Evaluation of Reopro and Stenting to Eliminate Restenosis - ERASER

Description:

Abciximab vs placebo to prevent in-stent restenosis.

Hypothesis:

The glycoprotein IIb/IIIa inhibitor abciximab would reduce neointimal hyperplasia following intracoronary stenting

Study Design

Study Design:

Patients Screened: Not reported
Patients Enrolled: 225
NYHA Class: Not reported
Mean Follow Up: 6 months
Mean Patient Age: Average 59 years
Female: 21%
Mean Ejection Fraction: Not evaluated

Patient Populations:

Target lesions were de novo 50% or greater stenoses in native coronary arteries with a diameter of 2.75–3.5 mm.

Exclusions:

MI in previous 72 hours, evident coronary thrombus, previous coronary intervention on nontarget lesion within past 6 months, planned debulking before stent placement, expected inability to access the target lesion by IVUS (e.g. calcified plaque, tortuous vessel), contraindications to abciximab

Primary Endpoints:

Percent in-stent volume obstruction (measured at six months with IVUS)

Secondary Endpoints:

Target lesion mean and minimal lumen diameter (MLD), late loss, and loss index by quantitative coroanry angiography; death + MI + target vessel revascularization

Drug/Procedures Used:

Patient randomized to one of three groups: 1.) placebo bolus plus placebo infusion, 2.) abciximab 0.25 mg/kg bolus plus 12 hour infusion at 0.125 ug/kg/min (maxium 10 ug/min), 3.) abciximab 0.25 mg/kg bolus plus infusion for 24 hours. Intravascular ultrasound was used to guide optimal stenting.

Concomitant Medications:

Aspirin, heparin, ticlopidine, nitroglycerin

Principal Findings:

There were no significant differences between groups in primary end point --> tissue volume as percentage of stent volume was 25%, 27%, and 29% in the placebo, abciximab12 hour, and abciximab 24 hour groups, respectively. Binary restenosis rates were 11.6%, 18.9%, and 19.4%, respectively (p=NS). Late loss indices were 0.33, 0.52, and 0.47, respectively (p=NS). There also no difference between the groups in the secondary composite endpoint of death, MI, and target vessel revascularization (25.4% in placebo and 21.4% in combined abciximab groups).

Interpretation:

Aggressive platelet inhibition with abciximab does not reduce the rate of in-stent restenosis. In the recent TARGET study comparing abciximab to aggrastat, the aggrastat group had a non-significant lower rate of target vessel revascularization (TVR), even among diabetic patients. Taken together, these results suggests that there is no durable benefit of glycoprotein 2b3a inhibitors in preventing restenosis, and no benefit of abciximab in particular.

References:

Circulation 1999; 100: 799–806.

Clinical Topics: Invasive Cardiovascular Angiography and Intervention

Keywords: Platelet Aggregation Inhibitors, Coronary Disease, Constriction, Pathologic, Coronary Vessels, Immunoglobulin Fab Fragments, Hyperplasia, Diabetes Mellitus, Stents, Platelet Glycoprotein GPIIb-IIIa Complex


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