Over many years doctors have used differing definitions as to what constitutes a myocardial infarction (MI). Hospitals in the same town and doctors in the same hospital have used differing definitions. Patients with similar MIs may be either reassured or frightened, have four or five medications or none, be able to drive or fly or not, based on the whim of which doctor may be on call on the particular day that an atheromatous plaque ruptures or fissures. Similarly, health statistics have been bedevilled by differing definitions. In 2000, the criteria for the diagnosis of myocardial infarction were redefined by a consensus group of the European Society of Cardiology and the American College of Cardiology.1

The new criteria recognised the fact that neither the clinical history nor the ECG has adequate sensitivity or specificity. The ECG is the prime investigation for determining eligibility for the administration of fibrinolytic therapy. For the diagnosis of MI, however, its sensitivity is only between 55 and 75%.2^–4 Central to the redefinition was the preferred use of troponins over creatine kinase myocardial band (CKMB) to detect myocyte necrosis and the requirement to have a rise and/or fall in troponin levels and either ischaemic symptoms or electrocardiographic (ECG) changes of ischaemia. Troponins have been shown to be more sensitive and specific markers of myocyte necrosis than CKMB5 and CKMB has been shown to be unsuitable as a diagnostic gold standard for the diagnosis of MI.6 Elevation of troponins is pathognomonic of cardiac myocyte necrosis5 and it has been 9 years since troponins were shown to be useful for the diagnosis of MI7 and 8 years since they were shown to be prognostically important.8

Several concerns were expressed about the redefinition, including the failure of the new definition …