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Troponins have recently been promoted to playing a pivotal role in the diagnosis of acute myocardial infarction. However, a number of problems arise as a result of this “redefinition” of acute MI The recent joint statement by the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) proposing a “redefinition” of myocardial infarction has aroused much interest but also sparked considerable controversy.1 The basis of the new definition is the promotion of troponins to a pivotal role in the diagnosis of acute myocardial infarction, coupled with the relegation of creatine kinase (CK-MB) to a secondary role; and, in the case of total CK, to the realms of history. Elevation of troponins to centre stage in the drama of acute myocardial infarction is a direct consequence of the recent emergence of new terminology for acute coronary disease. Thus the term “acute coronary syndromes”, coined to describe unstable angina and non-Q wave myocardial infarction, now also includes acute Q wave myocardial infarction. This has stimulated the formulation of management strategies based, at the time of presentation, on the ECG and, subsequently, on the biochemical detection of biomarkers, especially troponins. Thus patients with ST segment elevation myocardial infarction (STEMI) are candidates for thrombolysis while those without are considered to have suspected acute coronary syndromes. Those with typical ST-T changes of ischaemia are treated with low molecular heparin, aspirin, and a β blocker. Those with less typical histories and no acute ECG changes can be observed. It is at this point that measurement of troponins has its greatest value for, if positive at 12 hours after the onset of symptoms, a diagnosis of non-ST segment myocardial infarction (non-STEMI) can be made. Those with normal troponin values, but otherwise considered clinically to have acute ischaemia, are classified as unstable angina while …