2010, Volume 17, Supplement 1: Aspirin – reassessing its role in cardiovascular disease

Report from a scientific roundtable meeting held at the Royal Society of Medicine, London, in October 2009....

Identifying targets in the thrombosis pathway Figure 1 summarises the central role of platelets in the genesis of thrombosis.1 The platelet is initially activated in response to shear stress, events … Continue reading Aspirin – scope and limitations →...

Antithrombotic drugs act principally by inhibiting platelet function directly (for example, aspirin, clopidogrel and dipyridamole) or, via thrombin inhibition, by inhibiting platelet activation and fibrin formation (for example, heparins, warfarin and direct inhibitors of thrombin or factor Xa). Aspirin and other antiplatelet drugs reduce the risk of cardiovascular events such as thrombus formation (figure 1) by approximately 25 per cent in both primary and secondary prevention.(1) Inhibiting more than one pathway at a time significantly increases efficacy: dual antiplatelet therapy with aspirin plus clopidogrel is more effective than aspirin monotherapy in patients with acute coronary syndrome (ACS)(2) and aspirin plus dipyridamole is more effective than aspirin for secondary prevention of stroke.(3) All antiplatelet therapies are associated with an increased risk of bleeding; whereas the balance of benefit and the increased risk of bleeding is clear for secondary prevention, it is less certain for primary prevention....

The efficacy of aspirin in secondary prevention of cardiovascular disease is well understood but its position in primary prevention of cardiovascular events is less clear....

Variable and sometimes ineffective drug treatment is not uncommon in the treatment of cardiovascular disease.(1) In most cases lack of patient compliance is the explanation but other reasons may also exist. In the case of aspirin, “low responsiveness” or “resistance” to aspirin in pharmacological terms would mean that the compound fails to reach its therapeutic goal, i.e. inhibition of platelet COX-1-dependent thromboxane formation. However, in vivo there might be also changes in platelet sensitivity or “residual” platelet activity independent of aspirin treatment, probably unrelated to the drug’s pharmacodynamic actions.(2)...

Aspirin has revolutionised the management of cardiovascular disease (CVD) but it is apparent that clinical outcomes need to be improved further. The three-year follow-up of the Reduction of Atherothrombosis for Continued Health (REACH) registry shows that, despite optimal medical therapy with aspirin, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors and statins, the risk of recurrent myocardial infarction, stroke and vascular death remains high for patients with coronary artery disease, cerebrovascular disease and peripheral arterial disease, especially for those with a high symptom burden.(1)...