High-sensitivity Cardiac Troponin: From Theory to Clinical Practice

Abstract

Since 2000, cardiac troponin (cTn) has been the recommended biomarker for the evaluation of patients with a possible diagnosis of acute myocardial infarction (AMI). Most of the cTn immunoassays currently in use lack the analytical sensitivity to accurately measure the upper reference limit (URL), ie, the 99th percentile reference value, which is the guideline-mandated cutoff value for myocardial injury. Consequently, current methods fail to detect some cTn values slightly higher than the 99th percentile, which can be present during the earlier phases of non-ST-segment elevation myocardial infarctions, and miss some smaller infarctions all together. This shortcoming has led to the development of the so called high-sensitivity cTn assays (hs-cTn), which can measure cTn concentrations 5 to 10 times lower than current assays and do so with improved analytical imprecision. With these assays, the diagnosis of AMI will remain specific, but will increase in frequency. In addition, it is likely that the percentage of elevations due to ischemic heart disease will diminish, because other more occult causes of cardiac injury will be revealed as being more common than previously appreciated. Since 2010, cardiac troponin T (cTnT) has been the only high-sensitivity assay (hscTnT) available. Recently, a high-sensitivity assay for troponin I (hs-cTnI) was released for use in Europe and Asia and other assays will become available in the near term. This Editorial will attempt to clarify some of the controversial issues intrinsic to this developing field and will discuss the usefulness of hs-cTn in different clinical scenarios. It will also alert readers to gaps in our understanding, some of which have recently been revealed in an important Spanish study.