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Over 50 years ago, pathologists hotly debated the question of whether myocardial infarction was caused by coronary thrombosis.1 This reflected the observation that, in patients who had died from acute myocardial infarction (AMI), postmortem examinations often failed to demonstrate the presence of intracoronary thrombosis. Even when it had been identified, it was often attributed to postmortem change or artefact rather than having any aetiological or pathogenetic significance.1
The advent of coronary angiography allowed the time course of myocardial infarction to be characterised more precisely; it was soon appreciated that spontaneous coronary reperfusion is a common time dependent occurrence with 30% of infarct related arteries reperfusing within the first 12 h of presentation with ST segment elevation myocardial infarction.2 Moreover, with the more widespread use of primary percutaneous coronary angiography, we now recognise that 30% of patients will have normal or near normal blood flow in the infarct related coronary artery at presentation. This observation is attributable to endogenous fibrinolysis causing coronary thrombus dissolution. Indeed, endogenous fibrinolysis is an effective and powerful mechanism for causing coronary recanalisation, albeit more slowly than pharmacological thrombolytic therapy. By 2 weeks post-myocardial infarction, the residual coronary stenosis is identical whether patients have received thrombolytic therapy or not (figure 1).3 This underscores the effective clearance of coronary thrombus by endogenous fibrinolysis. This also explains why pathologists had been misled, with endogenous fibrinolysis rapidly clearing the culprit coronary thrombosis before death and postmortem examination occurred in the days after presentation.
The majority of atherosclerotic lesions responsible for the initiation of AMI do not cause major obstruction of the coronary lumen—86% being <70% diameter stenosis (figure 2).4 5 This is …