title: Differences in intravascular ultrasound and histological findings in culprit coronary plaques between ST-segment elevation myocardial infarction and stable angina.
abstract: A comprehensive evaluation of culprit coronary lesions may help to understand vulnerable plaques responsible for ST-segment elevation myocardial infarction (STEMI). We compared intravascular ultrasound (IVUS) and histological findings in culprit coronary plaques from 94 patients with STEMI (n = 54) or stable angina (n = 40). Tissue specimens were obtained by directional coronary atherectomy and IVUS was performed before percutaneous coronary intervention. IVUS and histological data were analyzed. Clinical characteristics were largely similar between the two groups. Plaque rupture and thrombi were more frequently found in the STEMI group than in the stable angina group. There were no significant differences between plaque types or proximal and distal reference measurements in the two groups. However, the site of minimal lumen area had a greater vessel area, remodeling index, and plaque burden with lesser lumen area in the STEMI group than in the stable angina group. Plaque areas immunopositive for CD68 and CD31 were significantly larger in the STEMI group, while the area immunopositive for α-smooth muscle actin was larger in the stable angina group. In conclusion, culprit lesions in STEMI patients showed a greater plaque burden, remodeling index, and more frequent thrombi with increased inflammation and neovascularization compared to the stable angina group, supporting the current concept of vulnerable plaques being responsible for STEMI.
authors.affiliation: Department of Medicine, University of Ulsan, Seoul, Korea.
authors.forename: Cheol Whan
authors.initials: CW
authors.lastname: Lee
authors.forename: Ilseon
authors.initials: I
authors.lastname: Hwang
authors.forename: Chan-Sik
authors.initials: CS
authors.lastname: Park
authors.forename: Hyangsin
authors.initials: H
authors.lastname: Lee
authors.forename: Duk-Woo
authors.initials: DW
authors.lastname: Park
authors.forename: Soo-Jin
authors.initials: SJ
authors.lastname: Kang
authors.forename: Seung-Whan
authors.initials: SW
authors.lastname: Lee
authors.forename: Young-Hak
authors.initials: YH
authors.lastname: Kim
authors.forename: Seong-Wook
authors.initials: SW
authors.lastname: Park
authors.forename: Seung-Jung
authors.initials: SJ
authors.lastname: Park
mesh_terms: D000199:Actins / Q000378:metabolism; D000368:Aged; D060050:Angina, Stable / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D062645:Percutaneous Coronary Intervention; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D018084:Ultrasonography, Interventional; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C067980:CD68 antigen, human; D000097382:CD68 Molecule