platelet reactivity compared to carriers of the G allele.
  • The FMO3 rs1736557 A allele was associated with a significantly decreased risk of HTPR, particularly in patients with CYP2C19 loss-of-function alleles on maintenance dose therapy.

Conclusions:

  • The FMO3 rs1736557 AA genotype is linked to enhanced antiplatelet potency of clopidogrel in Chinese CAD patients.
  • This finding suggests FMO3 rs1736557 may be a genetic marker influencing clopidogrel efficacy.
  • Further research is needed to validate these pharmacogenomic findings.
Abstract

Keywords:
CYP2C19Coronary artery diseaseFMO3High on-treatment platelet reactivityPlatelet reaction index

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