The separation of a diagnosis ofNSTEMI from unstable angina is dependent on the ability to show myocardial necrosis. Cardiac troponin T (cTnT) and cardiac troponin I (cTnl) are ideal biochemical markers for detection of myocardial necrosis owing to their high sensitivity and specificity and their wide time window (i.e., there is a long duration of elevated plasma levels after myocardial damage). These properties make the troponins especially suitable for detection of quantitatively small amounts of myocardial damage in unstable patients. However, it is important to remember that an elevated level oftroponin in blood signals only that myocardial damaged has occurred and does not indicate the cause of the damage. A number of other possible reasons for myocardial damage besides ischemia owing to a thrombotic or embolic occlusion of a coronary artery (Table 1) must be considered, and, thus, an abnormal troponin result must be interpreted in light of the clinical picture, rather than the other way around.
The introduction of troponins as part of the diagnostic arsenal has revealed that patients with NSTEACS have myocardial damage more frequently than previously thought, although in many cases the damage is quantitatively small. With the use of second- and third-generation troponin assays, with their increased diagnostic sensitivity, myocardial damage
is detected in an even higher proportion of NSTEACS patients (Fig. 2). Moreover, adoption of the new European Society of Cardiology/American College of Cardiology (ESC/ ACC) criteria for the diagnosis of acute MI (AMI) (8) using cTnT or cTnl and low decision limits has led to a shift in diagnoses among patients with NSTEACS from unstable angina to (NSTE) AMI, with an increase of 20-30% in the number of AMI diagnoses (9).
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