Abstract
After the introduction of troponin T (cTnT) and later troponin I (cTnI) as useful markers of myocardial necrosis,1 their testing has quickly redefined clinical cardiology. Indeed, the importance of troponin (cTn) for the diagnosis of myocardial injury has recently been reaffirmed in the ‘Universal Definition of Myocardial Infarction’: ‘if biomarkers have been measured … and are normal, the determinations of these take precedence over … imaging criteria’.2 This well illustrates that despite all technological developments in imaging techniques over the last two decades, cTn testing remains the gold standard for the identification of acute myocardial injury. There is, however, a potential weakness in cTn testing that is widely acknowledged: notwithstanding the superior accuracy of detecting myocardial injury, an elevated cTn concentration does not provide any insight into the mechanism of heart injury, and a broad differential diagnosis to explain cTn release in the absence of regional myocardial infarction (including cardiomyopathies, pulmonary embolism, renal failure, and even acute cerebral pathologies) should be routinely considered when using these valuable tests.2 While the foregoing differential diagnosis is well understood in the application of cTn in those with acute symptoms, what remains less well understood is the significance of cTn elevation—even at low levels—among ‘apparently well’ subjects. Providing some answer to this question, in a previous study, Wallace and colleagues demonstrated, in a population cohort, that measurable concentrations of cTnT were extremely uncommon, but, … *Corresponding author. Tel: +1 617 726 3443, Fax: +1 617 643 1620, Email: jjanuzzi{at}partners.org
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