MY APPROACH to low-level troponin elevations

Abstract

Cardiac troponin (cTn) I and T complement clinical assessment and the ECG in the early diagnosis of acute myocardial infarction (AMI). cTns are structural proteins unique to the heart. cTn levels in peripheral blood are quantitative markers of cardiomyocyte damage. Thereby, cTns are organ-specific, but not disease-specific, markers. Although AMI is a very important cause of cardiomyocyte damage, and clearly the dominant one in patients presenting with acute chest pain and substantial cTn elevations (eg, 50 times the 99th percentile), multiple other acute and chronic disorders seem to lead to cardiomyocyte damage that can be detected using modern cTn assays. Clinical evaluations of high-sensitivity cTn assays have taught us that detectable (but not elevated) cTn levels are normal and likely reflect cell turnover, and are observed in the majority of healthy individuals using state-of-the art cTn assays. The higher the cTn level at presentation and the higher the absolute change in cTn within the first hour, the higher is the likelihood of AMI. Low-level cTn elevations are those just above the 99th percentile (eg, up to three times the 99th percentile). In patients presenting with acute chest pain, the positive predictive value of low-level cTn elevations for AMI is only about 50%. In patients in whom low-level cTn elevations are detected for other presenting symptoms or possibly during screening, the positive predictive value of low-level cTn elevations for AMI is even lower. I try to answer three questions in order to rapidly identify the cause of low-level cTn elevations.