These findings are intriguing, but the reader should be aware of several limitations when interpreting the results of this study. First, the study group was small and highly selected. Exclusion criteria for the ROMICAT I trial included new diagnostic ECG changes, elevated cardiac biomarker, serum creatinine >1.3 mg/dl, or history of CAD revascularization (5). These criteria contributed to recruiting a low-risk population for the current study with mean age of 54 years, 54% female, and 82% Thrombolysis In Myocardial Infarction score 0 to 1. The results of this study might not be generalizable to other ED populations, which characteristically include older patients with more comorbidities, many of whom have established CAD. Second, hsTnT was measured at a single time point. The authors provide only the median time (4.2 h) but not the time range. The hsTnT measured at 4 h after presentation might not provide the same information as a measurement at 2 h or 6 h, even in the same patient. Serial measurements likely reflect optimal performance of the assay ((7),9). Third, 19 patients (14%) had abnormal SPECT, but only 10 of these patients had ischemia. The distinction between ischemic and fixed SPECT defects is clinically important, but the authors did not test for differences in hsTnT between these patient subsets. Only 7 of the 19 patients (37%) with abnormal SPECT had a significant stenosis (>50% diameter narrowing) by CTA or invasive angiography. What is the etiology of the “perfusion defect” in the other 12 patients? The authors suggest that these defects could be caused by plaque rupture in an insignificant stenosis with downstream embolization (Fig. 5 in Ahmed et al. ) but offer no proof for this concept. Of note, mean body mass index of the population was 30 ± 6 kg/m2, and attenuation correction was not applied for processing the SPECT images. Some of the perfusion defects might have represented attenuation artifacts, posing a challenge to explain a statistically significant association between hsTnT levels and the SPECT findings. Fourth, Ahmed et al. (10) analyzed the utility of hsTnT cut-points between 4.26 to 8.62 pg/ml for targeted sensitivities between 60% and 90% (Table 2). Inspection of Figure 1 in Ahmed et al. (10) reveals that these substantial differences in sensitivity thresholds are based on only a handful of data points crossing a narrow range of hsTnT cut-points. The findings would be more robust if based upon more data points. Fifth, the receiver-operating characteristic curve (Fig. 2 in Ahmed et al. ) reveals only fair operating characteristics for hsTnT, which might not result in dismissal of enough patients without performance of additional testing to be cost-effective. Sixth, Figure 3 in Ahmed et al. demonstrates statistically significant associations between log-transformed hsTnT and SPECT summed difference score and CTA coronary segments with plaque, but the correlation coefficients are weak (r2 = 0.15 and 0.08, respectively). Most of the data points line up along the y = 0 axis. The slope of the curve for the SPECT ischemia analysis is heavily influenced by 2 extreme data points in the northeast quadrant of the graph. Seventh, potentially interesting and useful information is not included in the manuscript. The authors allude to the performance of invasive angiography in some patients, but the number of these patients is not provided. The agreement between stenosis number and severity detected by CTA and invasive angiography is not stated. For discrepant results, the authors do not specify which result they selected for their statistical analyses. The original ROMICAT trial (5) reported outcome endpoints. Comparing the prognostic accuracy of hsTnT, SPECT, and CTA could provide insight substantiating the clinical value of these measurements.