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Pharmacogenetic Approach to Anti-platelet Therapy for the Treatment of ST-segment Elevation Myocardial Infarction (STEMI)

Phase 2
Completed
Conditions
STEMI
Interventions
Genetic: Point-of-Care Genetic Testing
Registration Number
NCT01452139
Lead Sponsor
Ottawa Heart Institute Research Corporation
Brief Summary

The objective of the RAPID STEMI study is to evaluate the feasibility, efficacy, and safety of a pharmacogenetic approach to anti-platelet therapy for the treatment of ST-segment elevation myocardial infarction (STEMI) patients following percutaneous coronary intervention (PCI) using point-of-care genetic testing for the CYP2C19\*2, \*17, and ABCB1 3435 C\>T alleles.

Detailed Description

Dual anti-platelet therapy following percutaneous coronary intervention (PCI) for the treatment of STEMI has traditionally consisted of aspirin and clopidogrel. Despite this treatment approach, a substantial portion of patients experience recurrent adverse cardiovascular events including death, myocardial infarction, and stent thrombosis. This persistent vulnerability has been associated with inadequate platelet inhibition in response to clopidogrel administration, a phenomenon referred to as high on-treatment platelet reactivity. Although multiple variables have been implicated in altered clopidogrel response, mounting evidence has suggested a crucial role for common genetic variants including: CYP2C19\*2, \*17, and ABCB1 3435 C\>T alleles.

Presence of the CYP2C19\*2 allele has been associated with a 1.5- to 6-fold increased risk of cardiovascular death, myocardial infarction, and stent thrombosis following PCI in patients treated with clopidogrel. These findings, recently bolstered by 2 separate meta-analyses, led the American Food and Drug Administration to issue a boxed warning for clopidogrel stating that poor metabolizers may not receive the full benefit of the drug. The ABCB1 3435 TT genotype has also been linked with increased adverse cardiovascular events in individuals treated with clopidogrel following PCI for an acute coronary syndrome. In contrast, the CYP2C19\*17 gain-of-function allele appears to enhance the activity of clopidogrel and has been associated with reduced ischemic events but increased bleeding.

As a result of these findings, experts have begun to advocate for routine genotyping in the context of PCI. A personalized approach to dual anti-platelet therapy following PCI is feasible given the presence of treatment alternatives such as prasugrel that are capable of overcoming clopidogrel resistance. Selective administration of prasugrel to patients at increased risk of clopidogrel resistance has the potential to successfully minimize adverse ischemic events, while simultaneously minimizing associated bleeding events and health care costs. A prospective pharmacogenomic approach to anti-platelet therapy has been previously hampered by limited access and the time-delay associated with genetic testing. The development of point-of-care genetic testing for the CYP2C19\*2, \*17, and ABCB1 3435 C\>T alleles that requires minimal training to perform carries the potential to overcome these obstacles and may facilitate the incorporation of pharmacogenetic strategies into routine clinical practice.

Patients receiving PCI in the context of STEMI will undergo point-of-care genetic testing for the CYP2C19\*2, \*17, and ABCB1 3435 C\>T alleles. CYP2C19\*2 carriers and individuals homozygous for the ABCB1 3435 T allele will subsequently be randomized to prasugrel 10mg daily for 1 month or clopidogrel 150mg daily for 1 week followed by 75mg daily. The remaining individuals without an at-risk genotype will receive standard therapy with clopidogrel. At the end of the 1 month period, efficacy of the treatment strategies will be evaluated using VerifyNow platelet function testing. The effect of the CYP2C19\*17 allele will be prospectively evaluated during the treatment period.

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
102
Inclusion Criteria
  • Males and Females between the ages of 18 and 75 years
  • STEMI patients treated with percutaneous coronary intervention
  • Able to provide informed consent
  • Able to comply with assigned treatment strategy and attend 1 month follow-up visit
Exclusion Criteria
  • Receiving anti-platelet therapy other than aspirin and clopidogrel
  • Receiving anti-coagulation with warfarin or dabigatran
  • History of stroke or transient ischemic attack
  • Platelet count < 100 000/μL
  • Known Bleeding Diathesis
  • Hematocrit <30% or >52%
  • Severe Liver Dysfunction
  • Renal Insufficiency (Creatinine Clearance < 30ml/min)
  • Pregnant females

Study & Design

Study Type
INTERVENTIONAL
Study Design
PARALLEL
Arm && Interventions
GroupInterventionDescription
At-Risk Genetics Arm: PrasugrelPoint-of-Care Genetic TestingTreatment of STEMI patients carrying at least 1 at-risk genetic variant with prasugrel 10mg daily for 1 month.
At-Risk Genetics Arm: ClopidogrelPoint-of-Care Genetic TestingTreatment of STEMI patients carrying at least 1 at-risk genetic variant with clopidogrel 150mg daily for 1 week followed by 75mg daily.
Low Risk Genetics Arm: ClopidogrelPoint-of-Care Genetic TestingTreatment of STEMI patients with no at-risk genetic variants with clopidogrel 75mg daily.
At-Risk Genetics Arm: PrasugrelPrasugrelTreatment of STEMI patients carrying at least 1 at-risk genetic variant with prasugrel 10mg daily for 1 month.
Primary Outcome Measures
NameTimeMethod
The rates of high on-treatment platelet reactivity as measured by the VerifyNow P2Y12 assay (Accumetrics, San Diego, CA) in CYP2C19*2 and ABCB1 3435 TT carriers treated with prasugrel relative to clopidogrel.1 month

High on-treatment platelet reactivity as measured by the VerifyNow P2Y12 assay with evidence based cutoffs.

Secondary Outcome Measures
NameTimeMethod
Between-group change in PRU and percent platelet inhibition in CYP2C19*2 and ABCB1 3435 TT carriers treated with prasugrel relative to clopidogrel.1 month
Effect of CYP2C19*17 allele on bleeding events1 month

Comparison of TIMI major \& minor bleeding rates in carriers and non-carriers of the CYP2C19\*17 allele.

Mean PRU and percent platelet inhibition in CYP2C19*2 and ABCB1 3435 TT carriers treated with prasugrel relative to clopidogrel1 month
Composite of death from cardiovascular causes, non-fatal myocardial infarction, and re-hospitalization.1 month
Bleeding risk1 month

Defined by TIMI major/minor

Concordance of point-of-care genetic screening with laboratory based genotyping methods1 month

Genotyping results from the Spartan RX device will be compared with the results of direct DNA sequencing.

Effect of the CYP2C19*17 allele on platelet inhibition.1 month

As measured by VerifyNow in P2Y12 Reaction Units (PRU) and percent platelet inhibition.

Trial Locations

Locations (1)

University of Ottawa Heart Institute

🇨🇦

Ottawa, Ontario, Canada

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