title: Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries.
abstract: -Retrospectively, plaque rupture is often colocalized with inflammation of the cap and shoulder of the atherosclerotic plaque. Local inflammation is therefore considered a potential marker for plaque vulnerability. However, high specificity of inflammation for plaque rupture is a requisite for application of inflammation markers to detect rupture-prone lesions. The objective of the present study was to investigate the prevalence and distribution (local versus general) of inflammatory cells in nonruptured atherosclerotic plaques. The cap and shoulder of the plaque were stained for the presence of macrophages and T lymphocytes in 282 and 262 cross sections obtained from 74 coronary and 50 femoral arteries, respectively. From most cases, 2 atherosclerotic arteries were studied to gain insight into the local and systemic distribution of the inflammatory process. In 45% and 41% of all cross sections, staining for macrophages was observed in the femoral and coronary arteries, respectively. Rupture of the fibrous cap was observed in 2 femoral and 3 coronary artery segments and was always colocalized with inflammatory cells. At least 1 cross section stained positively for CD68 or acid phosphatase in 84% and 71% of all femoral and coronary arteries, respectively. Only 1 femoral and 6 coronary arteries revealed a positive stain for CD68 in all investigated segments. Inflammation of the cap and shoulder of the plaque is a common feature, locally observed, in atherosclerotic femoral and coronary arteries. The high prevalence of local inflammatory responses should be considered if they are used as a diagnostic target to detect vulnerable, rupture-prone lesions.
authors.affiliation: Departments of Cardiology, Utrecht University Hospital, Utrecht, The Netherlands. g.pasterkamp@hli.azu.nl
authors.forename: G
authors.initials: G
authors.lastname: Pasterkamp
authors.forename: A H
authors.initials: AH
authors.lastname: Schoneveld
authors.forename: A C
authors.initials: AC
authors.lastname: van der Wal
authors.forename: D J
authors.initials: DJ
authors.lastname: Hijnen
authors.forename: W J
authors.initials: WJ
authors.lastname: van Wolveren
authors.forename: S
authors.initials: S
authors.lastname: Plomp
authors.forename: H L
authors.initials: HL
authors.lastname: Teepen
authors.forename: C
authors.initials: C
authors.lastname: Borst
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001161:Arteriosclerosis / Q000473:pathology*; D001167:Arteritis / Q000473:pathology*; D003324:Coronary Artery Disease / Q000473:pathology*; D005260:Female; D005263:Femoral Artery / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D017493:Leukocyte Common Antigens / Q000032:analysis; D008264:Macrophages / Q000737:chemistry / Q000473:pathology; D008297:Male; D012422:Rupture, Spontaneous; D000097382:CD68 Molecule
chemical_list: D000135:Acid Phosphatase; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017493:Leukocyte Common Antigens; C067980:CD68 antigen, human; D000097382:CD68 Molecule