Many patients self-present or are referred by primary care to the emergency department with chest pain because of the potential that they may be suffering an acute myocardial infarction, one of the most common causes of death worldwide.1 Owing to diagnostic uncertainty, the majority of these patients are admitted, and, in some centres, chest pain is responsible for up to 40% of all unplanned hospital admissions.2 The majority of these admissions are unnecessary and place additional burden on healthcare systems that are already struggling to cope with increasing emergency care attendances. Approaches to improve the accurate identification of patients with myocardial infarction would therefore be welcome and a potential major benefit.

Cardiac troponins are regulatory muscle proteins that are released into the circulation after acute myocardial injury. Assays that quantify cardiac isoforms of troponin have greater specificity and sensitivity for the diagnosis of myocardial infarction than traditional cardiac enzymes.3 ,4 Recent advances have led to greatly improved assay sensitivity, permitting quantification of extremely low serum concentrations of troponin with excellent precision. High-sensitivity cardiac troponin assays have limits of detection 10–100-fold lower than contemporary assays and are able to detect troponin in the circulation of the majority of healthy persons.4 These assays have the potential to transform how we assess patients with chest pain in the emergency room.

Myocardial infarction is defined as a rise and/or fall in cardiac troponin with at least one value above the 99th centile upper reference limit in the context …