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Weappreciate the interest ourmanuscript has raised and respond to the comments abridgedly pointing at recent literature. Our patient cohort consisted of consecutive ED patients having hs-cTn measurements (AMI n = 609; controls n = 964; see Fig. 1 from our manuscript) [6]. By this procedure only patients with an a priori suspicion of myocardial damage were included. However, a selection as suggested by Dr. Badertscher et al. would likewise be biased, as only about half of the AMI patients present with chest pain [1]. Retrospectively the physicians' intentions cannot be evaluated— heart failure and pulmonary embolism are exemplary for a wide variety of conditions leading to the release of cTn, necessitating an interpretation in a broader context [2]. Recent literature suggests that “there is now a large and convincing body of evidence to support the assertion that low hs-cTn cutoffs can be used to rule out AMI with a single blood test” [3]. Alone, combined with an electrocardiogram, or in modeling approaches, cTn can be used to rule out AMI [4]. While “the proportion of patients who could have AMI ruled out varies widely by cohort, with estimates ranging from 6% to 61%” [3], comparability between c-statistics depends on the homogeneity of the cohorts and the prevalence of non-T1MI therein. Serial measurements can improve the specificity of a given test, but not independently from pathophysiological dynamics. The purpose of