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PARADIGM SHIFT OF CARDIAC TROPONINS Until recently, cardiac troponins (troponin I and T) have been considered markers of myocardial necrosis, especially in the setting of acute coronary syndromes (ACS). Current percutaneous coronary intervention (PCI) guidelines also give a class I recommendation for the measurement of cardiac biomarkers including troponins in ACS patients who underwent PCI. However, more recent observations that very low levels of troponins are found circulating in patients with stable coronary artery disease (CAD), and even in the general population, has changed this paradigm. Alternative mechanisms for low-level troponin release have thus been advocated, including physiological cell turnover and cardiomyocyte apoptosis. Hence, troponin fragments after a short period of myocardial ischemia could be compatible with the chronic and lowgrade evaluations of cardiac troponins in patients with stable CAD and even in the general population (Figure 1). Using the conventional assays, troponin can be detected in 0.7% of the population. In contrast, the novel high-sensitivity troponin assay allows for the detection of troponin at levels far below previous detection limits, and permits not only the accurate diagnostic information, but also the prognostic value of circulating cardiac troponins in a variety of clinical settings. Using this novel assay, troponin levels below the conventional limit of detection have recently been shown to predict cardiovascular events and death in persons with congestive heart failure, CAD and in the general population. In the acute clinical settings, an early invasive strategy for patients with acute coronary syndrome has been shown to be of benefit only among patients with elevated troponin I concentrations. Meanwhile, it remains uncertain whether the use of high-sensitivity troponin assays facilitates the diagnostic and prognostic value in patients with stable CAD.

Prognostic impact of cardiac troponin T in patients with stable coronary artery disease and diabetes