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PKP-021 Results of the use of pharmacogenetics in the choice of antiplatelet therapy after percutaneous coronary intervention with stent
  1. JG Sanchez Ramos1,
  2. CL Dávila Fajardo2,
  3. X Díaz Villamarin2,
  4. LJ Martinez González3,
  5. F Burillo Gómez1,
  6. P Toledo Frías1,
  7. S Martínez Huertas1,
  8. A Bautista Pavés1,
  9. C Correa Vilches1,
  10. J Cabeza Barrera2
  1. 1Instituto de Investigación Biosanitaria de Granada Hospital Universitario San Cecilio, Department of Cardiology, Granada, Spain
  2. 2Instituto de Investigación Biosanitaria de Granada Hospital Universitario San Cecilio, Department of Clinical Pharmacy, Granada, Spain
  3. 3Centre for Genomics and Oncological Research GENYO – Pfizer-University of Granada-Andalusian Regional Government – Health Sciences Technology Park, Genomics Unit, Granada, Spain


Background Clopidogrel provides a reduction in cardiovascular events in acute coronary syndrome (ACS) patients, particularly for those who have undergone percutaneous coronary intervention (PCI). The cardiovascular response has been associated with some genetic polymorphisms. However, variability within the CYP2C19 and ABCB1 polymorphisms showed the higher level of evidence.

Purpose To compare the efficacy and safety of the choice of antiplatelet therapy guided by genotyping versus without genotyping after PCI.

Material and methods Quasi experimental design with retrospective control group including PCI patients requiring dual antiplatelet therapy for 1–12 months. In the genotyping group, CYP2C19*2 allele or ABCB1 TT genotype carrier patients (loss of function (LOF)) received prasugrel or ticagrelor and clopidogrel in non-LOF carrier patients. In the control group (without genotyping), patients received antiplatelet treatment according to medical criteria. Analysis was made by intention to treat during the first year under dual antiplatelet therapy.

Results 719 patients were included, 86.2% with ACS. In the genotyping group (317 patients), 41% were resistant to clopidogrel and 59% were sensitive to clopidogrel. The control group (402 patients) was treated with clopidogrel in the majority (7% received prasugrel). Baseline clinical characteristics were similar in both groups except for primary ICP (p = 0.001) and drug eluting stent (p = 0.0001). The primary endpoint was combined cardiovascular death, ACS, unstable angina or stroke. The primary endpoint occurred in 32 patients (10.1%) in the genotyping group and in 59 patients (14.7%) in the control group (HR 0.63, 95% CI 0.41 to 0.97, p = 0.037 (adjusted in multivariate analysis). There was no difference in TIMI major and minor bleeding between the two groups (4.1% vs 4.7%, HR 0.80, 95% CI 0.39 to 1.63, p = 0.55) and the net effect of efficacy and safety showed a favourable trend towards the genotyping group (13.9% vs 18.4%, HR 0.69, 95% CI 0.48 to 1.01, p = 0.058). Within the genotyping group, there was no difference in the rate of events in patients sensitive to clopidogrel versus resistant (9.1% vs 11.5% p = 0.44), or bleeding (3.7% vs 4.6%, p = 0.69).

Conclusion The choice of antiplatelet therapy after PCI guided by genotyping is more effective and safer than the previous strategy without genotyping.

No conflict of interest.

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