Abstract
We appreciate the very insightful comments by Drs Lippi and Cervellin regarding our study1 and agree that the exceptional analytic sensitivity of the novel high-sensitivity (hs) troponin (hsTn) assays raises several very important questions about their optimal use in the evaluation of patients with suspected or proven acute coronary syndrome (ACS), including those with acute myocardial infarction (MI). The tension created today by the hsTn assays is rather reminiscent of that when original cardiac troponin (cTn) methods were released nearly 20 years ago. Indeed, with the initial use of first-generation cardiac-specific cTnT or cTnI assays, it was immediately evident that these tests were more sensitive for acute MI than creatine kinase-MB (CK-MB); this led to confusion about the correct nomenclature of a cTn-positive/CK-MB–negative event. Subsequent studies demonstrated patients with such a syndrome had a risk comparable to that of an acute MI,2 and the biochemical redefinition of acute MI was changed to a cTn …
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