However, despite a robust evidence base supporting their routine measurement in ACS, troponins have several important limitations. In particular, because of troponins’ relative large size and location bound within the contractile apparatus of the cardiomyocyte, troponin release is typically delayed for several hours after the onset of ischemic injury. Thus, blood must be sampled at least 6 h after the onset of ischemic discomfort in order to achieve adequate sensitivity. As such, for a large number of patients without classic symptomatology or electrocardiographic changes, significant irreversible myocardial injury might occur before a definitive therapeutic plan is implemented. In addition, troponin levels might remain elevated for 7 to 14 days after the initial ischemic insult, thereby limiting sensitivity for detecting recurrent myocardial injury. Importantly, because current troponin assays are unable to detect ischemia in the absence of necrosis, troponins are unable to identify patients with unstable angina who are at increased risk of adverse outcomes and who might benefit from specific treatment strategies. Finally, it is increasingly recognized that, among hospitalized patients, a substantial proportion of elevated troponin levels are caused by conditions other than ACS (2). Troponins, although specific for myocardial necrosis, are by no means specific for acute plaque rupture leading to ischemic injury.