Antiplatelet therapy for preventing stroke and other vascular events after carotid endarterectomy

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Abstract
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). The objective of this review was 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 (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 reviewers selected trials for inclusion, assessed trial quality, and extracted data independently from each other. From each trial we extracted, first the number of patients originally allocated to each treatment group, and, second 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 0.48-1.24 did not show a statistically significant difference between both treatment groups. For 'stroke (any)' the Peto odds ratio of 0.58 (95%CI: 0.34-0.98) indicated a statistically significant benefit in favour of antiplatelet drugs (p=0.04). Concerning the secondary outcome events '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. 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.