High-Sensitivity Troponin Assays: Boon or Bane for the Cardiologist?

The Troponin Era The advent of the “troponin era” has its roots in the redefi nition of acute myocardial infarction (AMI) by the joint committee of European and American cardiologists in 2000.1 Troponin was identifi ed as the preferred serologic biomarker for acute coronary syndrome (ACS). Since then, troponin assays have continued to evolve with improved sensitivity and reproducibility, leading to a renewal of guidelines in 2007 and 2012.2 With increasing sensitivity of troponin assays, cutoff levels were lowered. A 99th percentile upper reference limit (URL) refers to the troponin concentration at the 99th percentile of a reference population. The use of the 99th percentile URL increases the ability of these assays to detect both early AMI and structural cardiac abnormalities. The fi rst-generation troponin assays were not suffi ciently sensitive to detect troponins in reference to “healthy” individuals and thus the cutoffs were set at levels at which the assays coeffi cient of variation (CV) were 10%. These early assays were thus not sensitive for early myocardial necrosis but highly specifi c, resulting in its use as a dichotomy tool for ACS rule-in. However, this should not be confused with newer generation high-sensitivity troponin (hsTn) assays, which are assays that have a CV of 10% or less at the 99th percentile URL and are able to detect cardiac troponin levels in at least 50% of the reference normal population.3 hsTn assays have only been available since 2010, with commercial availability still limited to a small number of hsTn assays. They are now able to measure tenfold lower concentrations with higher precision as compared to fi rst generation assays.3 Is the increased sensitivity afforded by hsTn a boon for the cardiologist, or a bane that could result in greater confusion for the physician interpreting these assays?