Coronary Artery Disease
Conditions
Keywords
coronary artery disease, prasugrel, platelet function tests
Brief summary
Although prasugrel, recently available thienopyridine derivative, exhibits rapid and potent platelet inhibition, concerns of low on-treatment platelet reactivity have been suggested especially in East Asian ethnicities. The investigators compared the effect of lower loading dose of prasugrel with conventional loading dose of clopidogrel and prasugrel.
Detailed description
Although clopidogrel together aspirin has been a backbone of anti-platelet therapy in coronary artery disease patients, clopidogrel has several limitations. It has delayed onset of peak concentration and pharmacodynamic inter-patient response variability resulting in high on-treatment platelet reactivity (HPR). Those demerits are known to be associated with adverse cardiovascular outcomes. Prasugrel has a more effective metabolism pathway than clopidogrel and exhibits more rapid and potent platelet inhibition. Recent guidelines recommend prasugrel as a first line antiplatelet agent or put precedence over clopidogrel for the patients with acute coronary syndrome. However, there have been concerns of different pharmacodynamic and pharmacokinetic response to prasugrel in East Asian ethnicities. In addition, lower loading dose of prasugrel exhibited more potent pharmacodynamic effect than clopidogrel 600 mg with comparable efficacy compared to conventional loading dose of prasugrel in healthy Korean subjects. The investigators compare the antiplatelet effect of lower loading dose of prasugrel 30 mg with conventional loading dose of clopidogrel 600 mg and prasugrel 60 mg in Korean coronary artery disease patients undergoing elective coronary angiography.
Interventions
Patients administer 600 mg of clopidogrel as conventional loading dose of clopidogrel
DRUGPrasugrel 30 mg
Patients administer 30 mg of prasugrel as lower loading dose of prasugrel.
DRUGPrasugrel 60 mg
Patients take 60 mg of prasugrel as conventional loading dose of prasugrel.
Sponsors
Dong-A University
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
TREATMENT
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
18 Years to 80 Years
Healthy volunteers
No
Inclusion criteria
* Patients between 18 and 80 years * Stable or unstable angina * Planned to undergo elective coronary angiography
Exclusion criteria
* Previous history of transient ischemic attack or stroke * Intracranial neoplasm * Uncontrolled malignant disease * History of antiplatelet or anticoagulation treatment within 1 month * Contraindication to the study drug * Bleeding diathesis * Hemoglobin \< 10 g/dl * Platelet count \< 100,000/mm3 * Significant renal insufficiency (glomerular filtration rate \<60 mL/min/1.73 m2) * Significant hepatic impairment (Serum liver enzyme or bilirubin \> 3 times normal limit) * Body weight \< 50 kg
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Platelet reactivity | at 6 hours after administration of study drug. (2 hours for prasugrel groups) | Platelet reactivity was measured using traditional light transmission aggregometry (LTA), VerifyNow (Accumetrics, San Diego, CA, USA), and multiple electrode aggregometry (MEA, Dynabyte Medical, Munich, Germany). The platelet reactivity was measured at 6 hours after study drug administration (after 2 hours for the prasugrel groups). |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Percent inhibition | at 6 hours after administration of study drug. (2 hours for prasugrel groups) | Percent inhibition is calculated using the following fomula: % inhibition = \[(baseline reactivity unit - peak reactivity unit) / baseline reactivity unit\] × 100. Percent inhibition is measured at the time of peak platelet inhibition. The platelet reactivity was measured at 6 hours after study drug administration (after 2 hours for the prasugrel groups). |
| HPR | at 6 hours after administration of study drug. (2 hours for prasugrel groups) | The high platelet reactivity (HPR) was defined as the results of LTA ≥ 48% or ≥ 55%, PRU ≥ 242 or ≥ 275, and result of MEA assay ≥ 37 U or 54 U at the time of peak platelet inhibition The platelet reactivity was measured at 6 hours after study drug administration (after 2 hours for the prasugrel groups). |
| LPR | at 6 hours after administration of study drug. (2 hours for prasugrel groups) | The low platelet reactivity (LPR) was defined as LTA \< 12, PRU \< 85, MEA \< 19 at the time of peak platelet inhibition. The platelet reactivity was measured at 6 hours after study drug administration (after 2 hours for the prasugrel groups). |
| Bleeding event | 30 days after study drug administration | Any event related to bleeding including access site bleeding and peri-procedural bleeding based on BARC and ACUITY criteria. |
| Adverse reaction | 30 days after study drug administration | Any adverse reaction related to study drug. |
Countries
South Korea
Outcome results
None listed