Anti platelet therapy and the vascular tree

Andrew D Blann ^1*

¹ City Hospital, Birmingham, United Kingdom

^* To whom correspondence should be addressed. E-mail: a.blann{at}bham.ac.uk.

Accepted 3 August 2005

Abstract

Aspirin is effective in reducing the risk of primary and secondary cardiovascular events such as myocardial infarction and stroke[1-3] and is a mainstay of both the adjuvant treatment of acute coronary syndromes and other cardiovascular disease[4-8], with a minor effect on reducing the risk of venous thromboembolism.[9,10] Whilst this impact is widely believed to be due to suppression of the platelet, aspirin also has desirable non-platelet effects, for example, in inhibiting nuclear transcription initiators such as NFb (implicated in the promotion of various genes with pro-inflammatory activity)[11], in protecting low-density lipoprotein cholesterol from oxidative modification[12], and in modulating endothelial dysfunction in atherosclerosis.[13] However, the precise value of these latter mechanisms in vivo and any possible contribution to a reduction in thrombotic events is speculative. However, although low to medium dose aspirin (32.5 - 75 mg daily) is well tolerated in the majority of patients, the principle adverse effects are gastro-intestinal bleeding and haemorrhagic stroke.[14-16] A meta-analysis of 16 placebo controlled trials of aspirin for cardiac and other indications found that aspirin increased the absolute risk of cerebral haemorrhage by 12 events per 30,000 person-years of follow up. Thus, the possible value of aspirin in reducing thrombosis may be weighed against the risk of bleeding, with the greatest value being in those at highest cardiovascular risk.[7,17]

Keywords: aspirin, clopidogrel, platelets, thrombosis

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