MJA
MJA

Troponin measurement and the new assays: how low can we go?

Con N Aroney, Peter E Hickman, Hans G Schneider, Jillian R Tate and Martin Than
Med J Aust 2010; 192 (5): . || doi: 10.5694/j.1326-5377.2010.tb03500.x
Published online: 1 March 2010

More sensitive assays may provide more information, but we are not yet sure of the clinical relevance of this information

The introduction of troponin measurement into clinical practice in Australia 10 years ago led rapidly to its widespread use as the marker of choice for diagnosis and risk stratification of patients with acute coronary syndrome (ACS). However, opportunities remain for improving risk assessment in “troponin-negative” patients, many of whom will have adverse events. This has led to the development of new, improved assays that are able to measure down to much lower concentrations than before (10–100-fold lower than current assays), and that increase the detection of acute myocardial infarction, as shown in two recent cohort studies.1,2 The improved analytical performance of these assays may be particularly useful in the early period following the onset of chest pain. These two studies indicated improved diagnostic accuracy of samples taken from patients with chest pain, both at the time of presentation to the emergency department (ED), and within 3 hours of symptom onset.1,2 This improved early sensitivity may lead to significant benefits in ruling out ACS, and in risk assessment, diagnosis and management of patients with ACS, although neither of these studies provided corroboration with clinical outcome.

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