Patients with narrowing of one of the major blood vessels to the brain, the internal carotid artery, are at risk of stroke. The surgical operation to remove the narrowing (carotid endarterectomy) can reduce the long-term risk of stroke. Drugs such as aspirin which prevent blood platelets forming clots (antiplatelet drugs) can also reduce the risk of stroke, but can sometimes cause serious bleeding. This review showed that antiplatelet drugs can also reduce the risk of stroke in patients undergoing carotid endarterectomy. There was limited information on bleeding risk. The review's conclusions supported the routine use of antiplatelet drugs such as aspirin in patients having carotid endarterectomy.
Our results may indicate that antiplatelet drugs did not significantly change the odds of death but reduce the outcome 'stroke of any cause' in patients undergoing carotid endarterectomy. However, it can not be excluded that the beneficial effect in reducing stroke is due to chance. There is a suggestion that antiplatelets may increase the odds of haemorrhage, but there are currently too few data to quantify this effect.
Antiplatelet drugs are effective and safe in a wide variety of patients at high risk of vascular ischaemic events. Among patients undergoing vascular surgical procedures, these agents significantly reduce the risk of graft or native vessel occlusion. In this context we wished to examine their effects in patients after carotid endarterectomy (CEA).
To evaluate whether antiplatelet agents are safe and beneficial after endarterectomy of the internal carotid artery.
We searched the Cochrane Stroke Group Trials Register (last searched 1 October 2002). In addition we performed comprehensive searches of the Cochrane Controlled Trials Register (The Cochrane Library Issue 3, 2002), MEDLINE (January 1966 to September 2002) and EMBASE (January 1980 to September 2002), and checked all relevant papers for additional eligible studies.
We selected randomised, controlled, unconfounded trials comparing antiplatelet agents with control after carotid endarterectomy in symptomatic or asymptomatic carotid stenosis of different degrees. Treatment duration had to be at least 30 days after CEA. Follow up should be at least three months.
Two review authors selected trials for inclusion, assessed trial quality, and extracted data independently from each other. From each trial we extracted the number of patients originally allocated to each treatment group, and the number of patients who met the criteria for each outcome (intention-to-treat analysis). We calculated a weighted estimate of the odds for each outcome event across studies using the Peto odds ratio method.
Six trials involving 907 patients were identified. For 'death (all causes)' the Peto odds ratio of 0.77 with a 95% confidence interval (CI) of 0.48 to 1.24 did not show a statistically significant difference between both treatment groups. For 'stroke (any)' the Peto odds ratio of 0.58 (95% CI: 0.34 to 0.98) indicated a statistically significant benefit in favour of antiplatelet drugs (P = 0.04). For 'vascular death', 'stroke or vascular death', 'serious vascular events', 'death or dependency', 'myocardial infarction', 'major extracranial haemorrhage', 'local haemorrhage requiring surgery', 'restenosis', 'TIA or amaurosis fugax', neither any benefit nor any hazard of antiplatelet drugs could be shown. For the outcome events 'intracranial haemorrhage', 'ischaemic stroke' and 'occurrence or progression of contralateral stenosis', data were either too sparse for meaningful analyses, or not available at all.