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


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


METHODS
We searched the Cochrane Stroke Group specialised Trials Register for relevant randomised trials and controlled clinical trials. In addition, we performed comprehensive searches of MEDLINE and EMBASE and checked reference lists of all relevant papers for additional eligible studies.


METHODS
Randomised controlled trials, controlled clinical trials assessing the efficacy of antiplatelet drugs or anticoagulants in the treatment of extracranial carotid artery dissection. For non-randomised trials, case series (studies), that reported on antithrombotic treatment with at least 4 patients, were eligible. All trials and studies were assessed for eligibility. 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: all deaths, vascular deaths, and 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 and 49 case series (including 683 treated patients) were identified. No reliable comparisons of antiplatelet drugs or anticoagulants with control were available. 24 eligible studies including 286 patients (who either received antiplatelet drugs or anticoagulants) were included in the analysis. There was no significant difference in odds of death comparing antiplatelet drugs with anticoagulants, odds ratio (OR) 2.41, 95% CI 0.27-21.80). There was also no significant difference in the odds of being alive but disabled (OR 1.65, 95% CI 0.50-5.42). Few major haemorrhages were reported.


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 1000 patients in each treatment arm with this condition is clearly needed.
Lyrer
P
P
Neurology Dept., University Hospital Basel, Petersgraben 4, Basel, Switzerland, CH-4031. plyrer@uhbs.ch
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*; D016032:Randomized Controlled Trials as Topic
D000925:Anticoagulants; D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors