Greater understanding of the underlying pathophysiology of acute myocardial infarction (AMI) has led to more aggressive management and lower mortality, both in-hospital and long term. AMI results mainly from thrombotic occlusion of the infarct-related coronary artery. The ensuing necrosis evolves over a 6-12 h period providing a time window for interventions designed to reduce eventual infarct size. The most appropriate interventions are those which restore coronary artery patency and hence myocardial blood flow as soon as possible. Occasionally, disruption of the occluding thrombus and compression of the underlying atheromatous lesion is best achieved by direct percutaneous transluminal coronary angioplasty. For the vast majority however, revascularisation by drug therapy is more appropriate. As soon as possible, all patients without contraindications should be offered oral aspirin and intravenous thrombolysis, usually with streptokinase but occasionally with tissue plasminogen activator. Patients in whom these agents are contraindicated should be considered for intravenous beta-blockade using atenolol or metoprolol to reduce myocardial demand and hence infarct size. Patients with large infarcts, impaired ventricular function, left ventricular failure or hypertension should be considered for early angiotensin-converting enzyme inhibitor therapy. Other agents may be valuable symptomatically, but have no proven role in reducing infarct size or mortality. After the first 24 h, the main aims of management are to assess the likelihood of later ischaemic events or death (risk stratification) and hence to choose appropriate long term secondary prophylaxis.