Updating an institutional chest pain algorithm
Thereby, c Tn T and I are organ specific, but not disease-specific markers.High-sensitivity and sensitive c Tn T and I assays exactly quantify the amount of cardiomyocyte injury.Several troponin-based strategies rely on serial hs-c Tn testing.Two of them, the 0/1h-algorithm and a 0/3h-algorithm, are currently recommended by the European Society of Cardiology (ESC) with a Class I recommendation.Absolute rather than relative hs-c Tn changes seem to be the best metric to differentiate MI from other causes of chest pain.
From a diagnostic perspective, it is highly inappropriate to label a patient as ‘c Tn-positive’, as this would lump together patients with only mildly elevated c Tn levels barely above the 99th percentile and an associated positive predictive value (PPV) for NSTEMI of only about 40–50% with patients with markedly elevated c Tn levels (e.g.
High-sensitivity cardiac troponin (hs-c Tn) assays have been used clinically in many countries throughout the world for years and complement detailed clinical assessment and the electrocardiogram in the early diagnosis of myocardial infarction (MI).
High-sensitivity cardiac troponin assays for the first time allow to precisely quantify cardiomyocyte injury around the 99th percentile and thereby substantially increase the accuracy for MI already for blood draws obtained at presentation to the emergency department (ED).
In case of a c Tn mismatch, contact the laboratory for ruling-out analytical interferences resulting in real but very rare ‘false-positive’ c Tn measurements (e.g.
troponin auto-antibodies affecting c Tn I or skeletal muscle disease affecting c Tn T The most important clinical advantage of the new, more-sensitive c Tn assays is their ability to substantially reduce the ‘troponin-blind’ interval in the first hours of an MI and thereby do allow for novel strategies to early rule-out or rule-in of NSTEMI.