New or presumably new LBBB has been considered a STEMI equivalent. Most cases of LBBB at time of presen- tation, however, are not known to be old because of prior electrocardiogram (ECG) is not available for comparison. New or presumably new LBBB at presentation occurs infre- quently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation.8 Criteria for ECG diagnosis of acute STEMI in the setting of LBBB have been proposed (see Online Data Supplement 1). Baseline ECG abnormalities other than LBBB (eg, paced rhythm, LV hypertrophy, Brugada syndrome) may obscure interpretation. In addition, ST depression in 2 precor- dial leads (V1 V4) may indicate transmural posterior injury; multilead ST depression with coexistent ST elevation in lead aVR has been described in patients with left main or proximal left anterior descending artery occlusion.9 Rarely, hyperacute T-wave changes may be observed in the very early phase of STEMI, before the development of ST elevation. Transtho- racic echocardiography may provide evidence of focal wall motion abnormalities and facilitate triage in patients with ECG findings that are difficult to interpret. If doubt persists, immediate referral for invasive angiography may be necessary to guide therapy in the appropriate clinical context.10,11 Car- diac troponin is the preferred biomarker for diagnosis of MI. In 2009, approximately 683000 patients were discharged from US hospitals with a diagnosis of acute coronary syndrome (ACS). Community incidence rates for STEMI have declined over the past decade, whereas those for non ST-elevation ACS have increased (Figure 1). 