Abstract

Accurate identification of the cause of chest pain is a challenge to the emergency physician because a significant proportion of patients with acute coronary syndrome (ACS) present atypically. Cardiac troponins are the most sensitive and specific biochemical markers of myocardial damage, and are an important diagnostic tool in the evaluation of ACS. High-sensitivity troponins (hsTn) have been introduced in recent years, and have been shown to have increased accuracy in the diagnosis of acute myocardial infarction (AMI), both at presentation and upon early onset of chest pain. A combination of hsTn readings at presentation and at either 2 hours or 3 hours after the onset of symptoms increases the sensitivity of diagnosing AMI as compared to at presentation alone, and this combination may negate the need for other cardiac markers. The absolute change in hsTn 2 hours after presentation was also found to be useful in the diagnosis of AMI, but not the relative change. However, hsTn has lower specificity in comparison with traditional troponin, and its levels may be elevated even in certain non-ACS settings. The interpretation of troponin values in patients with chronic renal failure must also be done with caution, as their baseline may be elevated, even in the absence of an acute event. Given these pitfalls, the assessment of ACS must still be global, comprising clinical history, electrocardiogram changes, troponin increase, and/or a new wall-motion abnormality on echocardiogram or nuclear scan showing new loss of viable myocardium. High-sensitivity troponin also has a potential use in prognosticating atherosclerotic disease in chronic renal patients as well as population screening of cardiovascular risk factors, although these uses have not been well studied. Identification of patients with unstable angina without myocardial infarction also remains a challenge, as the sensitivity of cardiac troponin in this area remains moderate to low. However, new cardiac markers such as copeptin, ischemia-modified albumin, and heart-type acid binding protein, are still being studied and provide a window of hope in the diagnosis of unstable angina.

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