The evidence that aspirin improves outcomes in unstable angina is both clear and overwhelming.1 The same cannot be said for the combination of aspirin and unfractionated heparin (UFH) compared with aspirin alone. All the trials conducted in this area have been underpowered to detect significant difference in the risk of death, myocardial infarction (MI), and recurrent ischaemia.2-4 A pooled analysis does suggest that UFH is superior to placebo in the presence of aspirin,5 but no single trial has been able to confirm this, nor have trials of sufficient size been performed. Treatment with UFH is associated with a significant failure rate, for which a number of explanations have been suggested. Firstly, the anticoagulant effect of UFH is unpredictable and, despite regular monitoring, many patients are not maintained within the optimum activated partial thromboplastin time (aPTT) range of 1.5–2.5 times control. Secondly, UFH is susceptible to binding by plasma proteins and neutralisation by platelet factor IV. Thirdly, a rebound phenomenon has been identified after the cessation of UFH. This has been demonstrated, especially in the absence of aspirin.3 6 Fourthly, the antiplatelet effects of aspirin may be overcome in the presence of a potent stimulus from disrupted plaque.

Low molecular weight heparins (LMWHs) have advantages over UFH that may result in greater efficacy and safety, as well as the practical advantages of subcutaneous administration and a predictable anticoagulant effect that removes the need for monitoring. The ESSENCE trial was designed to compare the safety and efficacy of enoxaparin with UFH in patients with unstable angina and non-Q wave myocardial infarction. Enoxaparin is an LMWH with a different chain length and anti-IIa:anti-Xa activity profile compared to other LMWHs.