High-Sensitivity Cardiac Troponin in Suspected MI
What are the key principles underlying the safe and effective use of high-sensitivity cardiac troponin (hs-cTn) in the emergency department (ED) in patients with suspected myocardial infarction (MI)?
The authors reviewed the existing data on the clinical use of hs-cTn in patients with suspected MI.
The most important clinical advantage of the new, more-sensitive cTn assays is their ability to substantially reduce the initial “troponin-blind” interval in the first hours after MI onset and to allow novel, rapid strategies for the early rule-out or rule-in of MI. It is important to highlight several aspects when applying troponin-based strategies in clinical practice. First, they should be used only in conjunction with full clinical assessment, including a pretest probability assessment to identify those patients at high risk who may not be suitable for early discharge. Second, these strategies should be considered triage strategies rather than definite diagnostic strategies, as additional imaging tests (e.g., invasive coronary angiography, stress testing, echocardiography, or computed tomography angiography) may be necessary for a definite diagnosis. Third, the percentage of patients eligible for rule-out or rule-in varies widely from 9.8% to 77% depending on the underlying algorithm, the cTn assay used, and the clinical setting including the prevalence of MI. Fourth, these strategies should only be applied after the initial electrocardiogram (ECG) has excluded ST-segment elevation MI since these high-risk patients need prompt identification based on the ECG and immediate reperfusion therapy without the need for cTn testing. Finally, to maximize utility, all triage strategies should be embedded in the local standard operating procedures of the ED.
The authors concluded that the clinical value of early rule-out algorithms for safe rule-out of MI is helping guide clinicians identifying patients at very low risk for MI and major adverse cardiac events.
This review suggests that hs-cTn assays improve and accelerate the early management of patients presenting with suspected MI and complements assessment using clinical signs and the ECG. The increased sensitivity reduces the ‘troponin-blind’ interval early after onset of MI and allows to substantially shorten timing of serial hs-cTn re-measurement. Furthermore, dynamic changes of hs-cTn during serial sampling help to distinguish ischemic from nonischemic causes of chest pain and mild troponin elevations. To maximize utility of hs-cTn assays in clinical practice, they should be embedded in an institutional standard operating procedure of the ED and in conjunction with a rapid triage algorithm enabling rapid and safe rule-out and, depending on which algorithm, also rule-in of MI within a few hours.
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