Troponin: A risk‐defining biomarker for emergency department physicians

See also pp. 490–501 In this issue of Emergency Medicine Australasia Jairam et al. report their findings on the clinical impact of using a new high-sensitivity troponin assay in a tertiary teaching hospital in New Zealand. Troponin testing was duplicated in patients in whom troponin (Tn) was ordered as part of their clinical management, using two assays: a 4th generation troponin T (cTnT) and the high-sensitivity TnT (hsTnT) assays. The authors aimed to identify changes in the positivity rate by using the high-sensitivity assay, and to characterize those patients in whom the hsTnT was positive, but the contemporary TnT was negative (the ‘new positive’ group). They described a significant increase in the numbers of patients with elevated troponin levels using the hsTnT assay (the ‘new positive’ group), but found that the diagnoses were often not AMI. Few biomarkers in clinical use are as important as troponin, and yet so complex. Troponin levels continue to define patient populations, and determine the management of those patients presenting with a possible acute coronary syndrome. Recommended management guidelines for admission and monitoring practices, and the use of an invasive strategy exist for those found to be troponin positive; i.e. those with a non-ST-elevation acute myocardial infarction (NSTEMI). Improvements in the sensitivity and precision of troponin assays have occurred since the assay was first developed. This evolution has confused and challenged clinicians, and there has been limited consideration of the broad implications of this change to individual patients, the clinician and health services in general. An elevated troponin has been defined as a value greater than the 99th percentile of a normal population. This value was rarely exceeded when using the early troponin assays, except in the setting of AMI. Historically, it was at this stage that troponin was therefore embraced as a ‘diagnostic’ test. Older biomarkers of AMI such as CK, CK-MB, aspartate amino transferase and lactate dehydrogenase became of limited importance. The conundrum of identifying a patient with AMI from the vast majority of ED patients with possible AMI symptoms appeared solved! With each new generation of troponin assays, clinicians have been forced to relearn the utility of this biomarker in clinical practice. The list of causes for an abnormally elevated troponin has increased, mirroring the improvements in the assays and the lowering of detection limits. Elevations are seen in pathological conditions, including structural heart disease, renal impairment and pulmonary embolism, but might also be seen in extreme exertion, such as marathon runners. It is now clear that when using a highly sensitive assay, circulating levels of troponin will be detected in many normal people. Despite the definitions of AMI always including clinical features of ischaemia, once troponin measurements became available, this biomarker was often used by clinicians as the defining marker for AMI. This can no longer be so when using hs-troponin assays. The key for the diagnosis of AMI again lies in finding the correct