Background: The presence of pathological Q waves in the infarct leads on the surface electrocardiogram in an ST-elevation acute myocardial infarction indicates myocardial necrosis. Clinically it might be difficult to ascertain the onset of acute myocardial infarction. Our aim was to assess whether the presence or absence of Q waves at presentation could be used as an indicator of the duration of acute myocardial infarction and predict mortality. Methods: 15 222 patients with ST-elevation acute myocardial infarction and normal intraventricular conduction were randomly assigned streptokinase and aspirin plus bivalirudin or unfractionated heparin in the HERO-2 trial; randomisation did not alter 30-day mortality. 10 244 patients(67%) had Q waves in the infarct territory at the time of randomisation, and 4978(33%) did not. The primary endpoint was 30-day mortality. Findings: There were more deaths at 30 days in patients with initial Q waves than in those without(1044[10%] vs 344[7%], p< 0.0001). These findings were similar in patients with a first acute myocardial infarction and when stratified by time to randomisation(0-2, >2-4, >4 h) and by acute myocardial infarction location(anterior or inferior). Both the presence of initial Q waves and time to randomisation were positive univariate predictors, but only the presence of initial Q waves independently predicted 30-day mortality on multivariate analysis(adjusted OR 1.44, 95%CI 1.25-1.65 with clinical indices, and 1.31, 1.12-1.54 with clinical plus ST indices included as predictors). Interpretation: The presence of Q waves in the infarct leads at presentation of ST-elevation acute myocardial infarction independently predicts higher 30-day mortality in patients treated with fibrinolytic therapy. Therefore, a more aggressive approach to reperfusion might be warranted in these patients. Background: The presence of pathological Q waves in the infarct leads on the surface electrocardiogram in an ST-elevation acute myocardial infarction indicates myocardial necrosis. Clinically it might be difficult to ascertain the onset of acute myocardial infarction. Our aim was to assess whether the presence or absence of Q waves at presentation could be used as an indicator of the duration of acute myocardial infarction and predict mortality. Methods: 15 222 patients with ST-elevation acute myocardial infarction and normal intraventricular conduction were randomly assigned streptokinase and aspirin plus bivalirudin or unfractionated heparin in the HERO-2 trial; randomisation did not alter 30-day mortality. 10 244 patients (67%) had Q waves in the infarct territory at the time of randomisation, and 4978 (33%) did not. The primary endpoint was 30-day mortality. Findings: There were more deaths at 30 days in patients with initial Q waves than in those without (1044 [10%] vs 344 [7%], p <0.0 001). These findings were similar in patients with a first acute myocardial infarction and when stratified by time to randomisation (0-2,> 2-4,> 4 h) and by acute myocardial infarction location (anterior or inferior). Both the presence of initial Q waves and time to randomisation were positive univariate predictors, but only the presence of initial Q waves based predicted 30-day mortality on multivariate analysis (adjusted OR 1.44, 95% CI 1.25-1.65 with clinical indices, and 1.31, 1.12 -1.54 with clinical plus ST indices included as predictors). Interpretation: The presence of Q waves in the infarct leads at presentation of ST-elevation acute myocardial infarction independent predicts higher 30-day mortality in patients treated with fibrinolytic therapy. Therefore, a more aggressive approach to reperfusion might be warranted in these patients.