What to expect when measuring high-sensitivity troponin: practical advice for clinicians.

T he path to the high-sensitivity cardiac troponin (hs-cTn) assays has taken more than 2 decades. Historically, after early studies showing superior diagnostic and prognostic performance compared with creatine kinase isoenzymes, conventional cTnI and T were adopted as gold standard biomarkers to evaluate patients with suspected acute coronary syndrome (ACS). Subsequently, work by the Third Global Myocardial Infarction Task Force (2) and others began to focus on exactly what defined an abnormal cTn, recognizing that ACS patients experienced a worse prognosis at cTnI or T concentrations below these biomarkers’ reference limits for myocardial infarction (MI) diagnosis. Indeed, any measurable cTnI or T in the context of an ACS appeared to portend a worse prognosis (3), suggesting the need to reconsider reference ranges for both biomarkers. Accordingly, consensus developed that upper reference limits for cTnI or T should be predicated on the 99th percentile of a healthy normal population (2). However, an important conundrum existed: although the risk of ACS complications appears at very low levels of cTnI or T, such concentrations