Measuring cardiac troponins is integral to diagnosing acute myocardial infarction (AMI); however, troponins may be elevated without AMI, and the use of multiple different assays confounds comparisons. We considered characteristics and serial troponin values in emergency department chest pain patients with and without AMI to interpret troponin excursions. We compared serial troponin in 124 AMI and non-AMI patients from the observational Performance of Triage Cardiac Markers in the Clinical Setting (PEARL) study who presented with chest pain and had at least one troponin value exceeding the 99th percentile of normal. Because 8 assays were used during data collection, we employed a method of scaling the troponin value to the corresponding assay's 99th percentile upper reference limit to standardize the results. In 81 AMI patients, 96% had elevated troponin at the first test following initial elevation, compared to 73% of the 43 non-AMI patients ( P < 0.001). Scaling troponin to the 99th percentile of normal yielded a median value that was 4.8 [2.2, 14.1] times higher than the 99th percentile cutpoint among AMI patients, compared to 2.3 [1.5, 6.5] times higher among non-AMI patients ( P = 0.04). The rise in serial scaled troponin values distinguished the AMI patients. Scaling to the 99th percentile was useful for comparing troponin when different assays were utilized. H igh-sensitivity troponin I testing has been shown to improve the early diagnosis of acute myocardial infarction (AMI) and aid with risk stratifi cation ( 1 -3 ). Investigators using a registry in Australia and New Zealand determined that high-sensitivity troponin I testing was associated with fewer in-hospital adverse events for patients hospitalized with possible acute coronary syndrome ( 4 ). Th ere are multiple non-AMI clinical scenarios, however, where troponin may exceed the 99th percentile, including renal failure, stroke, heart failure, pulmonary embolism, sepsis, and hypertension ( 5 ). We capitalized on a data set of chest pain patients who had serial troponin assays performed, had at least one positive value, and had central adjudication of the outcome of AMI. We compared the characteristics, as well as the dynamic rise and fall of troponin, in this group of patients to better understand how to quantitatively evaluate the excursion of troponin and relate it to the confi rmed diagnosis of AMI.