Antiplatelet therapy has inhibitor effects on platelets because of its suppression of an enzyme, cyclo-oxygenase, that is necessary for the synthesis of certain prostanoids. It has been shown in animal models to delay occlusion, and delay or prevent reocclusion in arteries after successful lysis.
Thus antiplatelet therapy is used in two different ways in ischaemic heart disease.
Firstly, antiplatelet therapy can be used to reduce the risk of complications, for example aspirin in unstable angina halves the risk of mortality.
Secondly aspirin improves the prognosis in acute myocardial infarction, as shown in ISIS-2, where aspirin reduces 5 week mortality from 13.2% to 10.7%.
Meta analysis of data from antiplatelet trials shows that in high risk patients there is a:
The Antithrombotic Trialists' Collaboration meta-analysis (2) showed that aspirin (or another antiplatelet drug) prevents serious vascular events in a wide range of high-risk patients, including people with previous MI, acute MI, previous stroke or TIA, acute stroke, stable angina, intermittent claudication and - if oral anticoagulants are unsuitable - atrial fibrillation. This meta-analysis also showed that low-dose aspirin (75-150mg daily) is as effective as higher aspirin doses for long-term use. A commentary on the meta-analysis (3) states that..'the documented effects of antiplatelet agents accross a wide range of patient groups suggests that low dose aspirin should be given routinely to patients at high or intermediate risk for cardiovascular events (above 2% per year).'
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