Carotid artery dissection means a tear in the lining in one of the main blood vessels carrying blood to the brain. Dissection can be caused by injury to the neck, but can sometimes develop for no obvious reason. Blood clots can form where the artery is torn. These blood clots can then block the artery and cause a stroke. Blood thinning drugs such as aspirin and anticoagulants might prevent clots forming and so prevent stroke in people with carotid artery dissection. We did not find any completed randomised trials testing these drugs in people with carotid artery dissection. However, there is one ongoing trial. We found only poor quality non-randomised studies that compared anticoagulants with aspirin. There was no evidence that anticoagulants were better than aspirin. Aspirin is likely to be similarly effective and safe as anticoagulants in such patients. More research is needed.
There were no randomised trials comparing either anticoagulants or antiplatelet drugs with control, thus there is no evidence to support their routine use for the treatment of extracranial internal carotid artery dissection. There were also no randomised trials that directly compared anticoagulants with antiplatelet drugs and the reported non-randomised studies did not show any evidence of a significant difference between the two.
Extracranial internal carotid artery dissection (eICAD) is a leading cause of stroke in younger patients.
1. To determine whether, in patients with eICAD, treatment with anticoagulants, antiplatelet agents or control was associated with a better functional outcome.
2. To compare, among patients treated with either anticoagulants or antiplatelet agents, the risk of ischaemic strokes and major bleeding episodes.
We searched the Cochrane Stroke Group Trials Register (last searched 3 October 2009). In addition, we performed comprehensive searches of the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2009), MEDLINE (January 1966 to November 2009) and EMBASE (January 1980 to November 2009), checked all relevant papers for additional eligible studies and contacted authors and researchers in the field.
Randomised controlled trials, controlled clinical trials and non-randomised studies (if they reported on outcome stratified by antithrombotic treatment and included at least four patients) of anticoagulants or antiplatelet agents for the treatment of extracranial internal carotid artery dissection. Two review authors independently extracted data.
Primary outcomes were death (all causes) and death or disability. Secondary outcomes were ischaemic stroke, symptomatic intracranial haemorrhage, and major extracranial haemorrhage during the reported follow-up period. The first choice treatment was taken for analyses.
We did not find any completed randomised trials. Comparing antiplatelets with anticoagulants across 36 observational studies (1285 patients), there were no significant differences in the odds of death (Peto odds ratio (Peto OR) 2.02, 95% CI 0.62 to 6.60), or the occurrence of ischaemic stroke (OR 0.63, 95% CI 0.21 to 1.86) (34 studies, 1262 patients). For the outcome of death or disability, there was a non-significant trend in favour of anticoagulants (OR 1.77, 95% CI 0.98 to 3.22; P = 0.06) (26 studies, 463 patients). Symptomatic intracranial haemorrhages (5/627; 0.8%) and major extracranial haemorrhages (7/425; 1.6%) occurred only in the anticoagulation group; however, for both these outcomes, the estimates were imprecise and indicated no significant difference between the two treatment modalities.