Earlier Detection of Myocardial Injury in a Preliminary Evaluation
Earlier Detection of Myocardial Injury in a Preliminary Evaluation
Cardiac troponins are important biochemical markers for defining the presence of myocardial injury. However, limitations in troponin testing exist, including the relatively late increase in troponin after onset of ischemia. We therefore evaluated a more sensitive troponin assay for detection of myocardial injury in "early presenters." Discarded serial specimens were obtained from 103 patients who had a negative cardiac troponin I (cTnI) result followed by a positive cTnI result. Results were obtained using our current cTnI method and a new more sensitive assay, TnI-Ultra (Siemens Medical Solutions, Diagnostics Division, Tarrytown, NY). Medical records were reviewed to determine the clinical diagnosis. Precision studies yielded a 10% coefficient of variation at the diagnostic cut points for cTnI (0.10 ng/mL [0.10 μg/L]) and TnIUltra (0.04 ng/mL [0.04 μg/L]). TnI-Ultra was positive before cTnI in 66 (64.1%) of 103 cases. We conclude that the more sensitive assay, TnI-Ultra, has better analytic performance and has the potential to detect myocardial injury earlier than the current cTnI assay.
Cardiac troponins I and T have a central role in the diagnosis and management of patients with suspected acute coronary syndrome (ACS). The biochemical diagnosis of myocardial infarction (MI) is defined by troponin status. In addition, troponin provides valuable information for assessing the risk of recurrent ischemic events and for guiding therapeutic decisions. The analytic performance of troponin assays, in particular their sensitivity, has improved significantly since their initial clinical implementation. The European Society of Cardiology (ESC) and the American College of Cardiology (ACC) jointly recommend using a diagnostic cut point at the 99th percentile of the reference population with an optimal coefficient of variation (CV) of less than or equal to 10%. Thus, the threshold for myocardial injury has been continually redefined as assay performance has improved, in conjunction with data demonstrating important clinical implications of increased concentrations of troponin in patients with suspected ACS.
Current troponin testing has limitations, including antibody specificity, assay imprecision, lack of standardization, and the relatively late increase in the circulating troponin level after the onset of ischemia. Studies of first- and second-generation assays have shown lower diagnostic sensitivity of troponin when measured early (<6 hours) after symptom onset. As such, patients seeking care early in the course of the myocardial injury, so called early presenters, will often have undetectable levels of troponin on initial evaluation, but will later have a positive troponin result. Early presenters carry a similar or worse prognosis compared with patients who have detectable troponin levels at initial examination. Given the central clinical goal of rapid triage for patients with chest pain syndromes and the potential benefits of early intervention, this delay in a detectable rise in the troponin level has led to interest in its combined use with "early markers" of necrosis such as myoglobin or fatty acid binding protein. However, it is possible that improvements in the early sensitivity of troponin would obviate the need for additional, potentially duplicative, biomarkers of necrosis.
We thus evaluated the potential of a newly available more sensitive assay for troponin I (TnI-Ultra, Siemens Medical Solutions, Diagnostics Division, Tarrytown, NY) to improve early detection of myocardial injury in patients whose serial cardiac TnI (cTnI) testing revealed an initially negative cTnI result followed by a positive cTnI result in at least 1 of the subsequently collected specimens.
Abstract and Introduction
Abstract
Cardiac troponins are important biochemical markers for defining the presence of myocardial injury. However, limitations in troponin testing exist, including the relatively late increase in troponin after onset of ischemia. We therefore evaluated a more sensitive troponin assay for detection of myocardial injury in "early presenters." Discarded serial specimens were obtained from 103 patients who had a negative cardiac troponin I (cTnI) result followed by a positive cTnI result. Results were obtained using our current cTnI method and a new more sensitive assay, TnI-Ultra (Siemens Medical Solutions, Diagnostics Division, Tarrytown, NY). Medical records were reviewed to determine the clinical diagnosis. Precision studies yielded a 10% coefficient of variation at the diagnostic cut points for cTnI (0.10 ng/mL [0.10 μg/L]) and TnIUltra (0.04 ng/mL [0.04 μg/L]). TnI-Ultra was positive before cTnI in 66 (64.1%) of 103 cases. We conclude that the more sensitive assay, TnI-Ultra, has better analytic performance and has the potential to detect myocardial injury earlier than the current cTnI assay.
Introduction
Cardiac troponins I and T have a central role in the diagnosis and management of patients with suspected acute coronary syndrome (ACS). The biochemical diagnosis of myocardial infarction (MI) is defined by troponin status. In addition, troponin provides valuable information for assessing the risk of recurrent ischemic events and for guiding therapeutic decisions. The analytic performance of troponin assays, in particular their sensitivity, has improved significantly since their initial clinical implementation. The European Society of Cardiology (ESC) and the American College of Cardiology (ACC) jointly recommend using a diagnostic cut point at the 99th percentile of the reference population with an optimal coefficient of variation (CV) of less than or equal to 10%. Thus, the threshold for myocardial injury has been continually redefined as assay performance has improved, in conjunction with data demonstrating important clinical implications of increased concentrations of troponin in patients with suspected ACS.
Current troponin testing has limitations, including antibody specificity, assay imprecision, lack of standardization, and the relatively late increase in the circulating troponin level after the onset of ischemia. Studies of first- and second-generation assays have shown lower diagnostic sensitivity of troponin when measured early (<6 hours) after symptom onset. As such, patients seeking care early in the course of the myocardial injury, so called early presenters, will often have undetectable levels of troponin on initial evaluation, but will later have a positive troponin result. Early presenters carry a similar or worse prognosis compared with patients who have detectable troponin levels at initial examination. Given the central clinical goal of rapid triage for patients with chest pain syndromes and the potential benefits of early intervention, this delay in a detectable rise in the troponin level has led to interest in its combined use with "early markers" of necrosis such as myoglobin or fatty acid binding protein. However, it is possible that improvements in the early sensitivity of troponin would obviate the need for additional, potentially duplicative, biomarkers of necrosis.
We thus evaluated the potential of a newly available more sensitive assay for troponin I (TnI-Ultra, Siemens Medical Solutions, Diagnostics Division, Tarrytown, NY) to improve early detection of myocardial injury in patients whose serial cardiac TnI (cTnI) testing revealed an initially negative cTnI result followed by a positive cTnI result in at least 1 of the subsequently collected specimens.
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