After reading the report by Pfortmueller et al, we are concerned that readers might be negatively influenced by the unsupported and wrong conclusions on the diagnostic performance of high-sensitivity troponin T (hsTnT) in patients with suspected acute coronary syndrome, particularly in those with renal insufficiency. The analyses are based on a cross-sectional survey on 1,514 consecutive patients admitted to the emergency department of the University Department of Bern. An elevated cardiac troponin T value greater than the ninety-ninth percentile of a healthy reference population was found in 346 consecutive patients (22.8%) admitted with suspected acute coronary syndrome, of whom 170 patients (49%) were diagnosed as having an acute myocardial infarction (AMI). In another 176 patients (51%), elevated cardiac troponin T values were related to noncardiac causes.

The most important finding of this survey was that a single hsTnT on presentation performed only moderately (area under the curve 0.741) for the diagnosis of an AMI in patients with preserved renal function (Modification of Diet in Renal Disease [MDRD]-estimated glomerular filtration rate [eGFR] >60 ml/min) and poorly (area under the curve 0.531) in patients with a moderately or severely reduced renal function (MDRD-eGFR <60 ml/min).

We believe that the study findings have not been analyzed and presented properly, not in accordance with the universal myocardial infarction definition criteria, in compliance with current European Society of Cardiology guideline recommendations, or with European or North American consensus recommendations. Although the investigators emphasize that inclusion of patients was restricted to cases with serial troponin measurements, the findings presented on the diagnostic performance of hsTnT are solely based on a single baseline value.

Not unexpectedly, implementation of analytically more sensitive or highly sensitive high-sensitivity troponin (hsTn) assays has been reported not only to increase clinical sensitivity, for example increase the number of patients with either an AMI and patients with true cardiac troponin elevations due to acute or chronic noncoronary or noncardiac reasons such as renal failure, but also to decrease clinical specificity as troponin release is not exclusively due to AMI. To restore clinical specificity, it has been endorsed to consider not only a single baseline value but also early kinetic changes. The disappointing findings of the present study are clearly explained by the inappropriate and unsupported way to diagnose an AMI from a single hsTnT value on presentation. Serial troponin measurements are deemed particularly important in the presence of small cardiac troponin elevations, nonspecific symptoms such as dyspnea, and confounding comorbidities such as renal failure. The impact of the latter is demonstrated nicely in Table 4 of the study. In patients with an MDRD-eGFR <60 ml/min presenting without chest pain or dyspnea, all patients demonstrated an hsTnT concentration greater than the ninety-ninth percentile yielding a sensitivity of 100% but only a clinical specificity of 10%.

Implementation of serial measurements would have increased clinical specificity at the cost of clinical sensitivity and would at least have helped to discriminate acute from chronic stable troponin elevations. This is paramount as in this study most patients did not have relative concentration changes high enough to support the presence of an acute relevant rise and/or fall as suggested by consensus groups on the appropriate use of hsTn. Relative changes were very low for patients with and without an MDRD-eGFR of <60 ml/min (0% [0 to 17] vs 0% [−8 to 14], p = 0.0759).

We strongly believe that all conclusions in this article are unsupported and misleading. Clinicians should know potential caveats and apply hsTn assays with scrutiny and a basic knowledge that is required for interpretation. However, even if hsTn assays are applied correctly, it may still be a challenge to identify the exact underlying reason for elevated cardiac troponin in many cases. Therefore, we strongly endorse following the recommendations of European Society of Cardiology guidelines for an extensive diagnostic work-up with additional biomarker testing and cardiac imaging.