Lower specificity and lower positive predictive value necessitate a cautious approach
The advent of cardiac troponin (cTn) assays has redefined acute myocardial infarction (AMI) and revolutionised the care of patients with suspected AMI presenting to emergency departments (EDs).1 So central has cTn measurement become to the diagnosis of AMI that, since 2000, the formal criteria start with detection of rise and/or fall in serum troponin levels (with at least one value above the 99th percentile of the value distribution of a reference population for an assay with optimal precision at this level, defined as a coefficient of variation ≤ 10%), to which clinical evidence of myocardial ischaemia is added in regard to symptoms, electrocardiogram (ECG) changes or findings on cardiac imaging.2 This revised definition of AMI, with cTn assays using 99th percentile cut-off values, has altered the epidemiology of the disease. Data from Western Australia suggest that in the two decades before the advent of cTn testing in 1998, age-specific hospitalisation rates for AMI had decreased by an average of 30%, but this downward trend was abolished between 1998 and 2004.3
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