Background: Inflammation is a significant factor contributing to atherosclerotic plaque development. Several inflammatory markers have been used to detect high risk patients with acute phase of ischemic heart disease. Recently, the long pentraxin family member, pentraxin 3 (PTX3) has been reported to be a significant predictor for clinical outcome in patients with acute coronary syndrome (ACS). However, the relationship between PTX3 and coronary plaque components has not been fully clarified. We tried to investigate the difference of plaque morphologies on intravascular ultrasound (IVUS) in ACS lesions among with elevating PTX3 or without. Methods: Eighteen target lesions in 18 ACS patients (ST-elevation MI (STEMI); 17 patients, non-STEMI; 1 patients), who underwent preintervention virtual histology (VH) - IVUS, were investigated. PTX3 was collected from all patients before percutaneous coronary intervention. The lesions were divided into two groups; group A with PTX3 ≥ 4ng/ml and group B with PTX3<4ng/ml. The differences of plaque morphologies on VH-IVUS were evaluated between the two groups. The presence of thin-cap fibroatheromas (TCFA), defined as a necrotic core ≥ 10% of plaque area at the minimal lumen area site without overlying fibrous tissue in the presence of >40% plaque burden characteristic. The presence of echo signal attenuation (EA) on IVUS, which recently has been reported to be related with no-reflow after PCI, was defined as atherosclerotic plaque showing ultrasound signal attenuation without very high intensity echo reflectors. Results: An elevation of PTX3 (≥4.0ng/ml) was detected in 10 lesions (55.6%). Lesion vessel area (20.1±3.3mm 2 vs. 14.8±4.9mm 2 , p<0.01) and plaque volume (312±118mm 3 vs. 200±93mm 3 , P<0.05) was significantly greater in group A than group B. Remodeling index was not significant but tended to be higher in lesion with group A than group B (1.19±0.19 vs. 1.06±0.17, p=0.13). The frequency of EA (60.0% vs. 0.0%, p<0.05) and TCFA (50.0% vs. 0 %, p<0.05) was significantly higher in lesions with group A than group B. Conclusions: In ACS lesions, pentraxin 3 might be a significant predictor for the presence of large amount of unstable and vulnerable plaque compositions, which might lead to a poor clinical outcome after PCI.