Background: Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI). Objectives and Methods: We used pre- and post-intervention intravascular ultrasound (IVUS) to assess 310 coronary culprit lesions (Group I: 125 lesions in ST segment elevation MI vs. Group II: 185 lesions in non-ST segment elevation MI). Culprit lesions were identified by a combination of electrocardiogram, wall motion abnormalities (ventriculogram or echocardiogram), and coronary angiogram. IVUS findings included ruptured plaque (a cavity that communicated with the lumen with an overlying residual fibrous cap fragment), thrombus (discrete intraluminal filling defects), lipid-pool like image (a pooling of hypoechoic or echolucent material covered with a hyperechoic layer), hypoechoic plaque (less bright compared with the reference adventitia), and plaque prolapse (tissue extrusion through the stent strut at post-stenting). Results: Culprit lesions had larger external elastic membrane area (13.5짹4.9 mm2 vs. 11.9짹4.3 mm2, p=0.002), larger plaque plus media area (10.8짹4.4 mm2 vs. 9.1짹4.1 mm2, p=0.001) and plaque burden (78.7짹10.1% vs. 74.8짹12.0%, p=0.002), and culprit lesion site calcium arc was smaller (96짹90째 vs. 153짹114째, p=0.002) in Group I than in Group II. Culprit lesions were more predominantly hypoechoic in Group I than in Group II (62% vs. 40%, p<0.001). Culprit lesion plaque ruptures, lipid-pool like images, and thrombus were observed more frequently in Group I compared with Group II (46% vs. 29%, p=0.002, 39% vs. 25%, p=0.010, and 34% vs. 21%, p=0.006, respectively). Post-stenting plaque prolapse was observed more frequently in Group I compared with Group II (36% vs. 22%, p=0.008). Conclusions: Culprit lesions in ST segment elevation MI have more markers of plaque vulnerability (more plaque rupture and thrombus, and larger plaque mass) and higher frequency of plaque prolapse compared with lesions in non-ST segment elevation MI.