It is now accepted that the earliest event in acute myocardial infarction is coronary occlusion caused by fissuring of an atherosclerotic plaque, with resultant platelet deposition on the mural flaw and build up of thrombus within the lumen. The symptoms generated are caused by myocardial ischaemia, as first described by Herrick and Levine some 80 years ago. If occlusion is not relieved, irreversible damage (infarction) begins in the ischaemic region within 30 minutes, is half completed by 2.5 hours, and is virtually completed by six hours. Thrombolysis is now accepted therapy for acute evolving myocardial infarction, but in most cases such therapy is not commenced for four hours after symptom onset, when most of the irreparable damage has already been done and when the potential for benefit has fallen substantially. The average time to thrombolysis in GUSTO worldwide, however, was two hours and, in Australia, 2.8 hours. Only patients who could be submitted to thrombolysis within six hours of the onset of pain were included. The results of thrombolytic therapy in acute thrombosis are likely to be improved if delays are minimised. This requires education of the public in the symptoms of this condition, and on the actions to take if such symptoms arise. It also requires expeditious transfer to hospital (or appropriate treatment outside) and above all it requires expeditious assessment and treatment when patients arrive in hospital. Use of the diagnosis 'myocardial infarction' for such patients implies that irreversible damage has already occurred and serves as a disincentive for the speedy, aggressive management that is logical and appropriate for dissolution of the offending coronary thrombus.