• Clin. Chim. Acta · Mar 2009

    Case Reports

    Interpretation of high sensitivity cardiac troponin I results: reference to biological variability in patients who present to the emergency room with chest pain: case report series.

    • Alan H B Wu.
    • Department of Laboratory Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, CA 94110, United States. wualan@labmed2.ucsf.edu
    • Clin. Chim. Acta. 2009 Mar 1;401(1-2):170-4.

    BackgroundThe development of highly sensitive cardiac troponin (cTnI) assays has increased the number of true and false positive results for patients suspected of acute myocardial infarction (AMI). Cases are reported whereby the use of serial testing, the 99th percentile cutoff, and the application of biological variation of cTnI were used to help determine ischemic vs. non-ischemic causes of myocardial injury.MethodscTnI was measured using the Siemens Ultra assay from 13 representative patients who presented to the emergency department with symptoms suggestive of acute cardiac disease. Based on a previous study, reference change values of a 46% increase and 32% decrease were used to interpret results. These differences were compared against the patient's discharge diagnosis.ResultsTwo patients who subsequently ruled in for AMI had a negative cTnI (<0.04 microg/l) and borderline positive cTnI (0.07 microg/l) at admission, respectively. While the 4-6 h results were also borderline, there was a significant increase from the baseline (+575% and +50%, respectively) to suggest the presence of an acute cardiac event. Two other AMI cases document the significant cTnI decline in results after peak values. In 7 other non-AMI cases (heart and renal failure, gastrointestinal bleeding, stroke and venous thrombosis), while baseline concentrations were clearly positive (0.18-2.12 microg/l), subsequent serial samples were not significantly increased or decreased from baseline. These findings were not typical for AMI. There were 2 cases with acute blunt cardiac trauma and intracranial hemorrhage, respectively, that produced cTnI results that were initially low (<0.04 and 0.05 microg/l, respectively), but significantly increased with serial testing thereby producing false positive Delta cTnI results for AMI.ConclusionsSerial testing for troponin was useful in differentiating early AMI from non-ischemic causes of troponin increases. However, non-AMI patients with acute cardiac injury can produce troponin results that mimic AMI. Therefore serial troponin testing must be used in conjunction with clinical presentation and other laboratory findings.

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