Unstable angina usually results from the rupture of an atheromatous plaque within the coronary circulation, which provides a stimulus for platelet deposition and thrombosis.1 If the thrombus is subocclusive it produces intense regional ischaemia, expressed clinically as unstable angina, and there is an ill defined risk of progression to thrombotic coronary occlusion and myocardial infarction. Chest pain is inevitable and treatment with opiates should not be delayed. Nitrates and β blockers are usually sufficient to correct myocardial ischaemia but dihydropyridine calcium antagonists (nifedipine, amlodipine) should be avoided, particularly in patients who are not taking β blockers.2

Because unstable angina is a thrombotic syndrome, treatment with antithrombotic drugs can reduce the risk of myocardial infarction and death. Thrombolytic therapy is unhelpful3 but three randomised trials have confirmed the benefits of aspirin for improving early prognosis.4-6 In one trial, unfractionated heparin was shown to have a similar beneficial effect, although there was no clear advantage over aspirin alone.6 Three further studies have confirmed that the combination of unfractionated heparin and aspirin confers little additional protection to that provided by aspirin alone.7-9 Nevertheless, meta-analysis has suggested that unfractionated heparin may make a small independent contribution to risk reduction in unstable angina (risk ratio 0.67, 95% confidence interval 0.44 to 1.02), and perhaps for this reason it remains widely used in combination with aspirin.10

A range of newer antithrombotic drugs has recently become available. Low molecular weight heparin, which has a more predictable anticoagulant effect than unfractionated heparin and can be given by subcutaneous injection without the …