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The advent of cardiac troponin assays has revolutionised the daily assessment and management of patients presenting to emergency rooms with undifferentiated chest symptoms suspicious for acute cardiac ischaemia. This has enhanced the identification of myocyte necrosis thus forming a key part of the contemporary definition for myocardial infarction (MI).1
Seminal work by Katus et al2 led to the demonstration by Hamm et al3 of the clinical applicability of the test in acute coronary syndromes (ACS). Negative troponin being associated with a good prognosis and a positive troponin with an increased frequency of adverse cardiovascular events. Subsequent technical refinements have produced four generations of assays in order to attain the guideline standard of <10% coefficient of variation at the 99th centile of a normal reference population. Point-of-care systems have also been developed and deployed by some to reduce the turnaround time of results and improve patient's flow in busy departments.
The relationship between troponin detection in these assays and poor prognosis has been seen not only in ACS but also in myocardial disease, following cardiac procedures, non-cardiac procedures, acute neurological disease, acute respiratory disease chronic renal disease, pulmonary embolism, exposure to certain toxins, sepsis and critical illness of any aetiology. Indeed, the prognosis …