Antithrombotic drugs for carotid artery dissection.
BACKGROUND
Extracranial internal carotid artery dissection can lead to occlusion of the artery and hence cause an ischaemic stroke. It is the underlying stroke mechanism in approximately 2.5% of all strokes. It is the second leading cause of stroke in patients younger than 45 years of age. Anticoagulants or antiplatelets may prevent arterial thrombosis in extracranial internal carotid artery dissection, but these benefits may be offset by increased bleeding.


OBJECTIVE
To determine whether antithrombotic drugs (antiplatelet drugs, anticoagulation) are effective and safe in the treatment of patients with extracranial internal carotid artery dissection, and which is the better treatment.


METHODS
We searched the Cochrane Stroke Group Trials Register (last searched 3 October 2002). In addition we performed comprehensive searches of the Cochrane Central Register of Controlled Trials (Cochrane Library Issue 2, 2002), MEDLINE (January 1966 to May 2002) and EMBASE (January 1980 to June 2002), and checked all relevant papers for additional eligible studies.


METHODS
Randomised controlled trials, controlled clinical trials assessing the efficacy of anticoagulants or antiplatelets for the treatment of extracranial internal carotid artery dissection, and non-randomised trials, e.g. case series (studies), that reported on any antithrombotic treatment with at least 4 patients, were eligible for inclusion. Data from all eligible studies were extracted independently by two reviewers. Disagreements were resolved by discussion.


METHODS
Data on the primary outcome measures were extracted systematically. These were: death (all causes) and death or disability. Secondary outcomes were: first stroke occurrence, stroke recurrence, any stroke during reported follow-up, extracranial haemorrhage, and intracranial haemorrhage. The first choice treatment was taken for analyses.


RESULTS
No randomised trials were identified. No reliable comparisons of antiplatelet drugs or anticoagulants with control were available. Twenty-six eligible studies including 327 patients (who either received antiplatelet drugs or anticoagulants) were to be included in the comparative analysis. There was no significant difference in odds of death comparing antiplatelet drugs with anticoagulants (Peto odds ratio (Peto OR) 1.59, 95% CI 0.22-11.59). There was also no significant difference in the odds of being dead or disabled (Peto OR 1.94, 95% CI 0.76-4.91). Few intracranial haemorrhages (0.5%) were reported for patients on anticoagulants, none for patients on antiplatelets.


CONCLUSIONS
There were no randomised trials comparing either anticoagulants or antiplatelet drugs with control. There is, therefore, 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. We suggest that a randomised trial including at least 1400 patients in each treatment arm with this condition is clearly needed.
Lyrer
P
P
Neurology, University Hospital Basel, Petersgraben 4, Basel, Switzerland.
Engelter
S
S
D000925:Anticoagulants / Q000627:therapeutic use*; D020215:Carotid Artery, Internal, Dissection / Q000188:drug therapy*; D018849:Controlled Clinical Trials as Topic; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*
D000925:Anticoagulants; D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors