BRIEF-PCI: Brief Infusion of Eptifibatide Following Percutaneous Coronary Intervention
This trial was designed to examine the efficacy of a brief versus a standard prolonged (18 hours) infusion of eptifibatide in preventing troponin I release following successful coronary stenting.
Coronary Artery Disease
|Study Design:||Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Treatment
|Official Title:||Brief Infusion of Eptifibatide Following Percutaneous Coronary Intervention|
- Ischemic injury is defined as troponin I release by 24 hours when the baseline troponin I is normal or by measuring creatine kinase (CK-MB) when the baseline troponin I is elevated. [ Time Frame: 24 Hours ]
- 30-day all-cause mortality, non-fatal myocardial infarction (MI), and unplanned target vessel revascularization (TVR) [ Time Frame: 30 days ]
- Composite event rate of non-coronary artery bypass graft (CABG) major bleeding, all-cause mortality, non-fatal MI, and urgent TVR at 30 days post PCI. [ Time Frame: 30 days ]
|Study Start Date:||December 2004|
|Study Completion Date:||August 2007|
|Primary Completion Date:||July 2007 (Final data collection date for primary outcome measure)|
Percutaneous coronary intervention (PCI) is a common treatment for patients with severe ischemic heart disease. In the majority of cases, the potent anti-platelet agent eptifibatide is administered (bolus followed by infusion for 18 hours). The principal reason to use eptifibatide for PCI is to prevent platelet aggregation and the associated ischemia and myocardial infarction (MI). With improved laminar flow following stenting, prolonged infusion of eptifibatide may no longer be necessary. We hypothesize that after successful stenting with good angiographic results, patients can have eptifibatide discontinued immediately without a higher risk of adverse ischemic outcome, i.e. death, MI or unplanned target vessel revascularization (TVR) by 30 days. MI is defined as creatine kinase-MB (CK-MB) concentrations elevated to more than three times the upper limit of normal or new pathologic Q wave as seen on electrocardiograms (ECG). In order to prove this hypothesis, we estimate a sample size of 2,100 patients.
Before embarking on a large-scale clinical trial, we propose a pilot study using serum troponin I elevation as a surrogate end-point. Troponin I is a sensitive biomarker of ischemic injury. The absence of troponin I release following PCI would suggest excellent short and intermediate term prognosis. For the pilot study, we seek to prove the hypothesis that following successful PCI with stenting, an abbreviated regimen of eptifibatide is not inferior to the standard infusion in preventing ischemic injury, defined as troponin I release if baseline value is normal, or as CK-MB more than 3 times upper limit of normal if baseline troponin I is elevated. For this pilot study, we estimate a sample size of 620 patients.
|Canada, British Columbia|
|Vancouver General Hospital|
|Vancouver, British Columbia, Canada, V5Z 1L8|
|Principal Investigator:||Anthony Fung, MB,BS, FRCPC||University of British Columbia|