Glycoprotein IIb‐IIIa inhibitors for acute ischaemic stroke
Abstract
Background
Glycoprotein (GP) IIb‐IIIa inhibitors block the final common pathway to platelet aggregation antagonising with receptors that bind fibrinogen molecules forming bridges between adjacent platelets. Thus, GP IIb‐IIIa inhibitors could favour endogenous thrombolysis by reducing thrombus growth and prevent thrombus re‐formation by competitive inhibition with fibrinogen. Currently used in clinical practice for acute coronary syndromes and percutaneous coronary interventions, they could also be useful for patients with acute ischaemic stroke.
Objectives
To assess efficacy and safety of GP IIb‐IIIa inhibitors in acute ischaemic stroke.
Search methods
We searched the Cochrane Stroke Group trials register (last searched 31 May 2005). In addition, we searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2005), MEDLINE (1966 to June 2005) and EMBASE (1980 to June 2005). In an effort to identify further published, unpublished and ongoing trials we searched reference lists and contacted trial authors and pharmaceutical companies.
Selection criteria
We aimed to analyse unconfounded randomised controlled trials comparing GP IIb‐IIIa inhibitors with placebo in patients with acute ischaemic stroke. Only patients who started the treatment within six hours of stroke onset were included.
Data collection and analysis
Three review authors independently selected trials for inclusion, assessed trial quality and extracted the data.
Main results
Two trials involving 474 patients were included. Only data for 414 patients treated within six hours were considered. Patients were treated with intravenous abciximab or placebo. Treatment with abciximab was associated with a non‐significant reduction of death and dependency combined (odds ratio (OR) 0.79; 95% confidence interval (CI) 0.54 to 1.17) and of death alone (OR 0.67; 95% CI 0.36 to 1.25). Treatment with abciximab was associated with a non‐significant increase of symptomatic intracranial haemorrhages (OR 4.13; 95% CI 0.86 to 19.67) and of major extracranial haemorrhages (OR 1.51; 95% CI 0.25 to 9.12).
Authors' conclusions
There is currently not enough evidence from randomised controlled trials regarding the efficacy or safety of GP IIb‐IIIa inhibitors therapy in acute ischaemic stroke. Results from ongoing trials will help to understand the risk to benefit ratio of these agents.
PICOs
Plain language summary
Glycoprotein IIb‐IIIa inhibitors for acute ischaemic stroke
Most strokes are due to a sudden blockage of an artery in the brain (this type of stroke is called an ischaemic stroke). In most ischaemic strokes, the blockage is caused by a blood clot. Glycoprotein (GP) IIb‐IIIa inhibitors might help to dissolve these blood clots, prevent new clots and so improve the blood supply to the brain. It is possible, if the drug is given within a few hours of the start of the stroke, that this would reduce brain damage and improve the chances of making a good recovery. However, GP IIb‐IIIa inhibitors may also cause bleeding in the brain, and so this complication could offset any benefits. This review aimed to evaluate whether GP IIb‐IIIa inhibitors administered within six hours from stroke onset increases the proportion of independent survivors. The results from two small included studies with 474 patients are inconclusive and cannot rule out a clinical benefit or harm. Future results from ongoing trials will be important to understand the balance of risk and benefit of GP IIb‐IIIa inhibitors for acute ischaemic stroke.
