Abstract
The diagnosis of acute myocardial infarction (AMI) relies strongly on the release of cardiac troponins (cTn) (either cardiac troponin I [cTnI] or T [cTnT]) into the blood-stream, which are the preferred biomarkers of myocardial injury. Recent improvement in the analytical performance of the troponin assays resulted in more accurate and sensitive detection of circulating cTn. These high-sensitivity (hs) assays are therefore able to detect cTn in almost every individual of the general population, enabling a precise determination of the 99th percentile cut-off value for the diagnosis of AMI.
The clinical introduction of the hs-cTn assays resulted in improved diagnostic sensitivity for AMI and therefore expedited an early initiation of evidence-based treatment and management. However, this improved sensitivity for AMI has come at a cost of specificity. Elevations of cTn exceeding the diagnostic cut-off for AMI are now detected in patients with acute or chronic cardiomyocyte injury other than AMI, and these elevations are invariably associated with adverse outcomes.
Defence date: 04/03/16