Clopidogrel loading dose adjustment according to platelet reactivity monitoring in patients carrying the 2C19*2 loss of function polymorphism

J Am Coll Cardiol. 2010 Nov 9;56(20):1630-6. doi: 10.1016/j.jacc.2010.07.004. Epub 2010 Aug 12.

Abstract

Objectives: We aimed to investigate the biological impact of a tailored clopidogrel loading dose (LD) according to platelet reactivity monitoring in carriers of the cytochrome (CYP) 2C19*2 loss-of-function polymorphism undergoing percutaneous coronary intervention for an acute coronary syndromes.

Background: CYP2C19*2 polymorphism is associated with reduced clopidogrel metabolism and a worse prognosis after percutaneous coronary intervention.

Method: A prospective multicenter study enrolling 411 patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention was performed. Platelet reactivity was measured using the vasodilator-stimulated phosphoprotein (VASP) index, and a cutoff value of ≥ 50% was used to define high on-treatment platelet reactivity (HTPR). The genetic polymorphism of CYP2C19 was determined by allele-specific polymerase chain reaction. In patients carrying CYP2C19*2 and exhibiting HTPR after a first 600-mg LD of clopidogrel, dose adjustment was performed by using up to 3 additional 600 mg LDs to obtain a VASP index <50%.

Results: One hundred thirty-four patients (35.3%) carried at least one 2C19*2 allele (11 homozygotes [2.7%] and 123 heterozygotes [32.6%]). The VASP index in these patients was significantly higher than in homozygotic patients for the wild-type alleles (61.7 ± 18.4% vs. 49.2 ± 24.2%; p < 0.001). Of the 134 carriers of the loss-of-function polymorphism, 103 were considered to have HTPR. After a second clopidogrel LD, the VASP index was significantly decreased in these patients (69.7 ± 10.1% vs. 50.6 ± 17.6%; p < 0.0001). Finally, dose adjustment according to platelet reactivity monitoring, enabled 88% of 2C19*2 carriers exhibiting HTPR to reach a VASP index <50%.

Conclusions: Increased and tailored clopidogrel loading dose according to platelet reactivity monitoring overcome HTPR in carriers of the loss-of-function CYP2C19*2 polymorphism.

Publication types

  • Comparative Study
  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Coronary Syndrome / blood
  • Acute Coronary Syndrome / genetics
  • Acute Coronary Syndrome / therapy*
  • Alleles
  • Angioplasty, Balloon, Coronary / methods*
  • Aryl Hydrocarbon Hydroxylases / genetics*
  • Blood Proteins
  • Cell Adhesion Molecules / blood
  • Cell Adhesion Molecules / drug effects
  • Clopidogrel
  • Cytochrome P-450 CYP2C19
  • DNA / genetics*
  • Dose-Response Relationship, Drug
  • Electrocardiography
  • Female
  • Follow-Up Studies
  • Genotype
  • Humans
  • Male
  • Microfilament Proteins / blood
  • Microfilament Proteins / drug effects
  • Middle Aged
  • Monitoring, Physiologic
  • Phosphoproteins / blood
  • Phosphoproteins / drug effects
  • Platelet Activation / drug effects*
  • Platelet Activation / genetics
  • Polymerase Chain Reaction
  • Polymorphism, Genetic*
  • Prospective Studies
  • Purinergic P2Y Receptor Antagonists / administration & dosage
  • Ticlopidine / administration & dosage
  • Ticlopidine / analogs & derivatives*
  • Treatment Outcome

Substances

  • Blood Proteins
  • Cell Adhesion Molecules
  • Microfilament Proteins
  • Phosphoproteins
  • Purinergic P2Y Receptor Antagonists
  • vasodilator-stimulated phosphoprotein
  • DNA
  • Clopidogrel
  • Aryl Hydrocarbon Hydroxylases
  • CYP2C19 protein, human
  • Cytochrome P-450 CYP2C19
  • Ticlopidine