title: Comparison of ruptured coronary plaques in patients with unstable and stable clinical presentation.
abstract: It remains uncertain why some plaque ruptures trigger acute coronary syndrome (ACS), whereas others do not. We investigated the anatomic features and tissue factor (TF) expression at the sites of plaque rupture in 42 patients presenting with ACS (n = 23) or stable angina (n = 19). Intravascular ultrasound examination was performed before directional coronary atherectomy. Specimens were stained with antibodies against TF, CD68 positive phagocytic cells, and smooth muscle cells; and intravascular ultrasound and immunohistochemistry results were compared. Baseline demographic and clinical characteristics, as well as vessel and lumen sizes at both reference and lesion sites, were comparable in the two groups. However, the remodeling index and plaque burden at lesion sites were significantly greater in the ACS than in the stable angina group. The TF-immunopositive areas were significantly greater in the ACS than in the stable angina group (0.07%; IQR [0.02-0.16%] vs. 0.02%; IQR [0.01-0.05%], P = 0.022), whereas the proportions of CD68-positive and smooth muscle cell areas were similar. There was a significant correlation between areas positive for TF and those positive for CD68 (r = 0.83, P < 0.001). In conclusion, ruptured plaques in patients with ACS show stronger TF expression, a greater plaque burden, and a higher remodeling index than do plaques in those with stable angina, suggesting that both lesion morphology and local thrombogenicity are related to clinical symptoms after plaque rupture.
authors.affiliation: Department of Medicine, Asan Medical Center, University of Ulsan, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, Korea.
authors.forename: Cheol Whan
authors.initials: CW
authors.lastname: Lee
authors.forename: Chan-Sik
authors.initials: CS
authors.lastname: Park
authors.forename: Ilseon
authors.initials: I
authors.lastname: Hwang
authors.forename: Hyangsin
authors.initials: H
authors.lastname: Lee
authors.forename: Duk-Woo
authors.initials: DW
authors.lastname: Park
authors.forename: Su-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: D054058:Acute Coronary Syndrome / Q000209:etiology / Q000378:metabolism* / Q000473:pathology*; D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000378:metabolism / Q000473:pathology; D015703:Antigens, CD / Q000096:biosynthesis*; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology; D010586:Phagocytes / Q000378:metabolism / Q000473:pathology; D058226:Plaque, Atherosclerotic / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D012422:Rupture, Spontaneous; D013925:Thromboplastin / Q000096:biosynthesis*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D013925:Thromboplastin; C067980:CD68 antigen, human; D000097382:CD68 Molecule