Some plaques lead to ST-segment elevation myocardial infarction (STEMI), whereas others cause non-ST-segment elevation acute coronary syndrome (NSTEACS). We used angiography and intravascular ultrasound (IVUS) to investigate the difference of culprit lesion morphologies in ACS.Consecutive 158 ACS patients whose culprit lesions were imaged by preintervention IVUS were enrolled (STEMI=81; NSTEACS=77). IVUS and angiographic findings of the culprit lesions, and clinical characteristics were compared between the groups.There were no significant differences in patients' characteristics except for lower rate of statin use in patients with STEMI (20% vs 44%, p=0.001). Although angiographic complex culprit morphology (Ambrose classification) and thrombus were more common in STEMI than in NSTEACS (84% vs 62%, p=0.002; 51% vs 5%, p<0.0001, respectively), SYNTAX score was lower in STEMI (8.6±5.4 vs 11.5±7.1, p=0.01). In patients with STEMI, culprit echogenicity was more hypoechoic (64% vs 40%, p=0.01), and the incidence of plaque rupture, attenuation and “microcalcification” were significantly higher (56% vs 17%, p<0.0001; 85% vs 69%, p=0.01; 77% vs 61%, p=0.04, respectively). Furthermore, the maximum area of ruptured cavity, echolucent zone and arc of microcalcification were significantly greater in STEMI compared with NSTEACS (1.80±0.99mm 2 vs 1.13±0.86mm 2 , p=0.006; 1.52±0.74mm 2 vs 1.21±0.81mm 2 , p=0.004; 99.9±54.6° vs 77.4±51.2°, p=0.01, respectively). Quantitative IVUS analysis showed that vessel and plaque area were significantly larger at minimum lumen area site (16.6±5.4mm 2 vs 14.2±5.5mm 2 , p=0.003; 13.9±5.1mm 2 vs 11.6±5.2mm 2 , p=0.003, respectively).Morphological feature (outward vessel remodeling, plaque buildup and IVUS vulnerability of culprit lesions) might relate to clinical presentation in patients with ACS.