BRIEF-PCI: Brief Infusion of Eptifibatide Following Percutaneous Coronary Intervention

Cardiology Research UBC

Status and phase

Completed

Phase 4

Conditions

Coronary Artery Disease

Myocardial Infarction

Treatments

Drug: eptifibatide

Study type

Interventional

Funder types

Other

Identifiers

NCT00111566

C04-0359

Details and patient eligibility

About

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.

Full description

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.

Enrollment

624 patients

Sex

All

Volunteers

No Healthy Volunteers

Inclusion criteria

Male and non-pregnant female subjects
18 years of age or older
Received aspirin, clopidogrel, heparin (unfractionated or low molecular weight [LMW]) and eptifibatide
Had a successful PCI procedure with at least one stent deployed
Availability of a hospital bed

Exclusion criteria

Use of alternative anti-thrombin therapy during PCI (e.g. bivalirudin)
High risk patients:
Acute ST elevation MI < 48 hours (either direct PCI or rescue PCI)
Unprotected left main PCI
Obvious large thrombus on angiography
Use of rotablation, atherectomy, or thrombectomy devices
Unsatisfactory PCI results:
Final thrombolysis in myocardial infarction (TIMI) flow < 3
High grade dissection (> type B, if not completely resolved at completion of PCI)
Evident or suspected thrombus
Distal embolization
Suboptimal stenting (> 20% residual stenosis)
Side branch closure (≥ 1.5 mm branch or with associated symptoms)
Abrupt closure during procedure (if prolonged > 15 min or not resolved at completion of PCI)
Clinical instability
Prolonged ischemia during PCI (> 15 min)
Increased hazard of eptifibatide infusion:
Unsatisfactory deployment of a closure device (if used)
Large peri-procedure hematoma making the continuation of eptifibatide hazardous
Any condition that will increase the hazard of continuing eptifibatide
Operator discretion
No informed consent
Active participation in other research studies (unless with special exemption)