Cardiac troponin elevations correlate with estimation of infarct size and risk of death; persistent elevation 72 to 96 hours after symptom onset may afford relevant information in this regard.164 Elevations of cardiac troponin can occur for multiple reasons other than MI. In these cases, there is often substantial risk of adverse outcomes, as troponin elevation indicates cardiomyocyte necrosis.181 3.4.4. CK-MB and Myoglobin Compared With Troponin Previously, CK-MB was used for early evidence of myocar- dial injury. Because myoglobin is a relatively small molecule, it is rapidly released from infarcted myocardium. CK-MB is much less sensitive for detection of myocardial injury than tro- ponin, and substantially more tissue injury is required for its detection. With the availability of cardiac troponin, CK-MB, myoglobin, and other diagnostic biomarkers are no longer CK-MB may be used to estimate MI size. Detection of MI after percutaneous coronary interven- tion (PCI) remains an area of controversy. Because of the increased sensitivity of cardiac troponin, the prognostic value associated with varying degrees of elevation remains unclear. See Online Data Supplements 5, 6, and 7 for additional information on cardiac injury markers. 3.5. Immediate Management 3.5.1. Discharge From the ED or Chest Pain Unit: Recommendations Class IIa 1. It is reasonable to observe patients with symptoms consistent with ACS without objective evidence of myocardial ischemia (nonischemic initial ECG and normal cardiac troponin) in a chest pain unit or te- lemetry unit with serial ECGs and cardiac troponin at (Level of Evidence: B) 2. It is reasonable for patients with possible ACS who have normal serial ECGs and cardiac troponins to have a treadmill ECG200 202 (Level of Evidence: A), stress myocardial perfusion imaging,200 or stress before discharge or within 72 hours after discharge. (Level of Evidence: B) 3. 