Aspirin is effective in reducing the risk of primary and secondary cardiovascular events, such as myocardial infarction and stroke, and is a mainstay of both the adjuvant treatment of acute coronary syndromes and other cardiovascular disease, with a minor effect on reducing the risk of venous thromboembolism. While this impact is widely believed to be caused by suppression of the platelet, aspirin also has likely desirable non-platelet effects—for example, in inhibiting nuclear transcription initiators such as NFκb (implicated in the promotion of various genes with pro-inflammatory activity), in protecting low density lipoprotein cholesterol from oxidative modification, and in modulating endothelial dysfunction in atherosclerosis. However, the precise value of these latter mechanisms in vivo and any possible contribution to a reduction in thrombotic events is speculative.

Although low to medium dose aspirin (32.5–75 mg daily) is well tolerated in the majority of patients, the principle adverse effects are gastrointestinal bleeding and haemorrhagic stroke. 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.^1–3

HOW VALUABLE IS ASPIRIN?

Despite the positive attributes of aspirin described above, several commentators have expressed other concerns that it may not be broadly valuable.⁴ For example, although recruiting patients with hypertension, the HOT trial reported no protective effect of aspirin on death, cardiovascular death, all cardiovascular events, all …